| First Author | Jones SA | Year | 2011 |
| Journal | J Immunol | Volume | 187 |
| Issue | 12 | Pages | 6318-26 |
| PubMed ID | 22075701 | Mgi Jnum | J:180409 |
| Mgi Id | MGI:5306212 | Doi | 10.4049/jimmunol.1102057 |
| Citation | Jones SA, et al. (2011) SOCS3 deletion in B cells alters cytokine responses and germinal center output. J Immunol 187(12):6318-26 |
| abstractText | B cell behavior is fine-tuned by internal regulatory mechanisms and external cues such as cytokines and chemokines. Suppressor of cytokine signaling 3 (SOCS3) is a key regulator of STAT3-dependent cytokine responses in many cell types and has been reported to inhibit CXCL12-induced retention of immature B cells in the bone marrow. Using mice with SOCS3 exclusively deleted in the B cell lineage (Socs3(Delta/Delta)mb1cre(+)), we analyzed the role of SOCS3 in the response of these cells to CXCL12 and the STAT3-inducing cytokines IL-6 and IL-21. Our findings refute a B cell-intrinsic role for SOCS3 in B cell development, because SOCS3 deletion in the B lineage did not affect B cell populations in naive mice. SOCS3 was strongly induced in B cells stimulated with IL-21 and in plasma cells exposed to IL-6. Its deletion permitted excessive and prolonged STAT3 signaling following IL-6 stimulation of plasma cells and, in a T cell-dependent immunization model, reduced the number of germinal center B cells formed and altered the production of Ag-specific IgM and IgE. These data demonstrate a novel regulatory signal transduction circuit in plasma cells, providing, to our knowledge, the first evidence of how these long-lived, sessile cells respond to the external signals that mediate their longevity. |
