| First Author | Escande-Beillard N | Year | 2010 |
| Journal | J Immunol | Volume | 184 |
| Issue | 2 | Pages | 816-23 |
| PubMed ID | 20018625 | Mgi Jnum | J:159396 |
| Mgi Id | MGI:4442543 | Doi | 10.4049/jimmunol.0902159 |
| Citation | Escande-Beillard N, et al. (2010) Neurons preferentially respond to self-MHC class I allele products regardless of peptide presented. J Immunol 184(2):816-23 |
| abstractText | Studies of mice lacking MHC class I (MHC I)-associated proteins have demonstrated a role for MHC I in neurodevelopment. A central question arising from these observations is whether neuronal recognition of MHC I has specificity for the MHC I allele product and the peptide presented. Using a well-established embryonic retina explant system, we observed that picomolar levels of a recombinant self-MHC I molecule inhibited neurite outgrowth. We then assessed the neurobiological activity of a panel of recombinant soluble MHC Is, consisting of different MHC I heavy chains with a defined self- or nonself-peptide presented, on cultured embryonic retinas from mice with different MHC I haplotypes. We observed that self-MHC I allele products had greater inhibitory neuroactivity than nonself-MHC I molecules, regardless of the nature of the peptide presented, a pattern akin to MHC I recognition by some innate immune system receptors. However, self-MHC I molecules had no effect on retinas from MHC I-deficient mice. These observations suggest that neuronal recognition of MHC I may be coordinated with the inherited MHC I alleles, as occurs in the innate immune system. Consistent with this notion, we show that MHC I and MHC I receptors are coexpressed by precursor cells at the earliest stages of retina development, which could enable such coordination. |
