| First Author | Westerberg L | Year | 2005 |
| Journal | Blood | Volume | 105 |
| Issue | 3 | Pages | 1144-52 |
| PubMed ID | 15383456 | Mgi Jnum | J:104994 |
| Mgi Id | MGI:3613263 | Doi | 10.1182/blood-2004-03-1003 |
| Citation | Westerberg L, et al. (2005) Wiskott-Aldrich syndrome protein deficiency leads to reduced B-cell adhesion, migration, and homing, and a delayed humoral immune response. Blood 105(3):1144-52 |
| abstractText | The Wiskott-Aldrich syndrome protein (WASp) is mutated in the severe immunodeficiency disease Wiskott-Aldrich syndrome (WAS). The function of B cells and the physiologic alterations in WAS remain unclear. We show that B cells from WAS patients exhibited decreased motility and had reduced capacity to migrate, adhere homotypically, and form long protrusions after in vitro culture. WASp-deficient murine B cells also migrated less well to chemokines. Upon antigen challenge, WASp-deficient mice mounted a reduced and delayed humoral immune response to both T-cell-dependent and -independent antigens. This was at least in part due to deficient migration and homing of B cells. In addition, the germinal center reaction was reduced in WASp-deficient mice. Thus, WASp is crucial for optimal B-cell responses and plays a pivotal role in the primary humoral immune response. |
