Oct-2 gene disruption eliminates the peritoneal B-1 lymphocyte lineage and attenuates B-2 cell maturation and function
- Author(s)
- Humbert, PO; Corcoran, LM;
- Details
- Publication Year 1997-12-01,Volume 159,Issue #11,Page 5273-5284
- Journal Title
- JOURNAL OF IMMUNOLOGY
- Publication Type
- Journal Article
- Abstract
- Targeted mutation of the gene for the Oct-2 transcription factor in mice caused neonatal lethality and abrogated mitogen-induced proliferation and differentiation of mature B lymphocytes in vitro. Here we show that Oct-2 is required for normal humoral responses upon immunization with T cell-dependent as well as T-independent Ags. oct-2-null T cell behavior was normal, implying a B cell-restricted lesion, oct-2(-/-) B cells displayed aberrant behavior during activation in vitro: both acquisition of markers of cellular activation and cell survival were diminished, Production of early B lineage cells in the bone marrow was normal, yet mature B cells were under-represented in blood and lymphoid organs. Furthermore, peritoneal B-1 lymphocytes were not detected in animals with a reconstituted oct-2(-/-) lymphoid system. We conclude that Oct-2 is required for B-1 cell maintenance and for normal Ag-driven maturation of conventional B cells in vivo.
- Publisher
- AMER ASSOC IMMUNOLOGISTS
- Keywords
- REMOTE ENHANCER POSITION; HEAT-STABLE ANTIGEN(HI); PERIPHERAL B-CELLS; OCTAMER DNA MOTIF; T-CELL; DEFICIENT MICE; IMMUNOGLOBULIN PROMOTERS; TYROSINE PHOSPHORYLATION; VAV PROTOONCOGENE; BINDING PROTEINS
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Creation Date: 1997-12-01 12:00:00