AI Article Synopsis
- The study investigates the role of c-Jun NH2-terminal kinase 2 (JNK2) in B cell activation, particularly regarding antibody production in response to different stimuli.
- Researchers found that JNK2-deficient B cells produced more of certain antibodies (IgG1 and IgG2a) when stimulated with anti-IgM and CpG ODN, compared to normal (wild-type) B cells.
- The increased antibody production in JNK2-deficient B cells is linked to higher TLR9 expression and occurs without changes in class switching or cell proliferation.
Article Abstract
Although c-Jun NH2-terminal kinase (JNK) 1 and JNK2 have been demonstrated to modulate T cell activation, role of JNKs in B cell activation remains largely unclear. Phosphorylation of JNK2 was increased in murine B cells following stimulation with either anti-IgM or CpG-1826 oligonucleotide (ODN) alone, with a further increase by a combined stimulation with anti-IgM and CpG-1826 ODN. In this study, we examined whether antibody production induced by CpG ODN and/or anti-IgM is affected in B cells from JNK2-deficient (JNK2-/-) mice. After stimulation with CpG ODN or both CpG ODN and anti-IgM, JNK2-/- B cells displayed an enhanced antibody production of IgG1 and IgG2a, with less pronounced in IgG2b production, as assessed by enzyme-linked immunoassay (ELISA). However, IgM production in JNK2-/- B cells by CpG ODN was comparable to that in WT B cells. TLR9 expression was increased in JNK2-/- B cells after stimulation with anti-IgM or both CpG ODN and anti-IgM, suggesting that the anti-IgM/CpG ODN-induced enhancement of antibody production is partly due to the increased expression of TLR9. The enhanced antibody production in JNK2-/- B cells by the combined stimulation does not appear to involve either increased class switch recombination or cell proliferation. Our results provide useful information on the role of JNK2 in antibody responses mediated by T cell-independent antigens.
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| http://dx.doi.org/10.1016/j.imlet.2010.05.006 | DOI Listing |
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