Cell Injury in Allergic Inflammation (Part 1 of 2)

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Abstract
Host resistance to microorganisms, in the broad sense, is compounded of diverse homeostatic mechanisms. Among these are the plasma-cell-antibody systems, the lymphoid delayed-type reaction system, various intrinsic tissue resistance systems, the nonspecific inflammatory granuloma, and perhaps other mechanisms yet to be described. Immune and allergic states which assume importance in virulent or chronic infections have received the greatest amount of attention. Other less easily studied "immune" mechanisms may be equally important. An attempt is made to clarify the relations between immediate and delayed-type hypersensitivity responses. Emphasis is placed on cell types responsible for hyper-sensitivity responses. Normal function of the antibody system may result in as much local tissue damage (Arthus reaction) as that caused by unmodified function of lymphoid systems which mediate delayed-type allergy (tuberculin reaction). Underfunction of one or another of these mechanisms can throw the activity of other systems into sharp relief. The relative usefulness to the host of these several homeostatic mechanisms is still further affected by sites of antigen location, by the cell types which are the larget for a reaction, and by the evolution of inflammatory responses. The complexity of these variables limits the value of any one laboratory method, such as serology or tissue culture, for explaining the mechanism of cell injury in allergic inflammation. 181 references are included.

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