期刊
BIOESSAYS
卷 41, 期 1, 页码 -出版社
WILEY
DOI: 10.1002/bies.201800128
关键词
CD38; CD4-Positive T lymphocytes; HIV/AIDS; immune activation; immunometabolism; NAD; Warburg effect
资金
- Mexican National Council for Science and Technology (CONACYT) [FC-2015-214]
- National Institutes of Health [AI091526, AI128864]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI128864] Funding Source: NIH RePORTER
Despite abundant evidence associating CD38 overexpression and CD4 T cell depletion in HIV infection, no causal relation has been investigated. To address this issue, a series of mechanisms are proposed, supported by evidence from different fields, by which CD38 overexpression can facilitate CD4 T cell depletion in HIV infection. According to this model, increased catalytic activity of CD38 may reduce CD4 T cells' cytoplasmic nicotin-amide adenine dinucleotide (NAD), leading to a chronic Warburg effect. This will reduce mitochondrial function. Simultaneously, CD38's catalytic products ADPR and cADPR may be transported to the cytoplasm, where they can activate calcium channels and increase cytoplasmic Ca2+ concentrations, further altering mitochondrial integrity. These mechanisms will decrease the viability and regenerative capacity of CD4 T cells. These hypotheses can be tested experimentally, and might reveal novel therapeutic targets. Also see the video abstract here https://youtu.be/k1LTyiTKPKs.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据