Journal
NATURE IMMUNOLOGY
Volume 10, Issue 12, Pages 1283-U8Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1820
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Funding
- Wellcome Trust
- Australian Research Council
- National Health and Medical Research Council
- Medical Research Council
- Ramaciotti Foundation
- Deutsche Forschungsgemeinschaft
- Cancer Research UK
- Andrew McMichael Trust Fund
- National Institute for Health Research Biomedical Research Centre Programme
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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.
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