Journal
EMBO JOURNAL
Volume 39, Issue 15, Pages -Publisher
WILEY
DOI: 10.15252/embj.2020104749
Keywords
ccr5[delta]32; humoral response; membrane phase; sphingolipid; T-cell receptor
Categories
Funding
- Spanish Ministerio de Ciencia, Innovacion y Universidades (AEI/FEDER, EU) [SAF2017-83732-R, FIS2016-78883-C2-2-P, CTQ2017-85378-R]
- Instituto de Salud Carlos III (ISCIII) [PI13/02434, PI16/01861]
- Comunidad de Madrid (IMMUNOTHERCAN-CM) [B2017/BMD-3733]
- Merck-Salud Foundation
- Deutsche Forschungsgemeinschaft (DFG) [BIOSS-EXC294, CIBSS-EXC 2189, 390939984, SCHA976/7-1, SFB1381]
- Fundacion Bancaria La Caixa
- Grifols SA
- Fundacio ACE
- ISCIII (Ministry of Health, Spain)
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CCR5 is not only a coreceptor forHIV-1 infection inCD4(+)T cells, but also contributes to their functional fitness. Here, we show that by limiting transcription of specific ceramide synthases,CCR5 signaling reduces ceramide levels and thereby increases T-cell antigen receptor (TCR) nanoclustering in antigen-experienced mouse and humanCD4(+)T cells. This activity isCCR5-specific and independent ofCCR5 co-stimulatory activity.CCR5-deficient mice showed reduced production of high-affinity class-switched antibodies, but only after antigen rechallenge, which implies an impaired memoryCD4(+)T-cell response. This study identifies aCCR5 function in the generation ofCD4(+)T-cell memory responses and establishes an antigen-independent mechanism that regulatesTCRnanoclustering by altering specific lipid species.
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