| First Author | Kelly-Scumpia KM | Year | 2011 |
| Journal | J Exp Med | Volume | 208 |
| Issue | 8 | Pages | 1673-82 |
| PubMed ID | 21746813 | Mgi Jnum | J:177607 |
| Mgi Id | MGI:5295543 | Doi | 10.1084/jem.20101715 |
| Citation | Kelly-Scumpia KM, et al. (2011) B cells enhance early innate immune responses during bacterial sepsis. J Exp Med 208(8):1673-82 |
| abstractText | Microbes activate pattern recognition receptors to initiate adaptive immunity. T cells affect early innate inflammatory responses to viral infection, but both activation and suppression have been demonstrated. We identify a novel role for B cells in the early innate immune response during bacterial sepsis. We demonstrate that Rag1(-/-) mice display deficient early inflammatory responses and reduced survival during sepsis. Interestingly, B cell-deficient or anti-CD20 B cell-depleted mice, but not alpha/beta T cell-deficient mice, display decreased inflammatory cytokine and chemokine production and reduced survival after sepsis. Both treatment of B cell-deficient mice with serum from wild-type (WT) mice and repletion of Rag1(-/-) mice with B cells improves sepsis survival, suggesting antibody-independent and antibody-dependent roles for B cells in the outcome to sepsis. During sepsis, marginal zone and follicular B cells are activated through type I interferon (IFN-I) receptor (IFN-alpha/beta receptor [IFNAR]), and repleting Rag1(-/-) mice with WT, but not IFNAR(-/-), B cells improves IFN-I-dependent and -independent early cytokine responses. Repleting B cell-deficient mice with the IFN-I-dependent chemokine, CXCL10 was also sufficient to improve sepsis survival. This study identifies a novel role for IFN-I-activated B cells in protective early innate immune responses during bacterial sepsis. |
