| First Author | Silva-Barrios S | Year | 2016 |
| Journal | Cell Rep | Volume | 15 |
| Issue | 11 | Pages | 2427-37 |
| PubMed ID | 27264176 | Mgi Jnum | J:238246 |
| Mgi Id | MGI:5818646 | Doi | 10.1016/j.celrep.2016.05.028 |
| Citation | Silva-Barrios S, et al. (2016) Innate Immune B Cell Activation by Leishmania donovani Exacerbates Disease and Mediates Hypergammaglobulinemia. Cell Rep 15(11):2427-37 |
| abstractText | Participation of B cells in the immune response by various antibody-independent mechanisms has recently been uncovered. B cells producing cytokines have been described for several infections and appear to regulate the adaptive immune response. B cell activation by Leishmania donovani results in disease exacerbation. How Leishmania activates B cells is still unknown. We show that L. donovani amastigotes activate B cells by triggering endosomal TLRs; this activation leads to the induction of various cytokines. Cytokine expression is completely abrogated in B cells from Ifnar(-/-) mice upon exposure to L. donovani, suggesting an involvement of IFN-I in a positive feedback loop. IFN-I also appears to enhance the expression of endosomal TLRs following exposure to L. donovani. Cell-specific ablation of endosomal TLR signaling in B cells revealed that innate B cell activation by L. donovani is responsible for disease exacerbation through IL-10 and IFN-I production and for the promotion of hypergammaglobulinemia. |
