期刊
SCIENCE IMMUNOLOGY
卷 3, 期 24, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciimmunol.aan2543
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资金
- U.S. NIH [R01DK67180]
- Agency for Science, Technology and Research
- European Research Council [280307-Epithelial_Immunol]
- Biotechnology and Biological Sciences Research Council [BBS/E/B/000C0407, BBS/E/B/000C0409]
- NC3R [NC/L001217/1]
- European Union H2020 ERA project [667824-EXCELLtoINNOV]
- projeto cofinanciado pelo FEDER atraves POR Lisboa 2020-Programa Operacional Regional de Lisboa, do PORTUGAL 2020, e pela Fundacao para a Ciencia e a Tecnologia [LISBOA-01-0145-FEDER-007391]
- BBSRC [BBS/E/B/000C0427, BBS/E/B/000C0409, BBS/E/B/000C0407] Funding Source: UKRI
Epithelial-resident T lymphocytes, such as intraepithelial lymphocytes (IELs) located at the intestinal barrier, can offer swift protection against invading pathogens. Lymphocyte activation is strictly regulated because of its potential harmful nature and metabolic cost, and most lymphocytes are maintained in a quiescent state. However, IELs are kept in a heightened state of activation resembling effector T cells but without cytokine production or clonal proliferation. We show that this controlled activation state correlates with alterations in the IEL mitochondria! membrane, especially the cardiolipin composition. Upon inflammation, the cardiolipin composition is altered to support IEL proliferation and effector function. Furthermore, we show that cardiolipin makeup can particularly restrict swift IEL proliferation and effector functions, reducing microbial containment capability. These findings uncover an alternative mechanism to control cellular activity, special to epithelial-resident T cells, and a novel role for mitochondria, maintaining cells in a metabolically poised state while enabling rapid progression to full functionality.
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