Chapter 20 & 21 Lecture

What lymphoid tissue is found in the oral cavity?

Tonsils are the simplest lymphoid organs; palatine tonsils are the largest tonsils and most often infected located at the posterior end of the oral cavity; lingual tonsils are lumpy collection of follicles at the base of the tongue; pharyngeal tonsils are also called adenoids and are located at the posterior wall of the nasopharynx; tubal tonsils surround the openings of the auditory tubes into the pharynx

What are lymphatic capillaries? Compare them to blood capillaries. Where are they found?

Vessels that weave between tissue cells and blood capillaries; absent from bones, teeth, bone marrow, and the CNS; similar to blood capillaries, but more permeable; can take up larger molecules and particles that blood capillaries cannot; can act as route for pathogens or cancer cells to travel through the body

What are interferons? What do they do?

Viruses are essentially nucleic acids surrounded by a protein envelope and lack the cellular machinery to generate ATP or synthesize proteins. They do their "dirty work" in the body by invading tissue cells and taking over the cellular metabolic machinery needed to reproduce themselves. Infected cells can do little to save themselves, but some can secrete small proteins called interferons to help protect cells that not yet been infected. The interferons diffuse to nearby cells, which they stimulate to synthesize proteins that block further protein synthesis and degrade viral RNA. They interfere with viral replication. Interferons produced against a particular virus protect against other viruses too. They also activate natural killer cells.

Trabeculae

divide the node into compartments

Afferent vessels

lymph enters convex side of node

Cortex

outer histological region of the node

List all the tonsils and locate where they are found.

palatine tonsils are the largest tonsils and most often infected located at the posterior end of the oral cavity; lingual tonsils are lumpy collection of follicles at the base of the tongue; pharyngeal tonsils are also called adenoids and are located at the posterior wall of the nasopharynx; tubal tonsils surround the openings of the auditory tubes into the pharynx

Antibodies that act against a particular foreign substance are released by

plasma cells of B cells

What is phagocytosis? Which immune cells are phagocytic?

A phagocyte is a cell that eats, ingests or engulfs another cell. Receptors on the flowing cytoplasmic extensions bind to the particle. The particle is then pulled inside, enclosed within a membrane-lined vesicle. The resulting phagosome then fuses with a lysosome. The process of phagocytosis starts when a phagocyte recognizes and adheres to pathogen's carbohydrate "signature". Some microorganisms have external capsules that hide their surface carbohydrates, helping them evade phagocytosis. Our immune system gets around this problem by coating pathogens with opsonins. Opsonins are complement proteins or antibodies. They provide "handles" to which phagocyte receptors can bind. Any pathogen can be coated with opsonins, a process called opsonization which greatly accelerates phagocytosis of that pathogen. Some pathogens are not killed with acidified lysosomal enzymes like the tuberculosis bacteria and some parasites. In this case, helper T cells release chemicals that stimulate the macrophage. This activates additional enzymes that produce a lethal respiratory burst. The respiratory burst promotes killing of pathogens by liberating highly destructive free radicals, producing oxidizing chemicals like hydrogen peroxide and bleach, and increasing the phagolysosome's pH and osmolarity, which activates other protein-digesting enzymes that digest the invader. Neutrophils also pierce the pathogen's membrane by using defensins.

What is a vaccine and why are they important? Why is it effective?

A vaccine is an artificially acquired humoral immune response; secondary responses are so much more vigorous than primary responses, vaccines were developed to "prime" the immune response by providing first encounter with the antigen. Most vaccines contain pathogens that are dead or attenuated (living, but extremely weakened), or their components. Vaccines provide two benefits: 1- Their weakened antigens provide functional antigenic determinants that are both immunogenic and reactive. 2- They spare us most of the symptoms and discomfort of the disease that would otherwise occur during the primary response. Vaccine booster shots are used in some cases to intensify the immune response at later encounters with the same antigen. Vaccines are wiped out smallpox and have substantially lessened the illness caused by such former childhood killers as whooping cough, polio, and measles. Although vaccines have dramatically reduced hepatitis B, tetanus, influenza, and pneumonia in adults, immunization of adults in the US has a much lower priority than that of children. As a result more than 65,000 Americans die each year from preventable infections (prior to COVID-19 data). Conventional vaccines have shortcomings. The biggest shortcoming is that they are not always as effective or long-lasting as we would like. In some individuals, contaminating proteins(egg, albumin, etc) cause allergic responses to the vaccine.

What is adaptive immunity?

Adaptive immunity is the body's built-in specific defensive system that stalks and eliminates with nearly equal precision almost any type of pathogen that intrudes the body. This is the third line of defense.

What is chemotaxis? Why is it important? What is diapedesis? What is margination?

After inflammation begins, phagocytes flood the damaged area. Neutrophils lead, followed by macrophages. There are 4 steps in which phagocytes are mobilized to infiltrate the injured site. 1. Leukocytosis: Injured cells release chemicals that increase the numbers of white blood cells. Neutrophils enter blood from the red bone marrow where they are produced within a few hours. The numbers of neutrophils increase 4-5 fold within a few hours. Leukocytosis is the increase in white blood cells and is a characteristic of inflammation. 2. Margination refers to the phenomenon of phagocytes clinging to the inner walls (margins) of the capillaries and postcapillary venules. Inflamed endothelial cells sprout cell adhesion molecules that signal "this is the place". As neutrophils encounter these CAMs, they bind briefly. This causes them to slow and roll along the inner surface of the blood vessel so they can be activated by inflammatory chemicals. Once activated, neutrophils sprout additional CAMs on their own plasma membranes. This allows neutrophils to bind endothelial cells tightly, creating an initial foothold. Endothelial cells line all capillaries and blood vessels. 3. Diapedesis: Continued chemical signaling prompts the neutrophils to flatten and squeeze between the endothelial cells of the capillary walls. This process is called diapedesis. 4. Chemotaxis: Inflammatory chemicals act as homing devices, or more precisely chemotactic agents. Neutrophils and other WBCs migrate up the gradient of chemotactic agents to the site of injury. Within an hour after the inflammatory response has begun, neutrophils have collected at the site and are devouring any foreign material present.

What is an autoimmune disease? What are some examples? What do they do?

An autoimmune disease occurs when the immune system loses its ability to distinguish self from nonself. When this happens, the artillery of the immune system turns against itself. The produces antibodies and cytotoxic T cells that destroy its own tissues. Names of specific autoimmune diseases are based on the part of the body they target. Examples include: 1- Rheumatoid arthritis systemically destroys joints 2- Myasthenia gravis impairs communication between the nerves and skeletal muscles 3- Multiple sclerosis which destroys the myelin sheaths of the brain and spinal cord as well as peripheral nerves. 4- Graves' disease prompts the thyroid gland to produce excessive amounts of thyroid hormone (thyroxine) 5- Type I (insulin-dependent) diabetes mellitus which destroys pancreatic beta cells, resulting in a deficit of insulin and the inability to use carbohydrates 6- Systemic lupus erythematosus (SLE) is a systemic disease that particularly effects the kidneys, heart, lungs and skin 7- Glomerulonephritis damages the kidney's filtration membrane and severely impairs renal function

Where is each of the immunoglobulins found? What do they do? IgG, IgM, IgA, IgD, IgE,

Antibodies are also called immunoglobulins (Igs) and constitute the gamma globulin part of blood proteins. Antibodies are proteins secreted in response to an antigen by effector B cells called plasma cells and the antibodies bind specifically with that antigen. Antibodies are grouped into 5 Ig classes. IgM is the first immunoglobulin class secreted by plasma cells during primary response. The presence of IgM diagnostically in plasma usually indicates current infection. It readily activates complement. It exists in monomer or pentamer forms. The monomer serves as antigen receptor for B cells. The pentamer circulates in the blood plasma. Numerous antigen-binding sites make it a potent agglutinating agent. IgA is referred to as secretory IgA and is found in body secretions such as saliva, sweat, intestinal juice and milk. Secretory IgA helps stop pathogens from attaching to epithelial cell surfaces including mucous membranes and the epidermis. The monomer exists in limited amount in plasma. IgD is found on the surface of B cells. It functions as a B cell antigen receptor as does IgM. IgG is the most abundant antibody in plasma accounting for 75-85% of circulating antibodies. The main antibody of both secondary and late primary responses. It readily activates complement and protects against bacteria, viruses, and toxins circulating in blood and lymph. It also crosses the placenta and confers passive immunity from the mother to the fetus. IgE is a monomer and the stem ends binds to mast cells or basophils. Antigen binding to its receptor end triggers these cells to release histamine and other chemicals that mediate inflammation and an allergic reaction. IgE is secreted by plasma cells in skin, mucosae of the gastrointestinal and respiratory tracts, and tonsils. Only traces of IgE are found in plasma. Levels rise during severe allergic attacks or chronic parasitic infections of the gastrointestinal tract.

What are APC? Helper T cells? Cytotoxic T cells? NK cells?

Antigen-presenting cells (APCs) engulf antigens and then present fragments of them, like signal flags, on their own surfaces where T cells can recognize them. APCs present antigens to the cells that deal with antigens. The major types of cells acting as APCs are dendritic cells, macrophages, and B lymphocytes. Helper T cells play a central role in adaptive immunity in both B cell mediated and T cell mediated immunity (humoral and adaptive). Helper T cells help activate B cells and T cells and induce proliferation in both. Without helper T cells, there is NO adaptive immune response. They are derived from CD4 cells. CD8 cells become active into cytotoxic T cells. The cytotoxic T cells directly attack and kill other cells. They roam the body, circulating in and out of the blood and lymph and throughout lymphoid organs in search of body cells displaying antigens that the cytotoxic T cells recognize. Their main targets are virus infected cells, but they can also attack tissue cells infected by certain intracellular bacteria or parasites, cancer cells, and foreign cells introduced into the body by blood transfusions or organ transplants. Cyotoxic t cells target specific infected or tumor cells. Natural killer cells police the body in blood and lymph. They are defensive cells that can kill cancer cells and virus-infected body cells before the adaptive immune system is activated. NK cells are a part of large granular lymphocytes. NK cells are less picky than cytotoxic T cells. NK cells are phagocytic, and kill by directly contacting the target cell inducing it to undergo programmed cell death. NK cells secrete potent chemicals that enhance the inflammatory response.

How does clonal selection of B cells work? Which substance is responsible for determining which cells become cloned?

B cells oversee humoral immunity. All B cells like other lymphocytes originate in the red bone marrow from hematopoietic stem cells. Lymphocytes are "educated" and go through a rigorous selection process as they mature. Immunocompetence occurs when a lymphocyte becomes competent or able to recognize its one specific antigen by binding to it. When B cells become immunocompetent, they display a unique type of receptor on their surface. These receptors enable lymphocytes to recognize and bind to a specific antigen. Once these receptors appear, the lymphocyte is committed to react to one and only one distinct antigenic determinant because all of its antigen receptors are the same. The receptors on B cells are membrane-bound antibodies. Self-Tolerance is the ability of the lymphocyte to be unresponsive to self-antigens so that it does not attack the body's own cells. Without self-tolerance, the lymphocyte would cause an autoimmune response resulting in some sort of disease based on where the lymphocytes respond. Those B cells that are self-reactive are eliminated by apoptosis. Maturation is a 2-3 day process that occurs in the red bone marrow for B cells. Immunocompetent B cells that have not been exposed to an antigen are called naïve. Naïve B cells are sent from the red bone marrow to other lymphoid organs to colonize (live) until they encounter antigen. They are more likely to encounter antigens in the secondary lymphoid organs (spleen, lymph nodes, etc). The first encounter between an immunocompetent but naïve lymphocyte and an invading antigen usually takes place in a lymph node or the spleen. Immune cells in lymph nodes are in a strategic position to encounter a large variety of antigens because lymphatic capillaries pick up proteins and pathogens from nearly all body tissues. When an antigen binds to the particular lymphocyte that has a receptor for it, the antigen selects that lymphocyte for further development. This is called clonal selection. If the proper signals are present, the selected lymphocyte will activate to complete its differentiation. Once activated, the lymphocyte rapidly proliferates to form an army of cells exactly like itself and having the same antigen specificity. This army of identical cells, all descended from the same ancestor cell is called a clone. Most members of the clone become effector cells, the cells that actually do the work of fighting infection. A few members of the clone become memory cells that are able to respond quickly after any subsequent encounter with the same antigen occurs. When a B cell encounters its antigen, that antigen provokes the humoral immune response, in which antibodies specific for that antigen are made. An immunocompetent but naïve B lymphocyte is activated when matching antigens bind its surface receptors and cross-link adjacent receptors together. Antigen binding is quickly followed by receptor-mediated endocytosis of the cross-linked antigen-receptor complexes. This is called clonal selection and is followed by proliferation and differentiation into effector cells. Most cells of the clone differentiate into plasma cells that secrete antibodies. Clone cells that do not become plasma cells become long-lived memory cells. This allows for immunological memory to occur and the immune response to be immediate if the same antigen is encountered again in the future.

What is the importance of B cells? What are the different kinds? Where are they? How do they mature? Where do they come from? How do B cells become active?

B lymphocytes are the humoral immune response. They secrete antibodies. They target extracellular pathogens, like bacteria, fungi, parasites, and some viruses in extracellular fluid. The originate in the red bone marrow. They also mature in the red bone marrow. The effector cells are called plasma cells that secrete the antibodies. They also form memory cells. Maturation and activation has been previously discussed.

What is the thymus? When is it most active?

Bi-lobed lymphoid organ found in inferior neck; extends into mediastinum and partially overlies the heart; functions as a lymphoid organ where T cells mature; most active and largest in size during childhood; stops growing during adolescence, then gradually atrophies; still produces immunocompetent cells, though more slowly

What are differences in how the immune system fights bacterial infections versus viral infections?

Both T cells and B cells fight both kinds of infections. However, usually T cells (cell mediated immunity) target viruses along with interferons and B cells (humoral immunity) target bacteria using phagocytes, complement, and antibodies.

What are the roles of activated complement?

Complement refers to a group of about 20 plasma proteins that normally circulate in the blood in an inactive state. The complement system provides a major mechanism for destroying foreign substances in the body. Its activation unleashes inflammatory chemicals that amplify virtually all aspects of the inflammatory process. Activated complement also lyses (ruptures or bursts) and kills certain bacteria and other cell types. Normally our cells are equipped with proteins that normally inhibit complement activation. Complement is a nonspecific defensive mechanism. It complements and enhances the effectiveness of both innate and adaptive defenses.

What are the innate immune system defenses?

Constitutes first and second lines of defense; the innate defenses reduce the workload of the adaptive system by preventing entry and spread of microorganisms in the body. The first line of defense is the skin and mucous membranes, along with secretions these membranes produce. This first line of defense serves as both a physical barrier and a chemical barrier. Your internal innate defenses are the second line of defense and include antimicrobial proteins, phagocytes, and other cells that inhibit the spread of invades. This second line of defense promotes inflammation which is the most important mechanism of warding off invasion.

Where are your large lymph node clusters found?

Head, face, neck, armpits, trunk, inguinal region

What causes proliferation of lymphocytes?

Helper T cells stimulate the proliferation of lymphocytes.

What is a fever? Why is it important? How does it occur? Why?

Inflammation is a nonspecific response to any tissue injury. Causes include physical trauma, intense heat, irritating chemicals or infection. Inflammation has several benefits: 1- it prevents the spread of damaging agents to nearby tissues 2- it disposes of cell debris and pathogens 3- it alerts the adaptive immune response 4- it sets the stage for repair There are 4 cardinal signs of inflammation: redness, heat, swelling, pain and possibly immobility Inflammation is a localized response to infection, but sometimes the body's response to the invasion of microorganisms is more widespread. Fever is the result of an abnormally high body temperature due to a systemic response to invading microorganisms. When leukocytes and macrophages are exposed to foreign substances in the body, they release chemicals called pyrogens. These pyrogens act on the body's thermostat (a cluster of neurons in the hypothalamus) raising the body's temperature above normal. Fever seems to benefit the body, but exactly how it does so is unclear. Fever causes the liver and spleen to sequester iron and zinc, which may make them less available to support bacterial growth. Additionally fever increases the metabolic rate of tissue cells, and may speed up the repair processes.

What is agglutination?

Let's begin with discussing why this happens. Antibodies themselves cannot destroy antigens, then inactivate antigens and tag them for destruction. The common event in all antibody-antigen interactions is the formation of antigen-antibody complexes. Defensive mechanisms used by antibodies include neutralization, agglutination, precipitation, and complement activation. Neutralization is the simplest defensive mechanism and occurs when antibodies block specific sites on viruses or bacterial exotoxins (toxic chemicals secreted by bacteria). As a result, the virus or exotoxin cannot bind to receptors on tissue cells. Phagocytes eventually destroy the antigen-antibody complexes. Agglutination: Because antibodies have more than one antigen-binding site, they can bind to the same determinant on more than one antigen at a time. Consequently, antigen-antibody complexes can be cross-linked into large lattices. When cell-bound antigens are cross-linked, the process causes clumping or agglutination of the foreign cells. IgM, with 10 antigen-binding sites, is an especially potent agglutinating agent. This is the same agglutination that occurs when blood is mismatched. Precipitation happens when soluble molecules (instead of cells) are cross-linked into large complexes that settle out of solution. Like agglutinated bacteria, precipitated antigen molecules are much easier for phagocytes to capture and engulf than are freely moving antigens. Complement activation is the chief antibody defense used against cellular antigens, such as bacteria or mismatched red blood cells. When several antibodies bind close together on the same cell, the complement-binding sites on their stem regions align and complement is activated. MAC may insert into the antigenic cell's surface triggering cell lysis. Complement activation amplifies the inflammatory response and promotes phagocytosis by opsonization. This sets into motion a positive feedback cycle that enlists more and more defensive elements.

What are lymphocytes? List the types and discuss each.. what they do? Where they are?

Lymphocytes are cells of the adaptive immune system; mature into two main types; 1-T cells 2- B cells; T cells manage the immune response by defending against intracellular antigens; examples are CD4 cells usually become T helper cells that can activate B cells and other T cells, Regulatory T cells, memory T cells, CD8 cells become cytotoxic T cells directly target and destroy pathogens; B cells produces plasma cells that secrete antibodies; All lymphocytes are found in lymphatic tissues and lymph nodes

What are monoclonal antibodies? What are they used for?

Monoclonal antibodies are pure antibody preparations specific for a single antigenic determinant. They are produced by descendants of a single cell. Commercially prepared monoclonal antibodies are essential in research, clinical testing, and treatment. Monoclonal antibodies are used to diagnose pregnancy, certain sexually transmitted infections, some cancers, hepatitis, and rabies. These monoclonal antibody tests are more specific, sensitive, and rapid than other tests. Monoclonal antibodies are also used to treat leukemia and lymphomas, cancers that are present in circulation and so are easily accessible to injected antibodies. They also serve as "guided missles" to deliver anticancer drugs only to cancerous tissue, and to treat certain autoimmune diseases.

What determines what specific foreign substance our adaptive immunity will be able to recognize and resist?

Our genes, not antigens we encounter, determine which specific foreign substances our immune system will be able to recognize and resist. The immune cell receptors represent our genetically acquired knowledge of the microbes that are likely to be in our environment.

What is passive immunity?

Passive humoral immunity occurs when ready-made antibodies are introduced into the body; B cells are not challenged by antigens; immunological memory does not occur; protection ends when antibodies degrade; Two Types 1- Naturally acquired passive humoral immunity occurs when antibodies are delivered to fetus via placenta or to infant through milk 2- Artificially acquired passive humoral immunity occurs when an injection of serum, such as gamma globulin is given, protection is immediate but ends when antibodies naturally degrade in body

What is opsonization?

Pathogens are coated with opsonins. Opsonins are complement proteins or antibodies which coat the pathogen and provide "handles" where phagocytes can bind. Any pathogen can be coated with opsonins, a process called opsonization which greatly accelerates phagocytosis of that pathogen.

What lymphatic structure drains lymph from the right upper limb and the right side of the head and thorax?

Right lymphatic duct drains lymph from the right upper limb and the right side of the head and thorax

What is the importance of T cells? What are the different kinds? Where are they? How do they mature? Where do they come from? How do T cells become active?

T cells are non-antibody producing lymphocytes that constitute the cellular arm of adaptive immunity. T lymphocytes share a common pattern of development with B cells. (See B cell maturation) 1-Origin- red bone marrow 2- Maturation- The receptors on T cells are not antibodies but are products of the same gene superfamily and have similar functions. Maturation of T cells occurs in the thymus. 3- Seeding secondary lymphoid organs and circulation- T cells account for 65-85% of bloodborne lymphocytes and circulate continuously throughout the body. 4- Antigen encounter and activation 5-Proliferation and differentiation The selection process that T cells undergo during maturation occurs in the thymus and consists of positive and negative selection. Positive selection of T cells is the first of two tests a developing T lymphocyte must pass. It ensures that only T cells with receptors that are able to recognize self-MHC proteins survive. (MHCs are the proteins that your body produces specifically for you. We call them our self identifying proteins. Everyone's MHCs are different, so your cells need to know your MHCs so that your immune cells don't attack itself.) T cells cannot bind antigens unless the antigens are presented on self-MHC proteins. T cells that are unable to recognize self MHC proteins are eliminated by apoptosis. Negative selection of T cells ensures that T cells do not recognize self-antigens displayed on self-MHC. If they do, they are eliminated by apoptosis. Negative selection is the basis for immunological self-tolerance, making sure that T cells don't attack the body's own cells, which would cause autoimmune disorders. Because the self-reactive lymphocyte and all of its potential progeny are eliminated, this is called clonal deletion. The education of T cells is expansive and only about 2% survive it and continue to become successful immunocompetent, self-tolerant T cells. Activated T cells can become either effector T cells or memory cells. Helper T cells play a central role in adaptive immunity, mobilizing both humoral and cellular mediated immunity. Basically without helper T cells, all adaptive immunity would suffer. This is in fact why AIDs is such a deadly virus. It wipes out helper T cells. Once activated by antigen presenting cells (APCs), helper T cells activate B and T cells and induce them both to proliferate. Helper T cells release cytokines that furnish the chemical help needed to recruit other immune cells. Helper T cells interact with B cells activation and proliferation. Helper T cells amplify the responses of the innate immune response. They activate macrophages to become more potent killers. The cytokines released by helper T cells not only mobilize lymphocytes and macrophages but also attract other types of white blood cells into the area. As the released chemicals summon more and more cells into battle, the immune response gains momentum, and the sheer number of immune elements overwhelms the antigens. Cytotoxic T cells are activated CD8 cells and are T cells that can directly attack and kill other cells. Cytotoxic T cells roam the body, circulating in and out of the blood and lymph and through lymphoid organs in search of body cells displaying antigens that the cytotoxic T cells recognize. Their main targets are virus-infected cells, but they also attack tissue cells infected by certain intracellular bacteria or parasites, cancer cells and foreign cells introduced into the body by blood transfusions or organ transplants. Before the onslaught can begin, the cytotoxic T cell must "dock" on the target cell by binding to a self-nonself complex. All body cells display MHC antigens, so Tc cells can destroy all infected or abnormal body cells. The attack on foreign human cells, such as those of a graft, is more difficult to explain because here all of the antigens are nonself. Apparently sometimes the Tc "see" the foreign MHCs as a combination of self MHCs bound to a foreign antigen. Once the Tc recognize their targets, they use two major mechanisms as a lethal hit. One involves perforins and granzymes. The other involves binding to a specific membrane receptor on the target cell that stimulates the target cell to undergo apoptosis. Regulatory T cells dampen the immune response. They act either by direct contact or by releasing inhibitory cytokines. Regulatory T cells are important in preventing autoimmune reactions because they suppress self-reactive lymphocytes outside the lymphoid organs.

What is complement? Why is it important? What are the different kinds? What all do they do? Which complement protein is important for opsonization? Inflammation?

The term complement system refers to a group of at least 20 plasma proteins that normally circulate in the blood in an inactive state. These proteins include those numbered C1 to C9 plus several others that act as regulatory proteins and other factors. Complement provides a major mechanism for destroying foreign substances in the body. Its activation unleashes inflammatory chemicals that amplify virtually all aspects of the inflammatory process. Activated complement also lyses and kills certain bacteria and other cell types. Complement is a nonspecific defense mechanism that enhances the effectiveness of both innate and adaptive defenses. Complement is activated three ways: 1- the classical pathway involving antibodies. Once an antibody binds to a pathogen it can also bind to complement activating the pathway. 2- the lectin pathway using water soluble proteins called lectin that the innate immune system produces to fight off foreign invaders. Lectins bind to carbohydrates on the surface of microorganisms and then bind and activate complement. 3- the alternative pathway is triggered when spontaneously activated C3 and other complement factors interact on the surface of microorganisms. Once complement is activated, it begins a cascade of events that each require the one before to proceed. It is a very orderly sequence of events. All three pathways converge at C3, which is split into C3a and C3b. Splitting C3 initiates a common terminal pathway that enhances inflammation, promotes phagocytosis and can cause cell lysis. Cell lysis begins when C3b binds to the target cell's surface and triggers the insertion of a group of complement proteins called MAC (membrane attack complexes) into the cell's membrane. MAC forms and stabilizes a hole in the membrane that allows a massive influx of water, causing the target cell to burst (lyse). The C3b molecules also act as opsonins. Opsonins coat the microorganism, providing "handles" that receptors on macrophages and neutrophils can adhere to. This allows them to engulf the particle more rapidly. C3a and other molecules formed during complement activation amplify the inflammatory response by stimulating mast cells and basophils to release histamine (a potent vasodilator) and by attracting neutrophils and other inflammatory cells to the area.