Micro 14-17

List the four major categories of nonspecific immunity

- inflammation - phagocytosis - fever - antimicrobial proteins

Maturation process of B cells

-develop in bone marrow -lymphocytes circulate blood, spleen, and lungs -adhere to binding sites and come into contact with antigens throughout life

List the four categories of acquired immunity, and provide examples of each.

1. Active natural immunity: This type of immunity is acquired naturally when the body is exposed to a pathogen and mounts an immune response. Examples include: - Getting infected with the chickenpox virus and developing immunity to future infections. - Contracting a bacterial infection and developing immunity to that specific bacteria. 2. Active artificial immunity: This type of immunity is acquired through deliberate exposure to a pathogen or its components, usually through vaccination. Examples include: - Receiving a flu vaccine to develop immunity against the influenza virus. - Getting vaccinated against measles to acquire immunity to the measles virus. 3. Passive natural immunity: This type of immunity is acquired naturally when an individual receives pre-formed antibodies from another source. Examples include: - A newborn receiving antibodies from their mother through breastfeeding, providing temporary protection against certain diseases. - Receiving antibodies through placental transfer during pregnancy, providing immunity to the fetus. 4. Passive artificial immunity: This type of immunity is acquired through the administration of pre-formed antibodies produced in another individual or animal. Examples include: - Receiving a tetanus shot after a puncture wound to provide immediate protection against tetanus. - Receiving immune globulin injections after exposure to hepatitis A to prevent infection.

Name three types of anti microbial proteins

1. Defensins: Defensins are small cationic peptides that are produced by various cells of the immune system, including neutrophils and epithelial cells. They have broad-spectrum antimicrobial activity and can kill a wide range of bacteria, fungi, and viruses. Defensins work by disrupting the microbial cell membrane and causing cell lysis. 2. Cathelicidins: Cathelicidins are a family of antimicrobial peptides that are produced by various cells, including immune cells such as neutrophils and macrophages. They exhibit antimicrobial activity against bacteria, fungi, and viruses. Cathelicidins work by disrupting microbial cell membranes, inhibiting microbial growth, and modulating the immune response. 3. Lysozyme: Lysozyme is an enzyme that is found in various body fluids, such as tears, saliva, and mucus, as well as in immune cells. It has antimicrobial activity against bacteria by breaking down the bacterial cell wall. Lysozyme hydrolyzes the bonds between the sugar residues in the peptidoglycan layer of the bacterial cell wall, leading to cell lysis and death.

Summarize the three lines of host defenses

1. First line- innate, nonspecific which includes: barriers to disease- physical, chemical, and genetic 2. Second-innate, nonspecific which includes: phagocytosis, inflammations, complement, interferon 3. Third- acquired, specific defenses which include: B and T lymphocyte

Characteristics of the 5 antibodies

1. IgM (Immunoglobulin M): - Structure: IgM is the largest antibody, consisting of five Y-shaped subunits connected by a central J chain. - Location: IgM is primarily found in the bloodstream and lymph fluid. - Function: IgM is the first antibody produced during the primary immune response. It is highly effective at activating complement proteins, which help to eliminate pathogens. - Role: IgM is crucial for the early recognition and neutralization of pathogens, especially bacteria. It is involved in the initiation of the immune response. 2. IgG (Immunoglobulin G): - Structure: IgG is the most abundant antibody in the bloodstream and tissues. It consists of two Y-shaped subunits connected by a hinge region. - Location: IgG is found in the bloodstream and can cross the placenta to provide passive immunity to the fetus. - Function: IgG is involved in long-term immunity and provides protection against bacterial and viral infections. It can neutralize toxins, opsonize pathogens for phagocytosis, and activate complement proteins. - Role: IgG plays a crucial role in secondary immune responses, providing memory and long-term immunity. 3. IgA (Immunoglobulin A): - Structure: IgA exists in two forms: IgA1 and IgA2. It is composed of two Y-shaped subunits connected by a J chain and a secretory component. - Location: IgA is primarily found in body secretions, such as saliva, tears, breast milk, and mucosal surfaces. - Function: IgA acts as the first line of defense against pathogens at mucosal surfaces. It can neutralize pathogens, prevent their attachment to host cells, and enhance local immune responses. - Role: IgA plays a crucial role in mucosal immunity and provides protection against respiratory, gastrointestinal, and genitourinary infections. 4. IgE (Immunoglobulin E): - Structure: IgE consists of two Y-shaped subunits

Outline the steps in inflammation

1. Injury and vasoconstriction 2. Vascular changes 3. Edema and pus formation 4. Scar and resolution

Discuss the qualities of an effective vaccine.

1. Low level of side effects 2. Protect against natural forms of the pathogen 3. Stimulate both antibody (B-cell) and cell (T-cell) mediated immune responses 4. Long-term lasting effects 5. Does not require boosters 6. Inexpensive, relatively long shelf-life, easy to administer

List the components of the mononuclear phagocyte system

1. Monocytes: These are circulating white blood cells that can differentiate into macrophages or dendritic cells. 2. Macrophages: These are large phagocytic cells that reside in tissues and play a key role in engulfing and destroying pathogens, dead cells, and debris. 3. Dendritic Cells: These are specialized antigen-presenting cells that capture and present antigens to T cells, initiating an immune response. 4. Langerhans Cells: These are dendritic cells found in the skin and mucosal tissues that play a role in skin immunity and antigen presentation. 5. Kupffer Cells: These are macrophages found in the liver that help in the clearance of bacteria, dead cells, and toxins. 6. Microglia: These are macrophages found in the central nervous system that act as the resident immune cells and play a role in maintaining brain homeostasis. 7. Osteoclasts: These are macrophage-like cells found in bones that are involved in bone remodeling and resorption. 8. Alveolar Macrophages: These are macrophages found in the lungs that help in the clearance of inhaled particles and pathogens. 9. Splenic Macrophages: These are macrophages found in the spleen that play a role in filtering the blood and removing old or damaged red blood cells. 10. Peritoneal Macrophages: These are macrophages found in the peritoneal cavity that help in the clearance of bacteria and debris. These components work together to form a network of cells that are involved in immune responses, tissue homeostasis, and pathogen clearance.

Name 6 types of blood cells that function in nonspecific immunity, and specify the most important function of each

1. Neutrophils: Neutrophils are the most abundant type of white blood cells and are the first responders to sites of infection. Their main function is phagocytosis, which involves engulfing and destroying bacteria and other pathogens. 2. Macrophages: Macrophages are large phagocytic cells that are present in tissues throughout the body. They engulf and destroy pathogens, dead cells, and debris. Macrophages also play a role in antigen presentation, initiating an immune response. 3. Natural Killer (NK) Cells: NK cells are a type of lymphocyte that can recognize and kill infected or cancerous cells. They release toxic substances that induce cell death in target cells. 4. Eosinophils: Eosinophils are involved in defending against parasitic infections and allergic reactions. They release toxic substances to kill parasites and are also involved in modulating the inflammatory response. 5. Basophils: Basophils are involved in allergic reactions and immune responses to parasites. They release histamine, which is responsible for the symptoms of allergies, and other chemical mediators of inflammation. 6. Mast Cells: Mast cells are similar to basophils and are primarily involved in allergic reactions. They release histamine and other inflammatory mediators in response to allergens. These blood cells work together to provide immediate defense against pathogens and initiate immune responses.

Identify two components of the first line of defense

1. Physical (Skin, Mucous membranes, Respiratory tract, Genitourinary tract, Resident microbiota) 2. Chemical (Sebaceous glands (secrete oil), tears (lysozyme) breaks down the peptidoglycan, sweat, low pH of our skin, high acidic environment in stomach acid, etc.)

Outline the natural history of disease

1. Susceptibility: In this stage, individuals are at risk of developing the disease but have not yet been exposed to the causative agent or risk factors. Factors such as genetics, age, sex, and environmental exposures can influence susceptibility. 2. Exposure: In this stage, individuals come in contact with the causative agent or risk factors that can lead to the development of the disease. Exposure can occur through various means, such as direct contact, inhalation, ingestion, or vector-borne transmission. 3. Latent period: After exposure, there is often a period of time where the disease remains asymptomatic or subclinical. This is known as the latent period. During this time, the causative agent may be replicating or causing cellular changes in the body, leading to the eventual development of symptoms. 4. Onset of symptoms: Once the latent period ends, individuals may start experiencing symptoms related to the disease. The specific symptoms depend on the type of disease and the affected body systems. Symptoms can range from mild to severe and can include pain, fever, fatigue, respiratory distress, and neurological manifestations, among others. 5. Clinical course: The clinical course of the disease refers to the progression of symptoms and their severity over time. It can include periods of improvement, exacerbation, or stability. Some diseases may follow a predictable course, while others may be more variable. 6. Complications: During the course of the disease, individuals may develop complications. Complications can be direct consequences of the disease or secondary to its treatment. These can include organ damage, infections, secondary illnesses, or adverse effects of medications. 7. Resolution or chronicity: The disease may resolve completely, leading to a return to normal health. Alternatively, it may beco

Name four body compartments that participate in immunity.

1. The *reticuloendothelial system (RES)* 2. The *extracellular fluid (ECF)*: spaces surrounding tissue cells 3. The *bloodstream* 4. The *lymphatic system*

Structure of B and T cell receptors

B and T cell receptors are specialized proteins that are crucial for the recognition and binding of antigens. While they have similar functions, there are differences in the structure and composition of B cell receptors (BCRs) and T cell receptors (TCRs). Here is an overview of the structure of BCRs and TCRs: B Cell Receptors (BCRs): 1. Immunoglobulin (Ig) Structure: BCRs are composed of membrane-bound immunoglobulin molecules. Immunoglobulins are also known as antibodies and have a Y-shaped structure. Each BCR consists of two identical heavy chains and two identical light chains that are linked by disulfide bonds. 2. Variable and Constant Regions: The BCR structure includes variable (V) regions and constant (C) regions. The V regions are responsible for antigen recognition and binding. The C regions provide structural stability and facilitate interactions with other immune cells and molecules. 3. Antigen-Binding Sites: The V regions of the heavy and light chains form the antigen-binding sites of the BCR. These regions contain hypervariable regions, also known as complementarity-determining regions (CDRs). The CDRs are responsible for recognizing specific antigenic epitopes. 4. Transmembrane Domain and Cytoplasmic Tail: The BCR also has a transmembrane domain that anchors the receptor to the B cell membrane. The cytoplasmic tail of the BCR is involved in signal transduction and interacts with intracellular signaling molecules. T Cell Receptors (TCRs): 1. TCR Complex: TCRs are composed of two chains: an α chain and a β chain. Each chain consists of a variable (V) region and a constant (C) region. TCRs are membrane-bound proteins that are associated with the CD3 complex, which is involved in signal transduction. 2. Variable and Constant Regions: The V regions of the α and β chains are responsible for antigen

Describe the major roles of T and B lymphocytes.

B-lymphocytes- production and activities of antibodies T-lymphocytes- cell mediated immunity

Severe Combined Immunodeficiency (SCID)

Both limbs of lymphocyte system are missing or defective; no adaptive immune response

Explain the role of cytotoxic T cell in apoptosis and list the potential targets of this process

Cytotoxic T cells (Tc cells), also known as CD8+ T cells, play a crucial role in inducing apoptosis, or programmed cell death, in target cells. This process is essential for eliminating infected, cancerous, or abnormal cells from the body. The role of cytotoxic T cells in apoptosis involves the following steps: 1. Recognition: Cytotoxic T cells are able to recognize specific antigens presented on the surface of target cells. These antigens are typically derived from foreign pathogens or abnormal proteins expressed by infected or cancerous cells. 2. Activation: When a cytotoxic T cell encounters a target cell displaying the specific antigen it recognizes, the T cell becomes activated. This activation involves the binding of the T cell receptor (TCR) to the antigen presented on the target cell, as well as additional co-stimulatory signals. 3. Effector functions: Once activated, cytotoxic T cells undergo a series of effector functions to initiate apoptosis in the target cell. - Secretion of cytotoxic molecules: Cytotoxic T cells release cytotoxic molecules, such as perforin and granzymes, which are stored in specialized granules called cytotoxic granules. Perforin creates pores in the target cell membrane, allowing the entry of granzymes into the target cell. - Induction of apoptosis: Granzymes enter the target cell through the perforin pores and initiate a caspase-dependent apoptotic pathway. Granzymes activate caspases, which are enzymes that play a key role in initiating and executing apoptosis. Caspases cleave various cellular components, leading to the dismantling of the target cell. - Fas ligand interaction: In some cases, cytotoxic T cells can also interact with target cells through the Fas-Fas ligand pathway. The binding of Fas ligand on the T cell to Fas receptors on the target cell triggers a signaling cas

What are the roles of two early epidemiologists of the modern era, Florence nightingale and John snow

Florence Nightingale contributed to epidemiology by emphasizing the importance of sanitary conditions in healthcare settings, while John Snow made significant contributions to the field by identifying the source of a cholera outbreak and challenging prevailing theories about disease transmission. Both Nightingale and Snow played crucial roles in advancing the understanding of disease patterns and prevention measures, laying the groundwork for modern epidemiology.

What's the role of the rare factor in hymolytic disease

Hemolytic disease of the newborn (HDN), also known as erythroblastosis fetalis, occurs when an Rh-negative mother carries an Rh-positive fetus. The rare factor in this disease refers to the presence of the Rh factor, an antigen found on the surface of red blood cells. If the mother is exposed to Rh-positive blood during pregnancy or childbirth, her immune system may produce antibodies against the Rh factor. In subsequent pregnancies with an Rh-positive fetus, these antibodies can attack and destroy the fetal red blood cells, leading to complications. To prevent HDN, Rh-negative mothers are given an injection of Rh immune globulin (RhIg) to prevent the production of Rh antibodies.

5 types of antibodies (immunoglobulins)

IgG, IgA, IgM, IgD, IgE

3 immune components causing cell lysis in type 2 hypersensitivity reactions

In type 2 hypersensitivity reactions, the immune system mistakenly recognizes and attacks healthy cells or tissues. This can occur through various mechanisms, including cell lysis. Here are three immune components that can contribute to cell lysis in type 2 hypersensitivity reactions: 1. Antibodies (IgG or IgM): In type 2 hypersensitivity reactions, antibodies, particularly IgG and IgM, can bind to antigens on the surface of target cells. This binding can trigger a series of immune responses that lead to cell lysis. Antibodies can activate the complement system, a group of proteins that can form pores in the cell membrane, leading to cell lysis by disrupting the cell's integrity and causing osmotic imbalances. 2. Complement System: The complement system plays a crucial role in type 2 hypersensitivity reactions and can contribute to cell lysis. When antibodies bind to antigens on the surface of target cells, they can activate the complement system through a process called complement fixation. This activation leads to the formation of membrane attack complexes (MACs) on the cell membrane, resulting in cell lysis. MACs create pores in the cell membrane, disrupting its integrity and causing the cell to lyse. 3. Natural Killer (NK) Cells: NK cells are a type of cytotoxic lymphocyte that can directly induce cell lysis. In type 2 hypersensitivity reactions, NK cells can be activated by antibody-dependent cell-mediated cytotoxicity (ADCC). Antibodies, such as IgG, can bind to antigens on the surface of target cells, marking them for destruction. NK cells recognize the bound antibodies through their Fc receptors and release cytotoxic substances, such as perforin and granzymes, that induce cell lysis.

Define marker, and discuss its importance in the second and third lines of defense.

Marker - extension on WBCs, "self" cells, and antigens that differentiate them from each other Important because when WBCs PRRs (Pathogen Recognition Receptor) comes into contact with "self" cells' "markers", the WBCs know to not destroy that cell. When WBCs PRRs come in contact with an antigen (pathogen), they identify the pathogen by contacting the pathogens "markers" or PAMPs (Pathogen Associated Molecular Pattern). Once the WBC recognizes the molecule to be an antigen (pathogen), it destroys the antigen (pathogen) thru phagocytosis.

Summarize the steps in phagocytosis, and describe the roles of PAMP's in this process

Phagocytosis is the process by which cells, such as macrophages and neutrophils, engulf and destroy foreign particles, such as bacteria and debris. The steps involved in phagocytosis are as follows: 1. Chemotaxis: The phagocytic cells are attracted to the site of infection or inflammation by chemical signals released by the invading microorganisms or damaged cells. 2. Recognition and attachment: The phagocytic cells recognize and bind to the foreign particles through specific receptors on their surface. These receptors can detect molecules on the surface of the foreign particles known as pathogen-associated molecular patterns (PAMPs). 3. Engulfment: The phagocytic cell extends its membrane around the foreign particle, forming a pocket called a phagosome. The phagosome then encloses the particle within the cell. 4. Phagosome maturation: The phagosome fuses with lysosomes, forming a phagolysosome. Lysosomes contain enzymes that can degrade the engulfed particle. 5. Degradation: The lysosomal enzymes within the phagolysosome break down the foreign particle into smaller molecules. 6. Killing and digestion: The degraded particles are destroyed and digested by the enzymes present in the phagolysosome. 7. Exocytosis: After digestion, the indigestible material is expelled from the cell through exocytosis. PAMPs, or pathogen-associated molecular patterns, are molecular structures found on the surface of pathogens that are recognized by phagocytic cells. These patterns can include molecules such as lipopolysaccharides, peptidoglycans, and flagellin, which are not typically found on the surface of host cells. Recognition of PAMPs by phagocytic cells triggers the immune response and initiates the process of phagocytosis. By recognizing PAMPs, phagocytic cells can differentiate between foreign pathogens and host cells, allo

Define point source,common source, and propagated epidemics, providing and indication of time frame for all 3.

Point source, common source, and propagated epidemics are terms used to describe different patterns of disease transmission in epidemiology. These patterns refer to how an infectious disease spreads within a population. 1. Point source epidemic: In a point source epidemic, a large number of people become infected with a disease after being exposed to a common source of infection within a relatively short period of time. The source of infection is usually a contaminated food or water source, or a shared exposure to a pathogen. The time frame for a point source epidemic is typically short, ranging from a few hours to a few days. Once the source of infection is identified and controlled, the number of new cases rapidly declines. 2. Common source epidemic: In a common source epidemic, a group of people are exposed to a common source of infection over a longer period of time, often through multiple exposures. The source of infection can be persistent, such as contaminated water supply or a continuous exposure to an infectious agent. The time frame for a common source epidemic can vary, lasting from days to weeks or even months. The number of new cases may peak and decline gradually as exposure to the common source is reduced or eliminated. 3. Propagated epidemic: In a propagated epidemic, the disease is transmitted from person to person, with each infected individual serving as a potential source of infection for others. The transmission occurs through direct contact, respiratory droplets, or vectors like mosquitoes. The time frame for a propagated epidemic is typically longer, lasting weeks to months or even years, as the infection spreads through the population. The number of cases may continue to increase over time until effective control measures, such as vaccination or isolation, are implemented. It is important to

Distinguish between primary and secondary immunodeficiencies

Primary Immunodeficiencies: 1. Genetic Origin: Primary immunodeficiencies, also known as inherited or congenital immunodeficiencies, are caused by genetic mutations or defects. These mutations are present from birth or are inherited from parents. 2. Onset: Primary immunodeficiencies are typically present from early childhood or infancy, although some may manifest later in life. 3. Nature: Primary immunodeficiencies are intrinsic to the immune system itself. They result from defects in specific components or functions of the immune system, such as B cells, T cells, phagocytes, complement system, or cytokines. 4. Types: There are over 400 known primary immunodeficiencies, each characterized by specific genetic defects and clinical manifestations. Examples include X-linked agammaglobulinemia, severe combined immunodeficiency (SCID), and common variable immunodeficiency (CVID). 5. Severity: The severity of primary immunodeficiencies can vary widely, ranging from mild to severe. Some primary immunodeficiencies may only affect specific branches of the immune system, while others can cause a global impairment of immune function. 6. Inheritance: Primary immunodeficiencies can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner, depending on the specific genetic mutation involved. 7. Treatment: Treatment options for primary immunodeficiencies may include immunoglobulin replacement therapy, antibiotic prophylaxis, stem cell transplantation, and gene therapy, depending on the specific disorder. Secondary Immunodeficiencies: 1. Acquired Causes: Secondary immunodeficiencies, also known as acquired immunodeficiencies, are not caused by genetic mutations but rather result from external factors or underlying medical conditions. 2. Onset: Secondary immunodeficiencies can develop at any age, depending on the

Connection between public health and epidemiology

Public health and epidemiology are closely connected fields that work together to improve the health of populations. Public health is a broad field that encompasses the efforts and strategies aimed at promoting and protecting the health of communities and populations. It focuses on preventing diseases, promoting healthy behaviors, and addressing social determinants of health. Public health professionals work in various areas such as health education, policy development, and community health promotion. Epidemiology is a specific discipline within public health that focuses on studying the patterns, causes, and effects of health and disease conditions in populations. Epidemiologists collect and analyze data to understand the distribution and determinants of diseases, as well as develop strategies for disease prevention and control. They investigate outbreaks, track disease trends, and inform public health policies and interventions. The connection between public health and epidemiology lies in the fact that epidemiology provides the scientific foundation for public health practice. Epidemiological studies provide crucial data and evidence that inform public health decision-making and interventions. Public health professionals rely on epidemiological findings to identify health risks, develop prevention strategies, and evaluate the impact of public health programs. In summary, epidemiology is a key component of public health, providing the necessary data and evidence for understanding disease patterns and developing effective interventions. Public health and epidemiology work hand in hand to improve the health of populations and prevent disease.

clonal selection and expansion

Selection = when a pathogen enters the body, it will select a particular lymphocyte that has a complementary binding site for expansion Expansion = the selected clone (the lymphocyte to which pathogen is bound) proliferates

Main function of the major T cell types and their subsets

T cells are a crucial type of white blood cell that coordinate and regulate the immune response. There are different types of T cells with specific functions: 1. Helper T cells (Th cells): Activate and assist other immune cells. Subsets include Th1, Th2, Th17, and Treg cells. 2. Cytotoxic T cells (Tc cells): Kill infected or abnormal cells. Subset includes CD8+ T cells. 3. Memory T cells: Long-lived cells that provide rapid and enhanced immune responses upon re-exposure to a pathogen. 4. Regulatory T cells (Tregs): Maintain immune tolerance and prevent excessive immune responses. 5. Natural Killer T cells (NKT cells): Have characteristics of T cells and natural killer cells, play a role in immune regulation and defense against infections and tumors.

Molecular basis for ABO blood groups

The ABO blood group system is determined by the presence or absence of specific antigens on the surface of red blood cells. These antigens are glycoproteins, meaning they consist of a protein core with attached carbohydrate molecules. The molecular basis for ABO blood groups lies in the different carbohydrate structures present on the antigens. 1. A antigen: Individuals with blood type A have the A antigen on their red blood cells. The A antigen is created by the addition of a specific carbohydrate molecule, N-acetylgalactosamine (GalNAc), to the protein core. This process is catalyzed by the enzyme A-transferase (also known as ABO gene product or ABO glycosyltransferase). 2. B antigen: Individuals with blood type B have the B antigen on their red blood cells. The B antigen is created by the addition of a different carbohydrate molecule, galactose, to the protein core. This process is catalyzed by the enzyme B-transferase (ABO gene product or B-transferase). 3. O antigen: Individuals with blood type O do not have either the A or B antigens on their red blood cells. This is because the O allele produces an inactive form of the ABO transferase enzyme, resulting in the absence of carbohydrate addition to the protein core. As a result, the O antigen is not formed. The ABO blood group system is determined by the inheritance of ABO alleles from both parents. There are three main alleles involved in ABO blood types: A, B, and O. The A allele produces the A-transferase enzyme, which adds GalNAc to the protein core, resulting in the A antigen. The B allele produces the B-transferase enzyme, which adds galactose to the protein core, resulting in the B antigen. The O allele produces an enzyme that is not functional, resulting in the absence of carbohydrate addition and the O antigen. The presence or absence of these antigens

Provide a clear distinction between correlation and causation

The article discusses the potential use of probiotics and prebiotics in the prevention and treatment of allergic diseases, such as asthma, eczema, and food allergies. It explains how these substances can modulate the immune system and improve gut health, leading to a reduction in allergic symptoms. The article also highlights the importance of early-life interventions and the potential of probiotics and prebiotics in reducing the risk of developing allergies later in life. It concludes that further research is needed to determine the optimal strains, doses, and duration of treatment for different allergic conditions.

Maturation of T cells

The maturation of T cells refers to the process by which immature T cells develop and acquire their functional characteristics in the thymus. T cell maturation involves several stages and is essential for the development of a diverse and properly functioning T cell repertoire. Here is an overview of the maturation process of T cells: 1. T Cell Precursor Entry: T cell precursors, also known as thymocytes, originate from hematopoietic stem cells in the bone marrow. Immature thymocytes migrate from the bone marrow to the thymus gland, where they undergo maturation. 2. Double-Negative (DN) Stage: In the thymus, thymocytes initially lack the expression of CD4 and CD8 co-receptors, making them "double-negative" (CD4-CD8-) cells. At this stage, they undergo rearrangement of their T cell receptor (TCR) genes to generate a diverse TCR repertoire. DN thymocytes progress through four sub-stages: DN1, DN2, DN3, and DN4. 3. β-Selection: During the DN3 stage, thymocytes undergo β-selection, which involves the rearrangement of the TCR β-chain genes. This process generates a functional pre-TCR complex composed of a TCR β-chain, pre-Tα chain, and CD3 proteins. Successful β-selection leads to the expression of CD4 and CD8 co-receptors and the transition to the double-positive (DP) stage. 4. Double-Positive (DP) Stage: DP thymocytes express both CD4 and CD8 co-receptors. They undergo positive and negative selection processes, which determine their fate based on their ability to recognize self-antigens presented by major histocompatibility complex (MHC) molecules. 5. Positive Selection: DP thymocytes are exposed to self-antigens presented by MHC molecules on thymic epithelial cells. Thymocytes with TCRs that can weakly interact with self-MHC molecules receive survival signals and undergo positive selection. Positive selection e

Identify the primary difference between the practice of medicine and epidemiology

The primary difference between the practice of medicine and epidemiology is their focus and scope. medicine focuses on the diagnosis and treatment of individual patients, epidemiology focuses on studying and improving the health of populations.

herd immunity

The resistance of a group to an attack by a disease to which a large proportion of the members of the group are immune

Fully describe the structure and function of the lymphatic system

The structures of the lymphatic system include the lymph fluid in lymph vessels, and the lymph organs. Collections of lymph nodes exist in the cervical, axillary, thoracic, inguinal, and mucosal areas of the body. The function of the lymphatic system includes: surveillance, recognition of antigens, destruction of antigens, and the memory of the encounter with the antigen - called "immunity" to disease. Provide return of extracellular fluid to the cardiovascular system. Also acts as a drain-off system for the inflammatory response.

Four major categories of hypersensitivity or overreaction to antigens

There are four major categories of hypersensitivity reactions, also known as overreactions to antigens. These categories are classified as Type I, Type II, Type III, and Type IV hypersensitivity reactions. 1. Type I Hypersensitivity (Immediate Hypersensitivity): Type I hypersensitivity reactions are immediate allergic responses mediated by the immune system. They occur within minutes to hours after exposure to an antigen (allergen). The antigen triggers the activation of IgE antibodies, which bind to mast cells and basophils. Upon subsequent exposure to the antigen, these antibodies cause the release of inflammatory mediators, such as histamine, leading to symptoms like itching, swelling, hives, and in severe cases, anaphylaxis. Examples include allergic asthma, hay fever, and food allergies. 2. Type II Hypersensitivity (Cytotoxic Hypersensitivity): Type II hypersensitivity reactions involve the destruction of cells or tissues by antibodies. The antibodies, usually IgG or IgM, bind to antigens present on the surface of host cells, leading to their destruction through various mechanisms. This can include complement-mediated lysis, opsonization and phagocytosis, or antibody-dependent cell-mediated cytotoxicity (ADCC). Examples include autoimmune hemolytic anemia, Rh incompatibility, and drug-induced immune reactions. 3. Type III Hypersensitivity (Immune Complex-Mediated Hypersensitivity): Type III hypersensitivity reactions occur when there is an excessive formation of immune complexes composed of antigens and antibodies (usually IgG or IgM). These immune complexes can deposit in tissues, leading to the activation of complement and recruitment of inflammatory cells. The persistent immune complex deposition can cause tissue damage and inflammation. Examples include systemic lupus erythematosus (SLE), rheumatoi

3 conditions that can lead to the development of secondary immunodeficiency diseases

There are several conditions that can lead to the development of secondary immunodeficiency diseases. Here are three examples: 1. Human Immunodeficiency Virus (HIV) Infection: HIV is a viral infection that targets and weakens the immune system, specifically the CD4+ T cells. As the virus replicates and destroys these immune cells, the body becomes more susceptible to opportunistic infections and certain types of cancers. HIV infection can progress to acquired immunodeficiency syndrome (AIDS), a severe form of secondary immunodeficiency. 2. Chronic Diseases and Medical Conditions: Certain chronic diseases and medical conditions can impair the immune system and lead to secondary immunodeficiency. Examples include: - Diabetes: Poorly controlled diabetes can weaken the immune system, making individuals more prone to infections. - Chronic kidney disease: Kidney disease can affect the production and function of immune cells, increasing the risk of infections. - Liver disease: Advanced liver disease, such as cirrhosis, can disrupt immune system functions, making individuals more susceptible to infections. 3. Cancer and Cancer Treatments: Both cancer itself and certain cancer treatments can weaken the immune system. Cancer cells can evade immune recognition and suppression, impairing the body's ability to mount an effective immune response. Additionally, treatments such as chemotherapy, radiation therapy, and immunosuppressive medications used in transplantation can suppress the immune system, increasing the risk of infections. It's important to note that these are just a few examples of conditions that can lead to secondary immunodeficiency. There are many other factors, such as malnutrition, autoimmune diseases, certain medications, and aging, that can also contribute to the development of secondary immunodefici

Identify commonalities and differences between type 2 and type 3 hypersensitivities

Type 2 and type 3 hypersensitivities are both classified as immune-mediated hypersensitivity reactions, but they differ in their underlying mechanisms and the specific immune responses involved. Here are the commonalities and differences between type 2 and type 3 hypersensitivities: Commonalities: 1. Both type 2 and type 3 hypersensitivities are mediated by antibodies produced by B cells. 2. Both types of hypersensitivities can result in tissue damage and inflammation. 3. Both type 2 and type 3 hypersensitivities are considered delayed hypersensitivity reactions, meaning that the symptoms do not appear immediately after exposure to the antigen. Differences: 1. Mechanism of antibody involvement: - Type 2 hypersensitivity: In type 2 hypersensitivity, antibodies, typically IgG or IgM, bind to antigens present on the surface of target cells or tissues. This leads to activation of the complement system and destruction of the target cells through various mechanisms, including antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis by macrophages. - Type 3 hypersensitivity: In type 3 hypersensitivity, immune complexes are formed when excessive amounts of antigens and antibodies (typically IgG or IgM) bind together. These immune complexes can deposit in various tissues, leading to activation of complement and recruitment of inflammatory cells. The inflammation caused by immune complex deposition can result in tissue damage. 2. Timeframe of the immune response: - Type 2 hypersensitivity: The immune response in type 2 hypersensitivity reactions is relatively rapid, occurring within hours to days after exposure to the antigen. - Type 3 hypersensitivity: The immune response in type 3 hypersensitivity reactions is delayed compared to type 2 hypersensitivity, typically occurring within 1-3 weeks after exposur

Differentiate between whole blood, plasma, and serum

Whole Blood Plasma: Clear, Yellowish fluid - clotting Serum: The same as plasma except it contains no clotting factors. used in immune testing and therapy

How does arthus reaction differ from serum sickness?

arthus reaction is a local dermal injury due to inflamed blood vessels in the vicinity of any injected antigen while serum sickness is systemic injury initiated by antigen-antibody complexes that circulate in the blood and settle into membranes at various sites

Compare and contrast the three different complement pathways

classical- begins when antibody binds to microbial cells lectin- activated by mannans alternative- activated by bacterial or fungal cell wall, viruses, or parasite surfaces

Discuss the mechanism of fever and its role in nonspecific immunity

impedes the nurtition of bacteria by reducing the availability of iron. Increase metabolism and stimulates immune reactions

What the difference between incidence and prevalence

incidence measures the number of new cases of a disease in a population over a specified time period, while prevalence measures the total number of existing cases of a disease in a population at a given point in time or within a specific time period. Incidence focuses on new cases and risk, while prevalence provides information about the overall burden of the disease in the population.

Discuss the role of normal biota as a first-line defense mechanism.

its presence can block the access of pathogens to epithelial surfaces and can create unfavorable environment for pathogens by competing for limited nutrients or by altering pH

Differentiate between screening tests and diagnostic tests

screening tests aim to identify individuals who may be at risk of a disease, while diagnostic tests are used to confirm or rule out the presence of a disease in individuals with symptoms or signs. Screening tests are generally applied to asymptomatic individuals, while diagnostic tests are used in individuals with clinical indications of a specific disease.

Define immunopathology, and describe the two major categories of immune dysfunction.

the study of disease states associated with overreactivity or underreactivity of the immune response. - Overreactivity "hypersensitivity" - Immunodeficiency "hyposensitivity"