Question

Compare how the inflammatory response is initiated by each of the following.

A. A Type IV hypersensitivity reaction

B. Endotoxin

C. A superantigen toxin

D. A Type III hypersensitivity response

Answer 1

inflammatory response initiated by Type IV hypersensitivity	inflammatory response initiated by endotoxins(Lipopolysacharides)	inflammatory response initiated by superantigen toxin	inflammatory response initiated by type III hypersensitivity
delayed-type hypersensitivity reactions are mediated by antigen-specific effector T cells.	Endotoxins represent the pyrogens (fever-inducing agents) of gram-negative bacteria, pyrogenicity being probably the first activity of endotoxin.	Superantigens are predominantly bacterial in origin, such as staphylococcal enterotoxin and toxin-1 responsible for toxic shock syndrome	Type III hypersensitivity is also known as immune complex injury. The damaging inflammatoryreaction is triggered by a soluble antigen capable of forming large insoluble immune complexes (IC) with IgM or IgG antibodies in the circulation.
They are distinguished from other hypersensitivity reactions by the lag time from exposure to the antigen until the response is evident (1 to 3 days).	Endotoxin interacts with cells and molecules of inflammation, immunity and haemostasis. Endotoxin is one of the most important bacterial components contributing to the inflammatory process. Levels of endotoxin correlate directly with severity of meningococcal disease and other forms of sepsis, and with elaboration and release of inflammatory mediators	Superantigens (SAgs) are the most powerful T cell mitogens Concentrations of less than 0·1 pg/ml of a bacterial superantigen are sufficient to stimulate the T lymphocytes in an uncontrolled manner resulting in fever, shock and death	Type III hypersensitivity. Type III hypersensitivity occurs when there is accumulation of immunecomplexes (antigen-antibody complexes) that have not been adequately cleared by innate immunecells, giving rise to an inflammatory response and attraction of leukocytes
Delayed-type hypersensitivity is part of the CMI response. This is a localized inflammatory reaction driven by sensitized T helper 1 cells and mediated by macrophages. This immune response is characterized by an influx of innate immune cells, with macrophages and the dendritic cells predominating	Endotoxin activates complement via the alternative pathway, but most of the biological activity of the molecule is attributable to lipid A. Both endotoxin and lipid A are potent activators of macrophages resulting in the induction of a range of cytokines involved in the regulation of immune and inflammatory responses	a large numbers of T cells (regardless of antigen specificity) may be activated by superantigens. This can lead to massive systemic disruption with symptoms similar to septic shock including occurrence of severe tissue injury and possible multiple organ failure.	The tissue damaging mechanisms are similar to those described for the antigen-antibody complexes that form in type II responses. The response times of types II and III hypersensitivity reactions are slower than that of type I reactions; they typically develop 3–6 h after exposure to antigen. The response can also become chronic, particularly in autoimmune reactions, where antigen persists.