| First Author | Vomhof-DeKrey EE | Year | 2015 |
| Journal | Proc Natl Acad Sci U S A | Volume | 112 |
| Issue | 40 | Pages | 12474-9 |
| PubMed ID | 26392556 | Mgi Jnum | J:227076 |
| Mgi Id | MGI:5699644 | Doi | 10.1073/pnas.1504790112 |
| Citation | Vomhof-DeKrey EE, et al. (2015) Cognate interaction with iNKT cells expands IL-10-producing B regulatory cells. Proc Natl Acad Sci U S A 112(40):12474-9 |
| abstractText | Successful induction of B-cell activation and memory depends on help from CD4(+) T cells. Invariant natural killer T (iNKT) cells (glycolipid-specific, CD1d-restricted innate lymphocytes) provide both cognate (direct) and noncognate (indirect) helper signals to enhance B-cell responses. Both forms of iNKT-cell help induce primary humoral immune responses, but only noncognate iNKT-cell help drives humoral memory and plasma cells. Here, we show that iNKT cognate help for B cells is fundamentally different from the help provided by conventional CD4(+) T cells. Cognate iNKT-cell help drives an early, unsustained germinal center B-cell expansion, less reduction of T follicular regulatory cells, an expansion of marginal zone B cells, and early increases in regulatory IL-10-producing B-cell numbers compared with noncognate activation. These results are consistent with a mechanism whereby iNKT cells preferentially provide an innate form of help that does not generate humoral memory and has important implications for the application of glycolipid molecules as vaccine adjuvants. |
