02965nas a2200457   4500000000100000008004100001260001300042653004400055653002200099653001700121653001800138653002800156653001400184653002000198653001100218653003800229653002100267653001200288653004500300653002700345653003100372653002700403653001800430653003200448100001500480700001100495700001300506700001400519700001400533700001300547700001400560700001200574700001400586700001500600245005700615856007700672300001200749490000700761520172500768022001402493       1991                            d  c1991 Nov10aAntigens, Differentiation, T-Lymphocyte10aAntigens, Surface10aCD2 Antigens10aCD58 Antigens10aCell Adhesion Molecules10aEpidermis10aGene Expression10aHumans10aIntercellular Adhesion Molecule-110aInterferon-gamma10aleprosy10aLymphocyte Function-Associated Antigen-110aMembrane Glycoproteins10aNucleic Acid Hybridization10aReceptors, Immunologic10aT-Lymphocytes10aTumor Necrosis Factor-alpha1 aSullivan L1 aSano S1 aPirmez C1 aSalgame P1 aMueller C1 aHofman F1 aUyemura K1 aRea T H1 aBloom B R1 aModlin R L00aExpression of adhesion molecules in leprosy lesions.  uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC259010/pdf/iai00047-0318.pdf  a4154-600 v593 a<p>Leprosy presents as a clinical spectrum that is precisely paralleled by a spectrum of immunological reactivity. The disease provides a useful and accessible model, in this case in the skin, in which to study the dynamics of cellular immune responses to an infectious pathogen, including the role of adhesion molecules in those responses. In lesions characterized by strong delayed-type hypersensitivity against Mycobacterium leprae (tuberculoid, reversal reaction, and Mitsuda reaction), the overlying epidermis exhibited pronounced keratinocyte intracellular adhesion molecule 1 (ICAM-1) expression and contained lymphocytes expressing the ICAM-1 ligand, LFA-1. Conversely, in lesions in which delayed-type hypersensitivity was lacking (lepromatous), keratinocyte ICAM-1 expression was low and LFA-1+ lymphocytes were rare. Expression of these adhesion molecules on the cells within the dermal granulomas was equivalent throughout the spectrum of leprosy. The percentage of lymphocytes in these granulomas containing mRNA coding for gamma interferon and tumor necrosis factor alpha, synergistic regulators of ICAM-1 expression, paralleled epidermal ICAM-1 expression. In lesions of erythema nodosum leprosum, a reactional state of lepromatous leprosy thought to be due to immune complex deposition, keratinocyte ICAM-1 expression and gamma interferon mRNA+ cells were both prominent. Antibodies to LFA-1 and ICAM-1 blocked the response of both alpha beta and gamma delta T-cell clones in vitro to mycobacteria. Overall, the expression of adhesion molecules by immunocompetent epidermal cells, as well as the cytokines which regulate such expression, correlates with the outcome of the host response to infection.</p>  a0019-9567