| First Author | Nanda NK | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 10 | Pages | 6473-80 |
| PubMed ID | 16272301 | Mgi Jnum | J:119397 |
| Mgi Id | MGI:3701938 | Doi | 10.4049/jimmunol.175.10.6473 |
| Citation | Nanda NK, et al. (2005) DM peptide-editing function leads to immunodominance in CD4 T cell responses in vivo. J Immunol 175(10):6473-80 |
| abstractText | DM functions as a peptide editor for MHC class II-bound peptides. We examined the hypothesis that DM peptide editing plays a key role in focusing the in vivo CD4 T cell responses against complex pathogens and protein Ags to only one, or at most a few, immunodominant peptides. Most CD4 T cells elicited in the wild-type BALB/c (H-2d) mice infected with Leishmania major predominantly recognize a single epitope 158-173 within Leishmania homologue of activated receptor for c-kinase (LACK), as is the case when these mice are immunized with rLACK. Using DM-deficient (DM-/-) H-2d mice, we now show that in the absence of DM, the in vivo CD4 T cell responses to rLACK are skewed away from the immunodominant epitopes and are diversified to include two novel epitopes (LACK 33-48 and 261-276). DM-/- B10.BR (H-2k) mice showed similar results. These results constitute the first demonstration of the role of DM peptide editing in sculpting the specificity and immunodominance in in vivo CD4 T cell responses. |
