Cytokine patterns in adults with aids

Abstract

The character of cytokine response in AIDS patients may be directly related to the stimulus employed in test systems. There is no evidence for Th1/Th2 dysregulation. Cytokine elevations in AIDS patients generally are reflective of chronic infection (the virus). Lymphocytes from AIDS patients do not respond as well to stimulation as do those from normal healthy volunteers. The stimulated lymphocyte response in AIDS patients suggests there is underlying low-grade host versus virus reaction in these patients (exaggerated responses of IL-3, IL-4, IL-8, TGF-B).

Simultaneous Measurement of 25 Inflammatory Markers and Neurotrophins in Neonatal Dried Blood Spots by Immunoassay with xMAP Technology

“…Because no reference methods have been published for the measurement of cytokines in serum and blood and because of the large variations in serum concentrations reported in the literature, it is difficult to evaluate the absolute concentrations reported by the present multiplex method (8,16,34,(42)(43)(44)(45)(46)(47)(48). However, to the best of our knowledge the cytokine concentrations measured in sera from healthy people fell within the ranges reported by several other assays, i.e., for IL-1␤, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, IL-17, IL-18, IFN-␥, TNF-␣, GM-CSF, and MCP-1 (35, 45, 49 -54 ) (60,61 ).…”

Cryptosporidium parvum is cytopathic for cultured human biliary epithelia via an apoptotic mechanism

“…Thus, it seems likely that, in vivo, the pathogenesis of biliary cryptosporidiosis is associated not only with the interactions between biliary epithelia and C. parvum, but also with the constellation of systemic dysfunctions after human immunodeficiency virus infection. It is entirely possible that human immunodeficiency virus-induced alterations in local or systemic cytokines, particularly tumor necrosis factor ␣, which has been reported to be increased in patients with AIDS, 27 could increase the susceptibility of biliary epithelia to C. parvum infection and to apoptosis. Recent data with other parasites such as Entamoeba histolytica, Schistosoma mansoni, Trypanosoma cruzi, and Toxoplasma gondii, as well as bacteria in other tissues, are also consistent with the concept that microbial pathogens can kill host cells by an apoptotic mechanism.…”

Increased expression of the inflammatory chemokine CXC chemokine ligand 9/monokine induced by interferon-γ in lymphoid tissues of rhesus macaques during simian immunodeficiency virus infection and acquired immunodeficiency syndrome

“…Furthermore, a reduction would occur in the proportion of circulating T lymphocytes that are type 1. Among studies examining shifts in cytokine profiles in peripheral blood of HIV-1-infected individuals from type 1 to type 0 or type 2 44 are reports that support [45][46][47][48] and do not support 25,49 the existence of such a shift. Nevertheless, IFN-␥ expression in lymph nodes increases 25 and IFN-␥ expression in peripheral blood decreases [45][46][47]49 in individuals with HIV-1 infection, and antiretroviral therapy increases IFN-␥ expression in peripheral blood.…”

“…Among studies examining shifts in cytokine profiles in peripheral blood of HIV-1-infected individuals from type 1 to type 0 or type 2 44 are reports that support [45][46][47][48] and do not support 25,49 the existence of such a shift. Nevertheless, IFN-␥ expression in lymph nodes increases 25 and IFN-␥ expression in peripheral blood decreases [45][46][47]49 in individuals with HIV-1 infection, and antiretroviral therapy increases IFN-␥ expression in peripheral blood. 50 Interestingly, CXCL9/Mig and IP-10/CXCL10 are antagonists for the CCR3 chemokine receptor 51 that is expressed on type 2 lymphocytes, 52 and increased expression of CXCL9/Mig in lymphoid tissues might lead selectively to decreased trafficking of type 2 cells out of the blood.…”