03032nas a2200469 4500000000100000008004100001260001300042653001000055653001900065653001100084653002500095653003100120653001100151653003500162653001400197653001900211653001100230653002200241653004100263653001200304653000900316653001600325653001500341653002900356653000900385653003000394653003500424653001600459100001300475700002300488700001300511700001300524700001400537700001400551700001200565700001300577245018400590300001000774490000800784520175600792022001402548 2011 d c2011 Aug10aAdult10aAntigens, CD2010aBiopsy10aCase-Control Studies10aCD8-Positive T-Lymphocytes10aFemale10aForkhead Transcription Factors10aGranuloma10aHIV Infections10aHumans10aImmunophenotyping10aInterleukin-3 Receptor alpha Subunit10aleprosy10aMale10aMiddle Aged10atratamento10aPoly(A)-Binding Proteins10aSkin10aSkin Diseases, Infectious10aT-Cell Intracellular Antigen-110aYoung Adult1 aTalhari 1 aRibeiro-Rodrigues 1 aTalhari 1 aMassone 1 aBrunasso 1 aCampbell 1 aCurcic 1 aCerroni 00aImmunophenotype of skin lymphocytic infiltrate in patients co-infected with Mycobacterium leprae and human immunodeficiency virus: a scenario dependent on CD8+ and/or CD20+ cells. a321-80 v1653 a

BACKGROUND: Leprosy occurs rarely in human immunodeficiency virus (HIV)-positive patients. In contrast to tuberculosis, there has been no report to date of an increase in HIV prevalence among patients with leprosy or of differences in leprosy's clinical spectrum. While several studies describe the systemic immune response profile in patients co-infected with HIV and leprosy, the local immune skin response has been evaluated in only a small number of case reports and limited series of patients.

OBJECTIVE: To investigate the interaction between Mycobacterium leprae and HIV infection in the skin.

METHODS: We investigated the presence and frequency of cells positive for CD4, CD8, CD20, TIA-1, FOXP3 and CD123 in lymphocytic infiltrates from 16 skin biopsies taken from 15 patients with HIV-leprosy co-infection.

RESULTS: CD4+ cells were absent in infiltrates from 6 (38%) skin biopsies and present in 10 (62%) cases at low levels (<1·16%) of the lymphocytic infiltrate. CD8+ was the predominant phenotype in the infiltrate (99·4%), followed by TIA-1, expressed by >75% of CD8+ cells. FOXP3+ cells were also present, representing 3·4% of the lymphocytic infiltrate. CD20+ cells were detected in 75% of the cases; however, in two cases (12%) these cells represented 25-50% of the infiltrate, while in the other 10 cases (62%) they were present only focally (<25% of the infiltrate). CD123+ cells were not observed in any of the studied specimens.

CONCLUSIONS: Data presented here suggest that cell-mediated immune responses to M. leprae are preserved at the site of disease and that in the absence of CD4+ cells, CD8+FOXP3+ and CD20+ cells may be involved in granuloma formation.

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