Induce Effector FunctionsThe effector functions can be divided into 2 chapters
The common denominator of each effector function is the induction of inflammatory processes for which cytokines, small molecular weight polypeptides, oxygen radicals and further, in part unidentified mediators, allow infiltration of tissues with polymorphonuclear leukocytes and upregulation of acute phase reactants to combat the inflammation inducing agents. Immune complexes potentiate the effector functions of certain cells, such as lymphocytes and monocytes/macrophages. Effector function can also be operative at the cellular level As an example, intestinal double-positive CD4(+)CD8(+) T cells kindle highly activated memory cells with an increased capacity to produce cytokines, of which IL-17 is currently on the forefront. Clinical evidence indicates that alleles and mutations that affect host cell recogniftion domains in factor H result in pathology involving complement activation as evidenced by inherited atypical hemolytic uremic syndrome (aHUS), age-related macular degeneration (ARMD) and dense deposit disease (membranoproliferative glomerulonephritis type II). Under the electron microscope, factor H, now in the limelight of the drug-developing industry (www.optherion.com, www.taligentherapeutics.com), looks like beads on a string with the ability to fold back on itself. For details go to: Molecular Immunology 2010, www.elsevier.com/locate/molimm
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The complement system is like an enzyme cascade with three different major inflows: activation of the crucial C3 component may be achieved be the phylogenetically older alternate and lectin pathways and by the younger classical pathway. Abbreviations: Man:mannose, MBL: mannose binding lectin, MASP: mannose activating surface protein. The regulatory proteins H and I are not shown; they regulate excessive complement activation. The complement receptor system on diverse cell types is not shown (soon to follow) print version pdf: (40 KB)
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