High affinity B cell receptor ligation by cognate antigen induces cytokine-independent isotype switching
The selection of an appropriate immunoglobulin (Ig) isotype is critical for an effective immune response against pathogens. Isotype regulation is sensitive to external signals, particularly cytokines secreted by T helper cells. For example, interleukin (IL)-4 induces isotype switching to IgG1 via a STAT6-dependent signalling pathway. Here, we show that B cell receptor (BCR) ligation also induces IgG1 switching. The extent of switch induction by antigen is affinity-dependent and high affinity antigen binding leads to IgG1 switching levels comparable to those induced by saturating IL-4. However, the antigen-induced IgG1 switch does not require additional cytokine signals and occurs in a STAT6-independent manner. Thus, BCR ligation represents a novel pathway for direct isotype switching leading to IgG1 secretion.
|Authors||Turner, M.L.; Corcoran, L.M.; Brink, R; Hodgkin, P.D.|
|Publisher Name||JOURNAL OF IMMUNOLOGY|
|DOI||jimmunol.0903437 [pii] 10.4049/jimmunol.0903437|
|URL link to publisher's version||http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=20483733|
|OpenAccess link to author's accepted manuscript version||https://publications.gimr.garvan.org.au/open-access/10347|