期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 200, 期 6, 页码 749-759出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20040874
关键词
HIV pathogenesis; CD4(+) T cell depletion; lymph nodes; gastrointestinal tract; HIV-specific T cells
资金
- NIAID NIH HHS [K24 AIO56986, R56 AI054232, R37 AI028246, K24 AI056986, R01 AI054232, R01 AI54232] Funding Source: Medline
- NIDCR NIH HHS [R01 DE-12934] Funding Source: Medline
The mechanisms underlying CD4(+) T cell depletion in human immunodeficiency virus (HIV) infection are not well understood. Comparative studies of lymphoid tissues, where the vast majority of T cells reside, and peripheral blood can potentially illuminate the pathogenesis of HIV-associated disease. Here, we studied the effect of HIV infection on the activation and depletion of defined subsets of CD4(+) and CD8(+) T cells in the blood, gastrointestinal (GI) tract, and lymph node (LN). We also measured HIV-specific T cell frequencies in LNs and blood, and LN collagen deposition to define architectural changes associated with chronic inflammation. The major findings to emerge are the following: the GI tract has the most substantial CD4(+) T cell depletion at all stages of HIV disease; this depletion occurs preferentially within CCR5(+) CD4(+) T cells; HIV-associated immune activation results in abnormal accumulation of effector-type T cells within LNs; HIV-specific T cells in LNs do not account for all effector T cells; and T cell activation in LNs is associated with abnormal collagen deposition. Taken together, these findings define the nature and extent of CD4(+) T cell depletion in lymphoid tissue and point to mechanisms of profound depletion of specific T cell subsets related to elimination of CCR5(+) CD4(+) T cell targets and disruption of T cell homeostasis that accompanies chronic immune activation.
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