01964nas a2200361 4500000000100000008004100001260001300042653002700055653001700082653002800099653001400127653001900141653001700160653001900177653001900196653001900215653002000234653001100254653002100265653001400286653002500300653002400325653001600349100001600365700001300381700001300394700001700407245014400424300001100568490000700579520100200586022001401588 1994 d c1994 Nov10aAntibodies, Monoclonal10aAntigens, CD10aCell Adhesion Molecules10aCell Line10aFlow Cytometry10aHLA Antigens10aHLA-A Antigens10aHLA-B Antigens10aHLA-C Antigens10aHLA-DR Antigens10aHumans10aInterferon-gamma10aMonocytes10aRecombinant Proteins10aSignal Transduction10aThalidomide1 aShannon E J1 aHowe R C1 aMcLean K1 aHastings R C00aThalidomide does not perturb CD2, CD4, CD5, CD8, HLA-DR, or HLA-A, B, C molecules in vitro on the membranes of cells with immune potential. a717-290 v163 a
Thalidomide dramatically relieves the signs and symptoms of erythema nodosum leprosum (ENL). ENL is an acute inflammatory complication of lepromatous leprosy. The cause(s) of ENL as well as the mechanism of action of thalidomide in arresting ENL are unknowns. It has been suggested that ENL is the consequence of a transient activation of a cell-mediated-immune (CMI) response to Mycobacterium leprae. To initiate a CMI response, an interaction between adhesion and/or signal transducing molecules on T-cells and molecules on antigen presenting cells would occur. An alteration, induced by thalidomide, of one or more of the molecules on T-cells or antigen presenting cells that are essential to maintaining the reactive state of ENL, could explain Thalidomide's ability to attenuate ENL. Thalidomide did not modify: (a) adhesion and/or signal transducing molecules such as CD2, CD4, CD5 and CD8, or (b) molecules that facilitate antigen presentation such as HLA-DR, HLA-A, HLA-B, or HLA-C.
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