1. Alteration in CD29(high) CD4(+) lymphocyte subset is a common feature of early HIV disease and of active tuberculosis.
- Author
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Diagbouga S, Chiron JP, Sanou O, and Ledru E
- Subjects
- Acquired Immunodeficiency Syndrome blood, Acquired Immunodeficiency Syndrome complications, Acquired Immunodeficiency Syndrome epidemiology, Acquired Immunodeficiency Syndrome immunology, Adult, Burkina Faso epidemiology, CD4 Antigens analysis, Comorbidity, Disease Progression, Female, HIV Infections blood, HIV Infections complications, HIV Infections epidemiology, Homeostasis, Humans, Leukocyte Common Antigens analysis, Male, Tuberculosis, Pulmonary blood, Tuberculosis, Pulmonary complications, Tuberculosis, Pulmonary epidemiology, CD4 Lymphocyte Count, CD4-Positive T-Lymphocytes classification, HIV Infections immunology, Integrin beta1 analysis, T-Lymphocyte Subsets, Tuberculosis, Pulmonary immunology
- Abstract
Peripheral CD4 T-cell depletion has been observed in human immunodeficiency virus (HIV)-negative patients with pulmonary tuberculosis (TB). To investigate more accurately this alteration, we studied peripheral blood CD45RA(+) and CD29(high) CD4 subsets in 79 TB patients with (HIV(+)TB(+)) or without (HIV(-)TB(+)) HIV infection, 85 HIV-infected patients without TB (HIV(+)TB(-)), and 43 healthy controls, all living in West Africa. The high proportion of CD4(+)CD29(high) T cells observed in controls was dramatically decreased in CDC-A stage HIV(+)TB(-) patients. CD45RA(+) CD4(+) T cells were depleted during the CDC-B stage. Both the percentage and the absolute count of CD29(high)CD4(+) T cells were decreased in HIV(-)TB(+) and HIV(+)TB(+) patients versus controls, but CD45RA(+)CD4(+) T cells were not decreased in TB patients without HIV-infection. Although distinct alterations in the CD4(+) T-cell homeostasis are involved in TB(-) versus HIV-infected subjects, our data suggest that the CD29(+)CD4(+) T-cell depletion observed during the early HIV disease contributes to the risk of active TB, by reducing the pool of T cells able to relocalize to the sites of the M. tuberculosis multiplication.
- Published
- 2001
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