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Mycobacterium tuberculosis Recall Antigens Suppress HIV-1 Replication in Anergic Donor Cells via CD8+ T Cell Expansion and Increased IL-10 Levels
- Source :
- Journal of Immunology, Journal of Immunology, Publisher : Baltimore : Williams & Wilkins, c1950-. Latest Publisher : Bethesda, MD : American Association of Immunologists, 2004, 172 (3), pp.1953-1959. 〈10.4049/jimmunol.172.3.1953〉
- Publication Year :
- 2004
- Publisher :
- The American Association of Immunologists, 2004.
-
Abstract
- Mycobacterium tuberculosis (MTb) is the leading cause of death in the setting of AIDS. MTb enhances the pathogenicity and accelerates the course of HIV disease and, furthermore, infection with HIV-1 increases the risk of reactivation or reinfection with MTb. In this study, we show that host-specific recall responses to one pathogen, MTb, has a direct effect upon the regulation of a second pathogen, HIV-1. Using cells from immunocompetent former tuberculosis (TB) patients who displayed either a persistently positive (responsive) or negative (anergic), delayed-type hypersensitivity (DTH) reaction to intradermal injection of purified protein derivative (PPD), we investigated the effect of recall Ags to MTb upon the replication of HIV-1 primary isolates in vitro. We show that HIV-1 replication of a T cell-tropic isolate was significantly impaired in MTb-stimulated PBMC from PPD-anergic donors. Furthermore, these donors displayed a significant increase in CD8+ T cells and IL-10 levels and lower levels of IL-2 and TNF-α relative to PPD-responsive donors in response to PPD stimulation. Strikingly, CD8+ T cell depletion and blocking of IL-10 significantly increased HIV-1 replication in these PPD-anergic donors, indicating that an immunosuppressive response to MTb recall Ags inhibits HIV-1 replication in PPD-anergic individuals. Therefore, immunotherapeutic approaches aimed at recapitulating Ag-specific MTb anergy in vivo could result in novel and effective approaches to inhibit HIV-1 disease progression in MTb/HIV-1 coinfection.
- Subjects :
- MESH : Tuberculosis, Pulmonary
MESH : Cytokines
CD8-Positive T-Lymphocytes
[ SDV.MP.BAC ] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology
Lymphocyte Activation
Virus Replication
[ SDV.IMM.IA ] Life Sciences [q-bio]/Immunology/Adaptive immunology
Immunology and Allergy
Cytotoxic T cell
MESH : Immunosuppressive Agents
Cells, Cultured
MESH : Tumor Necrosis Factor-alpha
biology
Clonal anergy
MESH : Antigens, Bacterial
MESH : Cell Division
MESH : CD8-Positive T-Lymphocytes
Interleukin-10
MESH : Virus Replication
[ SDV.MHEP.MI ] Life Sciences [q-bio]/Human health and pathology/Infectious diseases
Interleukin 10
Coinfection
Cytokines
Cell Division
Immunosuppressive Agents
MESH : HIV-1
Tuberculosis
Anti-HIV Agents
MESH : Immunologic Memory
Immunology
chemical and pharmacologic phenomena
Tuberculin
MESH : Clonal Anergy
MESH : Tuberculin
Mycobacterium tuberculosis
MESH : Mycobacterium tuberculosis
Antigen
MESH : Interleukin-10
[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathology
MESH : Cells, Cultured
medicine
Tuberculosis, Pulmonary
MESH : Lymphocyte Activation
Clonal Anergy
Antigens, Bacterial
Tumor Necrosis Factor-alpha
MESH : Anti-HIV Agents
bacterial infections and mycoses
biology.organism_classification
medicine.disease
Virology
MESH : Leukocytes, Mononuclear
HIV-1
Leukocytes, Mononuclear
Immunologic Memory
CD8
Subjects
Details
- ISSN :
- 15506606 and 00221767
- Volume :
- 172
- Database :
- OpenAIRE
- Journal :
- The Journal of Immunology
- Accession number :
- edsair.doi.dedup.....6c82d94a0757f1bcd710bad9c11ee166