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Immune cellular parameters of leprosy and human immunodeficiency virus‐1 co‐infected subjects
Author(s) -
Carvalho Karina I.,
Maeda Solange,
Marti Luciana,
Yamashita Jane,
Haslett Patrick A. J.,
Kallas Esper G.
Publication year - 2008
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2007.02756.x
Subject(s) - immunology , cd8 , cellular immunity , biology , immune system , mycobacterium leprae , immunopathology , t cell , peripheral blood mononuclear cell , immunity , population , flow cytometry , virology , t lymphocyte , virus , leprosy , medicine , in vitro , biochemistry , environmental health
Leprosy and human immunodeficiency virus‐1 (HIV‐1) are examples of human infections where interactions between the pathogen and the host cellular immunity determine the clinical manifestations of disease. Hence, a significant immunopathological interaction between HIV‐1 and leprosy might be expected. In the present study we explored several aspects of cellular immunity in patients co‐infected with HIV‐1 and Mycobacterium leprae . Twenty‐eight individuals were studied, comprising four groups: healthy controls, HIV‐1 and M. leprae co‐infection, HIV‐1 mono‐infection, and M. leprae mono‐infection. Subjects in the mono‐infection and co‐infection groups were matched as far as possible for bacillary load and HIV disease status, as appropriate. Peripheral blood mononuclear cells (PBMC) were analysed using six‐ and seven‐colour flow cytometry to evaluate T‐cell subpopulations and their activation status, dendritic cell (DC) distribution phenotypes and expression of IL‐4 by T cells. The co‐infected group exhibited lower CD4 : CD8 ratios, higher levels of CD8 + T‐cell activation, increased Vδ1 : Vδ2 T cell ratios and decreased percentages of plasmacytoid DC, compared with HIV‐1 mono‐infected subjects. Across infected groups, IL‐4 production by CD4 + T lymphocytes was positively correlated with the percentage of effector memory CD4 + T cells, suggesting antigenically driven differentiation of this population of T cells in both HIV‐1 and M. leprae infections. Co‐infection with M. leprae may exacerbate the immunopathology of HIV‐1 disease. A T helper 2 (Th2) bias in the CD4 + T‐cell response was evident in both HIV‐1 infection and leprosy, but no additive effect was apparent in co‐infected patients.