Linked Life Data

20665951

Source:http://linkedlifedata.com/resource/pubmed/id/20665951

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2010-7-27
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1879-0542
pubmed:author
pubmed:issnType
Electronic
pubmed:day
16
pubmed:volume
132
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
38-44
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Enhanced T cell-independent antibody responses in c-Jun N-terminal kinase 2 (JNK2)-deficient B cells following stimulation with CpG-1826 and anti-IgM.
pubmed:affiliation
Department of Immunology and Intractable Immunology Research Center, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, Tokyo 160-8402, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't