| First Author | Sacquin A | Year | 2017 |
| Journal | Eur J Immunol | Volume | 47 |
| Issue | 8 | Pages | 1295-1304 |
| PubMed ID | 28605013 | Mgi Jnum | J:248486 |
| Mgi Id | MGI:5918034 | Doi | 10.1002/eji.201746952 |
| Citation | Sacquin A, et al. (2017) The strength of BCR signaling shapes terminal development of follicular helper T cells in mice. Eur J Immunol 47(8):1295-1304 |
| abstractText | Antibody production is key for effective immune response and relies on follicular helper T (Tfh) cells. B cell-Tfh cell interactions result either in an extra-follicular low affinity B-cell response or in germinal center reactions producing high-affinity memory B cells and long-lived plasma cells. As Tfh cells influence B-cell commitment, it also became clear that B cells influence these interactions in ways that still remain unresolved. We observed that strong BCR signals decreased Tfh-cell differentiation in vitro, which correlated with decreased expression of ICOS-L at the surface of stimulated B cells. Further, we comprehensively demonstrated that ICOS-L expression correlated with the level of Tfh differentiation irrespective of antigen presentation at the surface of activated B cells. Our in vivo experiments could show that immunization with a high-affinity antigen for B cells resulted in much less Tfh development than immunization with low-affinity antigen. Furthermore, blocking ICOS-L in vivo inhibited Tfh development when using low-affinity antigen. Altogether, these results indicate that BCR affinity shapes Tfh-cell development in part through ICOS/ICOS-L interactions. Ultimately, we reveal new depths in the B cell-Tfh cell crosstalk that could eventually result in better vaccine protocols. |
