| First Author | Randall KL | Year | 2009 |
| Journal | Nat Immunol | Volume | 10 |
| Issue | 12 | Pages | 1283-91 |
| PubMed ID | 19898472 | Mgi Jnum | J:155516 |
| Mgi Id | MGI:4414646 | Doi | 10.1038/ni.1820 |
| Citation | Randall KL, et al. (2009) Dock8 mutations cripple B cell immunological synapses, germinal centers and long-lived antibody production. Nat Immunol 10(12):1283-91 |
| abstractText | To identify genes and mechanisms involved in humoral immunity, we did a mouse genetic screen for mutations that do not affect the first wave of antibody to immunization but disrupt response maturation and persistence. The first two mutants identified had loss-of-function mutations in the gene encoding a previously obscure member of a family of Rho-Rac GTP-exchange factors, DOCK8. DOCK8-mutant B cells were unable to form marginal zone B cells or to persist in germinal centers and undergo affinity maturation. Dock8 mutations disrupted accumulation of the integrin ligand ICAM-1 in the B cell immunological synapse but did not alter other aspects of B cell antigen receptor signaling. Humoral immunodeficiency due to Dock8 mutation provides evidence that organization of the immunological synapse is critical for signaling the survival of B cell subsets required for long-lasting immunity. |
