Journal
IMMUNITY
Volume 34, Issue 3, Pages 315-326Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2011.01.013
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Funding
- National Institutes of Health [AI076463, AI078246, AI187785, T32 AI07405]
- Howard Hughes Medical Institute
- Cancer Council of Victoria
- National Health and Medical Research Council of Australia
- NHMRC
- Australian Research Council
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The antigen receptor for natural killer T cells (NKT TCR) binds CD1d-restricted microbial and self-lipid antigens, although the molecular basis of self-CD1d recognition is unclear. Here, we have characterized NKT TCR recognition of CD1d molecules loaded with 0 natural self-antigens (Ags) and report the 2.3 angstrom resolution structure of an autoreactive NKT TCR-phosphatidylinositol-CD1d complex. NKT TCR recognition of self- and foreign antigens was underpinned by a similar mode of germline-encoded recognition of CD1d. However, NKT TCR autoreactivity is mediated by unique sequences within the non-germline-encoded CDR3 beta loop encoding for a hydrophobic motif that promotes self-association with CD1d. Accordingly, NKT cell autoreactivity may arise from the inherent affinity of the interaction between CD1d and the NKT TCR, resulting in the recognition of a broad range of CD1d-restricted self-antigens. This demonstrates that multiple self-antigens can be recognized in a similar manner by autoreactive NKT TCRs.
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