What is the principle difference between type II and type III hypersensitivity?

Whether the antibody reacts with the antigen on the cell or reacts with antigen before it interacts with the cell

IN TYPE II HYPERSENSITIVITY-- (or cytotoxic hypersensitivity) the antibodies produced by the immune response bind to antigens on the patients own cell surfaces. The antigens recognized in this way may either be intrinsic (self antigen, innately part of the patients cells) or extrinsic (adsorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen). These cells are recognized by macrophages or dendritic cells, which act as antigen-presenting cells. This causes a B cell response, wherein antibodies are produced against the foreign antigen. An example of type II hypersensitivity is the reaction to penicillin wherein the drug can bind to red blood cells, causing them to be recognized as different; B cell proliferation will take place and antibodies to the drug are produced. IgG and IgM antibodies bind to these antigens to form complexes that activate the classical pathway of complement activation to eliminate cells presenting foreign antigens (which are usually, but not in this case, pathogens). That is, mediators of acute inflammation are generated at the site and membrane attack complexes cause cell lysis and death. The reaction takes hours to a day. Another form of type II hypersensitivity is called antibody-dependent cell-mediated cytotoxicity (ADCC). Here, cells exhibiting the foreign antigen are tagged with antibodies (IgG or IgM). These tagged cells are then recognised by natural killer (NK) cells and macrophages (recognised via IgG bound (via the Fc region) to the effector cell surface receptor, CD16 (FcRIII)), which in turn kill these tagged cells. TYPE III HYPERSENSITIVITY --occurs when antigens and antibodies (IgG or IgM) are present in roughly equal amounts, causing extensive cross-linking. Presentation Type III hypersensitivity occurs when there is little antibody and an excess of antigen, leading to small immune complexes being formed that do not fix complement and are not cleared from the circulation. It is characterized by solvent antigens that are not bound to cell surfaces (which is the case in type II hypersensitivity). When these antigens bind antibodies, immune complexes of different sizes form. Large complexes can be cleared by macrophages but, comparatively macrophages have difficulty in the disposal of small immune complexes. These immune complexes insert themselves into small blood vessels, joints, and glomeruli, causing symptoms. Unlike the free variant, a small immune complex bound to sites of deposition (like blood vessel walls) are far more capable of interacting with complement; these medium-sized complexes, formed in the slight excess of antigen, are viewed as being highly pathogenic. Such depositions in tissues often induce an inflammatory response, and can cause damage wherever they precipitate. The cause of damage is as a result of the action of cleaved complement anaphylotoxins C3a and C5a, which, respectively, mediate the induction of granule release from mast cells (from which histamine can cause urticaria), and recruitment of inflammatory cells into the tissue (mainly those with lysosomal action, leading to tissue damage through frustrated phagocytosis by PMNs and macrophages) The reaction can take hours, days, or even weeks to develop, depending on whether or not there is immunlogic memory of the precipitating antigen. Typically, clinical features emerge a week following initial antigen challenge, when the deposited immune complexes can precipitate an inflammatory response. Because of the nature of the antibody aggregation, tissues that are associated with blood filtration at considerable osmotic and hydrostatic gradient (e.g. sites of urinary and synovial fluid formation, kidney glomeruli and joint tissues respectively) bear the brunt of the damage. Hence, vasculitis, glomerulonephritis and arthritis are commonly-associated conditions as a result of type III hypersensitivity responses As observed under methods of histopathology, acute necrotizing vasculitis within the affected tissues is observed concomitant to neutrophilic infiltration, along with notable eosinophilic deposition (FIBRINOID NECROSIS). Often, immunofluorescence microscopy can be used to visualize the immune complexes. Skin response to a hypersensitivity of this type is referred to as an ARTHUS REACTION, and is characterized by local erythema and some induration. Platelet aggregation, especially in microvasculature, can cause localized clot formation, leading to blotchy hemorrhages. This typifies the response to injection of foreign antigen sufficient to lead to the condition of SERUM SICKNESS

The correct answer to this question is B, Whether the antibody reacts with the antigen on the cell or reacts with antigen before it interacts with the cell. While this is the main difference, there are many other differences between type II and type III hypersensitivity.

Type II hypersensitivity includes tissue phagocytosis, while Type III has tissue necrosis. Another difference between them is that Type II hypersensitivity has a tissue-specific IgG response, while type III has non-specific IgG response. Lastly, type II hypersensitivity has AB targeted at something, while class III will form and depose of it, as well as have equal amounts of Ab and AG.

Hypersensitivities are of many types. There are 4 types of hypersensitivities, all characterized by their particular characteristics. For instance, type two hypersensitivity is mediated by antibodies while type 4 is delayed hypersensitivity. It depends on whether the antibody reacts with the antigen on the cell or reacts with the antigen before it interacts with the cell. In type 2 the antibodies can be extrinsic or intrinsic.

The cells are detected by special cells called macrophages or by dendritic cells and the antigen is then transferred to the lymphocytes which produce special antibodies against the particular invading cell to destroy it.