02236nas a2200397   4500000000100000008004100001260001300042653001000055653000900065653004400074653002300118653001100141653001900152653001100171653002300182653001200205653002500217653002500242653000900267653002700276653001600303653003300319653002500352653001800377100001500395700001400410700001300424700001000437700001400447245009200461856007700553300001100630490000800641520117500649022001401824       2007                            d  c2007 Apr10aAdult10aAged10aAntigens, Differentiation, T-Lymphocyte10aAntigens, Neoplasm10aFemale10aFlow Cytometry10aHumans10aImmunity, Cellular10aleprosy10aLeprosy, lepromatous10aLeprosy, Tuberculoid10aMale10aMembrane Glycoproteins10aMiddle Aged10aReceptors, Lymphocyte Homing10aT-Lymphocyte Subsets10aUp-Regulation1 aSieling PA1 aLegaspi A1 aOchoa MT1 aRea T1 aModlin RL00aRegulation of human T-cell homing receptor expression in cutaneous bacterial infection.  uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2265905/pdf/imm0120-0518.pdf  a518-250 v1203 a<p>We investigated the regulation of T-cell homing receptors in infectious disease by evaluating the cutaneous lymphocyte antigen (CLA) in human leprosy. We found that CLA-positive cells were enriched in the infectious lesions associated with restricting the growth of the pathogen Mycobacterium leprae, as assessed by the clinical course of infection. Moreover, CLA expression on T cells isolated from the peripheral blood of antigen-responsive tuberculoid leprosy patients increased in the presence of M. leprae (2.4-fold median increase; range 0.8-6.1, n = 17), but not in unresponsive lepromatous leprosy patients (1.0-fold median increase; range 0.1-2.2, n = 10; P < 0.005). Mycobacterium leprae specifically up-regulated the skin homing receptor, CLA, but not alpha(4)/beta(7), the intestinal homing receptor, which decreased on T cells of patients with tuberculoid leprosy after antigen stimulation (2.2-fold median decrease; range 1.6-3.4, n = 3). Our data indicate that CLA expression is regulated during the course of leprosy infection and suggest that T-cell responsiveness to a microbial antigen directs antigen-specific T cells to the site of infection.</p>  a0019-2805