Abstract
This chapter discusses relevant recent advances made in innate immunity, the complexity of lymphocyte participation, the mechanistic basis of granuloma formation/regulation, and the protective/destructive roles of the granulomatous responses through the presentation of various diseases and disease models. Advances made during the past decade revealed an extensive complexity in the granulomatous cellular response. A protective organized granulomatous response against intracellular pathogens encompasses the functional cell-mediated immunity (CMI) activity of several lymphocyte subsets; endothelial cell activation; participation of adhesion molecules; secretion of the necessary cytokines and chemokines; lymphocyte and macrophage homing; and macrophage-mediated microbicidal effects. The inefficient granulomatous response generates only loose cellular infiltration, without extracellular matrix (ECM) deposition and intimate cell-cell contact that prevent cellular activation. Virtually all granulomatous responses are accompanied by variable degrees of tissue damage. A large body of evidence indicates that most of the granulomatous inflammatory diseases (such as tuberculosis, sarcoidosis, Crohn's disease) are induced and maintained by the Th1 subset of lymphocytes. Though in chronic granulomatous diseases the inflammatory response is continuous, there occur cases of spontaneous recovery or periods of remission and downmodulation. It is likely that apoptotic mechanisms may also be active in regulating granulomatous sarcoidosis. The concerted efforts of basic and applied research will provide new and better tools in the treatment of granulomatous diseases.
Published Version
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