期刊
IMMUNITY
卷 31, 期 1, 页码 60-71出版社
CELL PRESS
DOI: 10.1016/j.immuni.2009.05.010
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类别
资金
- National Institute of Health [AI057485, A1076463, A1078246, 8785, A1057519, T32 A107405]
- Howard Hughes Medical Institute
- Australian Research Council Federation Fellowship
- National Health and Medical Research Council (NHMRC) Research Fellowship
- Cancer Research UK [11331] Funding Source: researchfish
- Medical Research Council [MC_U137884181] Funding Source: researchfish
- MRC [MC_U137884181] Funding Source: UKRI
Mouse type I natural killer T cell receptors (iNKT TCRs) use a single V alpha 14-J alpha 18 sequence and V beta s that are almost always V beta 8.2, V beta 7, or V beta 2, although the basis of this differential usage is unclear. We showed that the V beta bias occurred as a consequence of the CDR2 beta loops determining the affinity of the iNKT TCR for CD1d-glycolipids, thus controlling positive selection. Within a conserved iNKT-TCR-CD1d docking framework, these inherent V beta-CD1d affinities are further modulated by the hypervariable CDR3 beta loop, thereby defining a functional interplay between the two iNKT TCR CDR beta loops. These V beta biases revealed a broadly hierarchical response in which V beta 8.2>V beta 7>V beta 2 in the recognition of diverse CD1d ligands. This restriction of the iNKT TCR repertoire during thymic selection paradoxically ensures that each peripheral iNKT cell recognizes a similar spectrum of antigens.
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