[Bactericidal activity of cells of the immune system]

The acquisition of a bactericidal activity by the cellular immune system is one of the mechanisms of prime importance for the development of the cellular resistance to infection. It involves the specific recognition of the pathogenic microorganism associated with the direct or indirect activation of effector cells. The in vivo type of replication of the infectious microorganism provides the adaptive response of the host. This response differs according to extracellular or intracellular multiplying microorganism. The acquired resistance to extracellular multiplying bacteria (ie, capsulated bacteria) is linked to the B cell production of specific antibodies that are associated with the activated complement fragments, that enable bacterial opsonization, activation and recruiting of polymorphonuclear phagocytes. These cells did acquired a greater capacity to ingest and to kill bacteria at sites of infection. Such phenomenon could be also associated with acute purulent necrotizing lesions. On the other hand, intracellular multiplying bacteria are mostly associated with chronic granulomatous non pyogenic lesions, and such bacteria are also able to survive and to replicate into the non activated professional mononuclear phagocytes. The acquired resistance against such bacteria is linked to the occurrence of a non specific bactericidal capacity of macrophages, that inhibit and/or kill replicative intracellular microorganisms. Such macrophage bactericidal capacity is dependent upon the gradual and stepwise cellular activation provided by several extracellular and membrane associated signals. Sequential signals are produced by the specific recognition of committed T CD4+ lymphocytes mediated by the infected macrophages through the MHC class 2 restriction of the peptide presentation. One of the major signal of cellular communication to induce macrophage priming involves the production of Interferon gamma (IFN gamma). Secondary signals are needed to induced full macrophage activation defined by phenotypic, metabolic and functional alterations which include their acquired increase capacity to kill intracellular bacteria and tumor cells. Secondary signals involve the production of cytokines such as TNF alpha, IL2 and GM-CSF being transduced by bacterial cell wall products (such as lipopolysaccharide, teichoic acid, or lipoarabinomanan) or by the calcitriol pathway recently described during mycobacterial infection.(ABSTRACT TRUNCATED AT 250 WORDS)