01967nas a2200361   4500000000100000008004100001260001300042653001500055653002000070653001700090653001100107653002100118653001700139653001900156653002500175653002600200653001600226653001400242653001400256100001200270700001700282700001200299700001600311700001300327700001400340700001100354245013800365300001100503490000700514050001500521520105500536022001401591       1995                            d  c1995 Dec10aAntibodies10aCells, Cultured10aDinoprostone10aHumans10aImmune Tolerance10aIndomethacin10aInterleukin-1010aLeprosy, lepromatous10aLymphocyte Activation10aLymphopenia10aMonocytes10aTh1 Cells1 aMisra N1 aSelvakumar M1 aSingh S1 aBharadwaj M1 aRamesh V1 aMisra R S1 aNath I00aMonocyte derived IL 10 and PGE2 are associated with the absence of Th 1 cells and in vitro T cell suppression in lepromatous leprosy.  a123-280 v48  aMISRA 19953 a<p>Our previous studies had shown that the clinicopathological spectrum in leprosy was associated with discrete T cell subsets in circulation, with tuberculoid patients having antigen-induced Th 1, whereas lepromatous leprosy patients with antigen-specific T cell anergy possessed Th 2 cells. The present study shows that infected monocytes from lepromatous but not tuberculoid leprosy patients released soluble factors (MoF(s)) containing IL-10 and PGE2 which inhibited M. leprae induced in vitro lymphoproliferation of previously sensitised healthy or tuberculoid leprosy subjects. A strong negative correlation was observed between adherent cell derived IL-10 and IL-2 at the level of both the product and cytokine mRNA. Moreover, anti-IL-10 antibodies and indomethacin partially reversed the suppressor effects of MoF(s). Taken together these studies indicate that infected monocytes contribute to the development of T cell anergy by releasing factors that affect regulatory cytokines and T cell subset differentiation in lepromatous leprosy.</p>  a0165-2478