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Perspective Hemophagocytic Syndromes and InfectionDavid N. Fisman |
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| Back to article Figure 2. Schematic representation of possible immunopathologic mechanisms in infection-associated hemophagocytic lymphohistiocytosis (HLH). In Epstein-Barr virus (EBV)-associated HLH, infection of T lymphocytes results in clonal proliferation, with production of high levels of activating cytokines. Elaboration of TNF-a and other cytokines causes fever and systemic illness. TNF-a and IFN-g production contributes to macrophage activation with resulting hemophagocytosis, as demonstrated by the ability of anti-TNF-a and anti-IFN-g antibodies to attenuate hemophagocytosis. The immunopathology of infection with nonviral pathogens is less well understood, but may be related to exaggerated production of TNF-a and IFN-g in response to infection. TNF-a = tumor necrosis factor-a; IFN-g = interferon-gamma; IL-1 = interleukin-1; IL-2 = interleukin-2; IL-6 = interleukin-6; IL-18 = interleukin-18; sFasL = soluble Fas ligand; T = T-lymphocyte; M = macrophage; EBV = Epstein-Barr virus. |
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Home | Top of Page | Current Issue | Expedited | Upcoming Issue | Past Issue | EID Search | Contact Us CDC Home | Search | Health Topics A-Z This page last reviewed December 08, 2001 Emerging Infectious Diseases Journal
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