02065nas a2200337   4500000000100000008004100001260001600042653002000058653003100078653001100109653002100120653001900141653001900160653001700179653001200196653002800208653001800236100001600254700001400270700001400284700001400298700001600312700001200328700001500340245010300355856007000458300001100528490000700539520116700546022001401713       1997                            d  c1997 Jan 1510aDown-Regulation10aGene Expression Regulation10aHumans10aInterferon-gamma10aInterleukin-1010aInterleukin-1210aInterleukins10aleprosy10aLeukocytes, Mononuclear10aUp-Regulation1 aLibraty D H1 aAiran L E1 aUyemura K1 aJullien D1 aSpellberg B1 aRea T H1 aModlin R L00aInterferon-gamma differentially regulates interleukin-12 and interleukin-10 production in leprosy.  uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC507801/pdf/990336.pdf  a336-410 v993 a<p>The ability of monocytes to influence the nature of the T cell response to microbial pathogens is mediated in part by the release of cytokines. Of particular importance is the release of IL-12 and IL-10 by cells of the monocyte/macrophage lineage upon encountering the infectious agent. IL-12 promotes cell mediated immunity (CMI) to intracellular pathogens by augmenting T-helper type 1 responses, whereas IL-10 downregulates these responses. The ability of IFN-gamma to modulate the balance between IL-12 and IL-10 production was examined by studying leprosy as a model. In response to Mycobacterium leprae stimulation, IFN-gamma differentially regulated IL-12 and IL-10 production resulting in upregulation of IL-12 release and downregulation of IL-10 release. Furthermore, we determined that the mechanism by which IFN-gamma downregulates IL-10 was through the induction of IL-12. The data suggest a model of lymphocyte-monocyte interaction whereby the relative presence or absence of IFN-gamma in the local microenvironment is a key determinant of the type of monocyte cytokine response, and hence the degree of CMI in the host response to infection.</p>  a0021-9738