| First Author | Quemeneur L | Year | 2008 |
| Journal | Blood | Volume | 111 |
| Issue | 5 | Pages | 2714-24 |
| PubMed ID | 18094331 | Mgi Jnum | J:131581 |
| Mgi Id | MGI:3773984 | Doi | 10.1182/blood-2007-07-102822 |
| Citation | Quemeneur L, et al. (2008) SWAP-70 deficiency causes high-affinity plasma cell generation despite impaired germinal center formation. Blood 111(5):2714-24 |
| abstractText | Germinal centers (GCs) are lymphoid tissue structures central to the generation of long-lived, high-affinity, antibody-forming B cells. However, induction, maintenance, and regulation of GCs are not sufficiently understood. The F-actin-binding, Rac-interacting protein SWAP-70 is strongly expressed in activated B cells like those in B follicles. Recent work suggests that SWAP-70 is involved in B-cell activation, migration, and homing. Therefore, we investigated the role of SWAP-70 in the T-dependent immune response, in GC formation, and in differentiation into plasma and memory B cells. Compared with wt, sheep red blood cell (SRBC)-, or NP-KLH-immunized SWAP-70(-/-) mice have strongly reduced numbers of GCs and GC-specific B cells. However, SWAP-70(-/-) NP-specific B cells accumulate outside of the B follicles, and SWAP-70(-/-) mice show more plasma cells in the red pulp and in the bone marrow, and increased NP-specific Ig and antibody-forming B cells. Yet the memory response is impaired. Thus, SWAP-70 deficiency uncouples GC formation from T-dependent antibody and long-lived plasma cell production and causes extrafollicular generation of high-affinity plasma cells, but does not adequately support the memory response. |
