02016nas a2200373   4500000000100000008004100001260001300042653001000055653002300065653002000088653002100108653001100129653001100140653001200151653003300163653000900196653001600205653001400221653002500235653001800260653003200278100001600310700001700326700002100343700001300364700001600377700001700393245011300410300001200523490000800535050001700543520106800560022001401628       2000                            d  c2000 Nov10aAdult10aCell Communication10aCells, Cultured10aErythema Nodosum10aFemale10aHumans10aleprosy10aLipopolysaccharide Receptors10aMale10aMiddle Aged10aMonocytes10aMycobacterium leprae10aT-Lymphocytes10aTumor Necrosis Factor-alpha1 aSampaio E P1 aOliveira R B1 aWarwick-Davies J1 aNeto R B1 aGriffin G E1 aShattock R J00aT cell-monocyte contact enhances tumor necrosis factor-alpha production in response to Mycobacterium leprae.  a1463-720 v182  aSAMPAIO 20003 a<p>Tumor necrosis factor (TNF)-alpha has been implicated as a key factor in inflammatory processes occurring in erythema nodosum leprosum (ENL). In the present study, the roles of soluble factors and contact-mediated interaction in the induction of enhanced TNF-alpha secretion in leprosy have been investigated. In vitro studies have demonstrated that Mycobacterium leprae per se is a poor stimulus for TNF-alpha production by purified monocytes obtained from normal subjects, although this could be enhanced by either exogenous interferon-gamma or cell contact with fixed activated T lymphocytes. Further investigations demonstrated that monocyte-T cell contact enhanced M. leprae-induced TNF-alpha production by peripheral blood mononuclear cells of ENL patients and was modulated by blocking antibodies to CD40L, CD69, and CD18. These results suggest that physical contact with T cells isolated from patients in a particular disease state (ENL) modulates monocyte function and may contribute to the secretion of proinflammatory cytokines described in ENL.</p>  a0022-1899