Journal
NATURE COMMUNICATIONS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-017-01605-1
Keywords
-
Categories
Funding
- National Health and Medical Research Council (NHMRC) of Australia [1054925, 1058238, 1060675]
- Victorian State Government Operational Infrastructure Support
- Australian Government NHMRC IRIIS
- Lupus Research Alliance
- Multiple Myeloma Research Foundation (MMRF)
- Walter and Eliza Hall Trust Centenary Fellowship
- Commonwealth Serum Laboratories Centenary Fellowship
- National Health and Medical Research Council of Australia [1058238, 1060675] Funding Source: NHMRC
Ask authors/readers for more resources
Humoral immunity requires B cells to respond to multiple stimuli, including antigen, membrane and soluble ligands, and microbial products. Ets family transcription factors regulate many aspects of haematopoiesis, although their functions in humoral immunity are difficult to decipher as a result of redundancy between the family members. Here we show that mice lacking both PU.1 and SpiB in mature B cells do not generate germinal centers and highaffinity antibody after protein immunization. PU. 1 and SpiB double-deficient B cells have a survival defect after engagement of CD40 or Toll-like receptors ( TLR), despite paradoxically enhanced plasma cell differentiation. PU. 1 and SpiB regulate the expression of many components of the B cell receptor signaling pathway and the receptors for CD40L, BAFF and TLR ligands. Thus, PU.1 and SpiB enable B cells to appropriately respond to environmental cues.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available
Share Paper
