期刊
NATURE IMMUNOLOGY
卷 18, 期 1, 页码 36-44出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3622
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资金
- NIAID of the US National Institutes of Health [R01 AI083988, AI059739]
- NIMH of the US National Institutes of Health [MH092906, NSF BRAIN EAGER MCB-1450895]
- New Jersey Commission on Cancer Research Fellowship
- Robert Wood Johnson Foundation [67038]
- Century for the Cure (Fellowship in Translational Immunology)
The interaction between the T cell antigen receptor (TCR) expressed by natural killer T cells (NKT cells) and the antigen-presenting molecule CD1d is distinct from interactions between the TCR and major histocompatibility complex (MHC). Our molecular modeling suggested that a hydrophobic patch created after TCR alpha-TCR beta pairing has a role in maintaining the conformation of the NKT cell TCR. Disruption of this patch ablated recognition of CD1d by the NKT cell TCR but not interactions of the TCR with MHC. Partial disruption of the patch, while permissive to the recognition of CD1d, significantly altered NKT cell development, which resulted in the selective accumulation of adipose-tissue-resident NKT cells. These results indicate that a key component of the TCR is essential for the development of a distinct population of NKT cells.
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