| First Author | Stadinski BD | Year | 2016 |
| Journal | Nat Immunol | Volume | 17 |
| Issue | 8 | Pages | 946-55 |
| PubMed ID | 27348411 | Mgi Jnum | J:259367 |
| Mgi Id | MGI:6142291 | Doi | 10.1038/ni.3491 |
| Citation | Stadinski BD, et al. (2016) Hydrophobic CDR3 residues promote the development of self-reactive T cells. Nat Immunol 17(8):946-55 |
| abstractText | Studies of individual T cell antigen receptors (TCRs) have shed some light on structural features that underlie self-reactivity. However, the general rules that can be used to predict whether TCRs are self-reactive have not been fully elucidated. Here we found that the interfacial hydrophobicity of amino acids at positions 6 and 7 of the complementarity-determining region CDR3beta robustly promoted the development of self-reactive TCRs. This property was found irrespective of the member of the beta-chain variable region (Vbeta) family present in the TCR or the length of the CDR3beta. An index based on these findings distinguished Vbeta2(+), Vbeta6(+) and Vbeta8.2(+) regulatory T cells from conventional T cells and also distinguished CD4(+) T cells selected by the major histocompatibility complex (MHC) class II molecule I-A(g7) (associated with the development of type 1 diabetes in NOD mice) from those selected by a non-autoimmunity-promoting MHC class II molecule I-A(b). Our results provide a means for distinguishing normal T cell repertoires versus autoimmunity-prone T cell repertoires. |
