| First Author | Letran SE | Year | 2011 |
| Journal | Eur J Immunol | Volume | 41 |
| Issue | 1 | Pages | 29-38 |
| PubMed ID | 21182074 | Mgi Jnum | J:174661 |
| Mgi Id | MGI:5140292 | Doi | 10.1002/eji.201040717 |
| Citation | Letran SE, et al. (2011) TLR5 functions as an endocytic receptor to enhance flagellin-specific adaptive immunity. Eur J Immunol 41(1):29-38 |
| abstractText | Innate immune activation via TLR induces dendritic cell maturation and secretion of inflammatory mediators, generating favorable conditions for naive T-cell activation. Here, we demonstrate a previously unknown function for TLR5, namely that it enhances MHC class-II presentation of flagellin epitopes to CD4(+) T cells and is required for induction of robust flagellin-specific adaptive immune responses. Flagellin-specific CD4(+) T cells expanded poorly in TLR5-deficient mice immunized with flagellin, a deficiency that persisted even when additional TLR agonists were provided. Flagellin-specific IgG responses were similarly depressed in the absence of TLR5. In marked contrast, TLR5-deficient mice developed robust flagellin-specific T-cell responses when immunized with processed flagellin peptide. Surprisingly, the adaptor molecule Myd88 was not required for robust CD4(+) T-cell responses to flagellin, indicating that TLR5 enhances flagellin-specific CD4(+) T-cell responses in the absence of conventional TLR signaling. A requirement for TLR5 in generating flagellin-specific CD4(+) T-cell activation was also observed when using an in vitro dendritic cell culture system. Together, these data uncover an Myd88-independent function for dendritic cell TLR5 in enhancing the presentation of peptides to flagellin-specific CD4(+) T cells. |
