期刊
JOURNAL OF IMMUNOLOGY
卷 180, 期 8, 页码 5530-5536出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.8.5530
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资金
- NCRR NIH HHS [U54 RR022241, U54 RR02241, U54 RR022241-01] Funding Source: Medline
- NHLBI NIH HHS [HL072682, R01 HL072682, R01 HL072682-01] Funding Source: Medline
- NIAID NIH HHS [R01 AI060422-02, R01 AI060422, AI060422] Funding Source: Medline
Regulatory T cells (T-reg) play key roles in immune regulation through multiple modes of suppression. The effects of HIV-1 infection on T-reg levels in lymphoid tissues remain incompletely understood. To explore this issue, we have measured the levels of forkhead box protein 3 (FOXP3)-positive cells and associated immunomodulatory genes in a pathogenic simian immunodeficiency virus/macaque model and found that a loss of T-reg in lymph nodes occurred following simian immunodeficiency virus infection. Changes in expression of the ligands for CXCR3, CCR4, and CCR7 and the cytokines TGF-beta and IL-2 were all linked to this loss of T-reg, which in turn was linked with increased levels of cellular activation. Our findings identify three mechanisms that likely contribute to SIV-driven loss of T-reg, including reduced levels of cytokines associated with T-reg differentiation and altered expression of agonist and antagonist chemokines. The loss of T-reg and the associated cellular activation in lymphoid tissues is consistent with the events in HIV-1-infected individuals and suggest that components of the T-reg differentiation and trafficking network could be targets for therapeutic intervention.
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