title: Cellular and vascular manifestations of cell-mediated immunity.
abstract: The studies reviewed here emphasize both the complexity and the heterogeneity of cell-mediated immunity. In addition to the round cell infiltrate of the classic descriptions, cell-mediated immunity includes reactions that feature many types of inflammatory cells, that exert profound effects on the blood microvasculature, and that initiate extravascular clotting and, possibly, angiogenesis. The common denominator of all of these reactions is a subset or subsets of sensitized T lymphocytes that, on exposure to specific antigen, recruit and collaborate in other ways with one or more populations of circulating bone marrow-derived cells. Although the reactions generally resemble chronic inflammation by virtue of the lymphocytes and monocytes present, cell-mediated immunity may also take the guise of acute or subacute inflammation when neutrophils or eosinophils predominate and an entirely different morphologic pattern when basophils predominate, as in CBH. Tissue mast cells undergo changes (activation, proliferation) that are generally observed at later stages of delayed hypersensitivity, but no convincing evidence has been presented that these cells play an essential role in the elicitation of cell-mediated immunity. The concept that an essential prerequisite for the elicitation of delayed hypersensitivity is the mast cell-dependent generation of microvascular gaps, favoring inflammatory cell diapedesis, is clearly incorrect. First, lymphocytes fail to traverse certain of the vessels that exhibit such gaps (i.e., those of the SCV) in delayed hypersensitivity reactions in humans. Second, there is no diminution in the cellular infiltration associated with cell-mediated immunity reactions in mast cell-deficient mice. Cell-mediated immunity does not consist of an inflammatory cell infiltrate alone. The local microvasculature is rendered hyperpermeable to varying extents, with resulting extravasation of plasma proteins, including fibrinogen. The majority of extravasated fibrinogen is clotted to cross-linked fibrin, presumably as the result of the actions of procoagulants associated with fixed connective tissue cells and perhaps also because of the activity of infiltrating cells, such as monocytes/macrophages. Clotted fibrin forms a water-trapping gel, which accounts for the induration seen in many delayed hypersensitivity reactions. The microvasculature may also be affected in other ways. Endothelial cells may undergo hypertrophy and cell division or, alternatively, may exhibit profound and progressive injury.(ABSTRACT TRUNCATED AT 400 WORDS)
mesh_terms: D000818:Animals; D001491:Basophils / Q000473:pathology; D001798:Blood Proteins / Q000378:metabolism; D001808:Blood Vessels / Q000276:immunology*; D002196:Capillaries / Q000473:pathology; D002199:Capillary Permeability; D003877:Dermatitis, Contact / Q000473:pathology; D004727:Endothelium / Q000473:pathology; D005337:Fibrin / Q000378:metabolism; D006168:Guinea Pigs; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000276:immunology / Q000473:pathology; D006984:Hypertrophy; D007111:Immunity, Cellular; D051379:Mice; D014664:Vasodilation
chemical_list: D001798:Blood Proteins; D005337:Fibrin