Ch 17 LO
Discuss the relative importance of humoral immunity and cellular immunity in host resistance to free viruses, toxins, extracellular bacteria, intracellular bacteria, or intracellular viruses (virus-infected cells), see Fig. 17.20.
Humoral immunity -directed at freely circulating pathogens and depends on B cells -involves antibodies, which are found in serum and lymph and are produced by B cells. Cellular immunity -control of intracellular pathogens or cells already infected by pathogen -depends on T cells to eliminate the intracellular pathogens -rejects foreign tissue recognized as nonself -destroys tumor cells-
Rank the five classes of antibodies in terms of their serum concentrations, see Table 17.
IgG: 80% IgA: 13% IgM: 6% IgD: 0.02% IgE: 0.002
Define T-cell receptor, MHC I, MHC II, effector T cell, memory T cell.
T cell receptor: help T cells to respond to antigens MHC I: are found on plasma membranes od mammalian nucleated cells; they ID the "self" cells preventing the immune system from attacking host cells MHC II: exist only on surface of antigen-presenting molecules (APC's )- including B cells effector T cell: perform a cellmediated function Memory T cell: provide a basis for a secondary immune response.
Describe antibody response to a T-independent antigen and to a T-dependent antigen, see Fig. 17.7 and Fig. 17.5.
T independent antigens stimulate the B cell to make antibodies without the aid of T helper cells. Activation of B cells to produce antibodies: -B cell receptors recognize and attach to antigen (ex extracellular antigen) -antigen is internalized into B cell -fragments of the antigen are presented on MHC proteins on the surface of the cell. -A T helper cell that recognizes this antigen fragment is activated and releases cytokines, activating the B cell. -The activated B cell begins clonal expansion, producing an army of antibody-producing plasma cells and memory cells.
Clinical applications (p. 491). Solve problem #1. A woman had life threatening salmonellosis that was successfully treated with anti-salmonella. why did this treatment work, when antibiotics and her own immune system failed?
The antigen( pathogen) was able to escape the innate immunity and had resistance to the antibiotics, but when her adaptive immunity recognized the pathogen, it was able to kill it.
Explain why lymph nodes swell during an infection.
They respond to an infection and activate B and T cells and TRAP microbes
. Recognize the variable region (V), constant region (C), Fab, Fc, antigen binding site, light chain, and heavy chain as shown in Fig. 17.4 and explain the significance of variability in the antigen binding site. 17
V: 2 sections located at the ends of the Y arms; bind to epitopes C: stem of antibody monomer and lower parts of arms of the Y Fab: Fc: stem of the Y shaped antibody monomer antigen binding site: Variability in antigen binding site is important because??
Explain why both innate and adaptive immunities are important in host resistance to microbial infections
they both attack microbes with both of these systems working then have a greater opportunity to kill the microbe
Clinical Case - It's just a scratch. Read the article and answer its questions.
What caused Mrs. Vasquez to die from disseminated intravascular coagulation and septic shock? Read on to find out. A: Describe the bacteria in the figure A: its a gram negative rod bacteria, there are other big gram negative cells, and white blood cells. the gram - was specifically Capnocytophaga canimorsus and is found in cats or dogs and can be transmitted through a scratch What molecules normally made by the b cells combat bacterial infections? A: IgM antibodies are made in response to bacterial infections. What steps are required for an antibody response to these antigens? A: immune response to antigens takes place primarily in the secondary lymphoid organs: lymph nodes, mucosa-associated lymphoid tissue, and spleen. During 1* immune response, pathogens and consituents are transported to these tissues, where the microbial antigens are presented to B cells that constantly leave and enter the 2* lymphoid organs . Why is the fact that the patient has no spleen important? A: because she contracted the bacteria and since her spleen had been removed some time before, she did not have the immune response necessary to combat the resulting deadly infection. (did not have the t, b and dendritic cells found in spleen)
Define seroconversion
a change in a person's response to an antigen in a serological test
Clinical applications (p. 491). Solve problem #3.
a patient with chronic diarrhea was found to lack IgA in his secretions, although he had a normal level of IgA serum. what was this patient found to be unable to produce. A: ???
Define antigen and epitope (antigenic determinant), see Fig. 17.2 and Fig. 17.4.
antigen: substances that cause production of antibodies epitope: antigenic determinant; specific regions on antigens that antibodies recognize
Explain what is responsible for the binding specificity of each different antibody.
epitopes???
Define immunity, innate immunity, and adaptive immunity
immunity: The ability to resist/protect innate immunity: (constitutive, nonspecific) immunity; Does not target a specific pathogen • Exists prior to exposure to a microbe or a microbial product adaptive immunity: (acquired, induced, specific) immunity; •Targets a specific pathogen/antigen •Develops only after exposure to a microbe or a microbial product; Adaptive/acquired •Is "remembered" (memory) •Is strengthened after repeated encounters
Define immunoglobulin and antibody. Draw a typical antibody molecule as shown in Fig. 17.4.
immunoglobin (Ig): antibodies antibodies: globular proteins; made in response to an antigen and can recognize and bind to the antigen.
Compare and contrast innate immunity and adaptive immunity.
innate: -responses are same regardless of pathogen -more immediate responses adaptive -responses target specific pathogens -defenses take few days to develop -can differentiate between "self cells" and non "self"
Define cytokine and name two specific cytokines.
•Small proteins -chemical messengers •Produced and secreted by cells in response to stimuli •Regulation of immune responses of different cell types (as a "messenger" or "regulator") -small protein released from human cells that regulate the immune response; directly or indirectly may induce fever, pain, or T cell proliferation -interleukins( serve as communicators btween leukocytes) -chemokines ( induce migration of leukocytes into areas of infection or tissue damage)
Identify the components of the lymphatic system (Fig. 16.5) and assign one function to each.
lymphatic capillaries: permit interstitial fluid derived from blood plasma to flow into them but not out; converge to form vessels lymphatic vessels: lymph flows in one way movement lymph nodes: are found within vessels; site where T cells and B cells activate- immune response; phagocytosis of trapped microbes thoracic duct (left) and lymphatic duct (right): lymph eventually passes through these then onto subclavian veins (fluid becomes blood plasma) Thymus, bone marrow • Producing lymphocytes -Thymus: site of T cell maturation; contains dendritic cells and macrophages -bone marrow: site of B cell maturation; -Tonsils and Peyer's patches: protected against microbes that are ingested or inhaled -Spleen: contains lymphocytes and macrophages that monitor blood for microbes and secreted products such as toxins, much like lymph nodes monitor lymph - Asplenia - absence of spleen or its normal functions
List the types of cells and non-cell components involved in generation of specific immune responses.
- Immunogen (stimulates immune system) - T lymphocyte (helper or cytotoxic) - B lymphocyte - Antigens - Antibodies - Antigen processing cell or APC (macrophage, NOT NEUTROPHIL, dendritic cell, b cell) -presenting protein antigens -MHC(major histocompatibilitycomplex): - Proteins that are selfmarkers - Presentation of a processed antigen -cytokines
IgD
-.02% antibody serum -B cell surface, blood, lymph -serum function not known -presence on B cells functions in initiation of immune response
IgE
-0.002% antibody serum -bound to mast and basophil cells throughout body and blood -allergic reactions; possibly lysis of parasitic worms
IgA
-13% total antibody serumm -secretions: tears, mucus, intestine, milk, saliva, blood, lymph -local protection on mucosal surface
IgM
-6 % total antibody serum -blood, lymph, B-cell surface -effective against microorganisms and agglutination of antigens -1st antibodies produced in response to intial infection
IgG characteristics
-80% total serumm antibody -location: blood, lymph, intestine -placental transfer -protects fetus and newborn -enhances phagocytosis (opsonin) -neutralizes toxins and viruses
Watch the animation on immune responses to rhinovirus infection at https://massasoit.instructure.com/courses/181005/pages/microflix-immunology?module_item_id=2296184
-cold caused by rhinovirus -virus escaped by 1st line of defenses: mucus and cilia -enter respiratory epithelial cells and replicate -In tissue fluids cells, cells of 2nd line of innate defense ex. dendritic cells carry out surveillance -dendritic cells engulf virus w/in endosome and that fuses with lysosome and lyzosymes digest virus into rhinovirus epitopes -then dendritic cell binds epitopes to presentation molecules called MHC-2 -then complex folds outwards sitting on membrane of dendritic cell -dendritic cell (innate immune system) then enters lymphatic vessel and travels to a lymph node and encounters a helper t cell (adaptive immune system) -TCR (t cell receptor) of t cell recognizes rhinovirus epitope while CD4 receptor of t cell recognnizes the MHC-2 -Dendritic cell thus stimulates activation of helper t cell Adaptive defenses (B cells and humoral immunity) -Adaptive defenses help control current infections and also provide immunity against future infections -carried out by b cells and t cells -immature b cells conduct surveilance of lymph nodes using b cell receptors to recognize one specific epitope - b cells whose receptors recognize epitopes are selected for activation in clonal selection -selected b cell takes in rhinovirus and degrades it and presents the virus to MHC -2 -mature helper t cell recognizes virus epitope with TCR and the MHC-2 with CD4 -helper t cells secretes cytokines (chemical messengers ) that activate b cell - b cell proliferates and differentiates in clonal expansion into either memory b cells or plasma cells -memory b cells carry memory of the pathogen -plasma cells secrete antibodies that conduct surveillance for more rhinoviruses grouping them together so they are easy targets for phagocytes -antibodies in blood and tissue fluids seek out free rhinoviruses (and other free pathogens) -antibodies (humoral defenses) neutralize the viruses by binding to surface molecules and thus prevent attachment to host cells T cells and cellular immunity -Cytotoxic t cell (tc cell) can locate and destroy rhinovirus infected cells; provides cell mediated immunity -TCR of tc cell is genetically programed to recognize rhinovirus epitope on MCH-1 of dendritic cell when presented and MCH-1 is recognize by CD8 glycoprotein -cytotoxic t cell (tc cell) is activated by cytokines released by helper t cell and then clonal expansion occurs differentiat into memory t cells and many active Cytotoxic cells (Ctl's) [they leave lymph vessel to search for infected cells that present the rhinovirus epitope with their MHC-1) -epitope is recognized by tcr of cytotoxic t cell and and MHC-1 recognized by tc cells's CD8 glycoprotein -tc cell secretes perforin molecules which form channels in infected cell's membrane -granzyme from tc cell passes through perforin channel and activated enzymes that lead to apoptosis cytotoxic t cell then moves on to look for other infected cells Summary of adaptive immunity -humoral and cellular defenses are the bodies 3rd line of defense in fighting a very specific pathogen -humoral defenses in form of antibodies conduct surveillance for rhinoviruses outside the body cells, tissue spaces, and bloodstream -cellular defenses in form of tc cells search for rhinovirus infected cells inducing apoptosis when found -memory t and b cells help body to recognize and rapidly fight the same rhinovirus
Describe the protective mechanisms of the adaptive immune system
-consists of humoral and cell mediated immunity -humoral: (antibody mediated) -cellular (cell mediated)
Applications of Microbiology - Interleuking-12: The next "magic bullet"? (p. 471) Explain why interleukin-12 has been considered as the next "magic bullet" against cancer and a host of other diseases by some scientists.
-inhibits about 20 kinds of tumors in mice by stimulating wbc's to kill tumor cells -activates the Th1 pathway, causing activation of cellular immunity, macrophages and promotion of phagocytosis through opsonization and inflammation -to prevent side effects of pathway mentioned above, researchers developed concept of blocking IL-12 w/ monoclonal antibodies that bind secretede IL-12
Distinguish a primary response from a secondary immune response (Fig. 17.17) and explain why the secondary antibody response occurs faster (and stronger) than the primary response, see also Fig. 17.6.
1* response: first time the adaptive immune system meets and combats a pathogen PRIMARY - IgM first to respond then IgG - IgG also provides long term immunity which is shown in a faster growth rate in secondary response - IgG higher than IgM 2* response: more rapid - IgM still the same level or growth - IgG has faster rate of growth since memory cells utilized
Describe each of the five antibody-mediated protective mechanisms as illustrated in Fig. 17.8.
1. Agglutination: antibodies cause antigens to clump together, making it easier to engulf (phagocytosis); reduces number of infectious to be dealt w/. 2. Opsonization: the antigen (ex bacterium) is coated w/ antibodies, or complement proteins that enhance its ingestion and lysis by phagocytic cells. 3. Antibody dependent cell mediated cytotoxicity: antibodies attach to target cell and is destroyed by immune cells(macrophages, eosinophils, and NK cells) that remain external to target cell. 4. neutralization: IgG antibodies inactivate microbes by blocking their adhesion to host cells (or mucosa) and they neutralize toxins in similar manner 5. activation of complement system: causes inflammation and cell lysis either by IgG or IgM antibodies -inflammation causes microbes in area to become coated w/ certain proteins --> leads to attachment to microbe of an antibody-complement complex. complex lyses the microbe and attacts phagocytes and other immune cells to the area
. List the five classes of antibodies and describe their functions, see Table 17.1.
1. IgG: enhances phagocytosis and neutralizes toxins and viruses, protects fetus and newborn 2. IgM: especially effective against microorganisms and agglutinating antigens; first antibodies produced in resonse to initial infection 3. IgA: localized protection on mucosal surfaces 4. IgD: serum function not known; presence on B cell functions in initiation of immune response. 5. IgE: allergic reactions; possibly lysis of parasitic worms
. Describe clonal selection, see Fig. 17.6.
1. Stem cells differentiate into mature B cells, each bearing surface immunoglobins against a specific antigen. 2. B cell II encounters its specific antigen and proliferates 3. Some B cells proliferate into long-lived memory cells, which at a later date can be stimulated to become antibody-producing plasma cells. 4. Other B cells proliferate into antibody-producing plasma cells 5. Plasma cells secrete antibodies into circulation
Explain why many diseases, such as measles, occur only once in a person, yet others, such colds, occur more than once.
??? zhang lecture
Clinical applications (p. 491). Solve problem #2.
A patient w/ aids has a low Thc count. why does this patient have trouble making antibodies? How does this pateint make any antibodies? A: because dont have enough Th cell to release cytokines into B cell to stimulate it to differentiate it into a plasma cell (that produces antibodies) Makes some because has low ThC count.
Define vaccine and vaccination, attenuated microorganism, toxoid, passive immunization.
A preparation of killed, inactivated, or attenuated microorganisms or toxoids to induce artificially acquired active immunity vaccination: introduction of vaccine into body to induce an active immunity attenuated microorganism: weakened microorganism toxoid: an inactivated toxin passive immunization: Injection of preformed antibodies or antiserum( blood derived fluid containing antibodies) to obtain a temporary immunity
Describe the function of antigen-presenting cells (APCs) and major histocompatibility complex (MHC II) in the activation of T helper cells, see Fig. 17.12.
APC: To present antigen to a helper t cell -MHC II:
Compare and contrast the four ways to acquire adaptive immunity (Fig. 17.18); Explain why active immunity lasts longer than passive immunity and give three applications of passive immunization.
naturally aquired immunity: when person gets sick because exposed to antigen. When immunity aquired it can be lifelong or for some diseases can last few years. Naturally aquired passive natural transfer of antibodies from mother to fetus. if mother is immune to diseases so will newborn temporarily. Breastfeeding also transfers antibodies but the effects last few weeks or months Artificially aquired immunity active -result of vaccination (immunization).: introduces vaccines (antigens such as killed or nonliving microorganisms or inactivated bacterial toxins) into body Artificially aquired passive immunity -injection of antibodies into body. come from an animal or a human who is already immune to disease.
Define B cell, plasma cell, and memory B cell.
B cell: they remove viruses, bacteria, and toxins from body tissue fluids and blood by recognizing antigens and making antibodies against them. Participate in humoral immunity. Type of lymphocytes which differentiates into an antibody-producing plasma cell and memory cells. Plasma cell: produce antibodies against antigen memory B cell: Long-lived cells produced from B cell which can be stimulated by immune response to become a plasma cell which produces antibodies for an already encountered microorganism