Linked Life Data

21900180

Source:http://linkedlifedata.com/resource/pubmed/id/21900180

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2011-10-4
pubmed:abstractText
I?BNS has been identified as a member of the I?B family of NF-?B inhibitors, which undergoes induction upon TCR signaling. Mice carrying a targeted gene disruption of I?BNS demonstrate dysregulation of cytokines in T cells, macrophages, and dendritic cells. I?BNS mediates both positive and negative gene regulation, depending on individual cell type and/or cytokine. In this study, we demonstrate an additional role for I?BNS in the B cell lineage. B cells from I?BNS knockout (KO) mice were impaired in proliferative responses to LPS and anti-CD40. IgM and IgG3 Igs were drastically reduced in the serum of I?BNS KO mice, although I?BNS KO B cells exhibited a higher level of surface IgM than that found in wild-type mice. Switching to IgG3 was significantly reduced in I?BNS KO B cells. The in vitro induction of plasma cell development demonstrated that progression to Ab-secreting cells was impaired in I?BNS KO B cells. In agreement with this finding, the number of Ab-secreting cells in the spleens of I?BNS KO mice was reduced and production of Ag-specific Igs was lower in I?BNS KO mice after influenza infection as compared with wild-type mice. Additionally, I?BNS KO mice lacked B1 B cells and exhibited a reduction in marginal zone B cells. Thus, I?BNS significantly impacts the development and functions of B cells and plasma cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
187
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3942-52
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Impaired B cell development and function in the absence of IkappaBNS.
pubmed:affiliation
Laboratory of Immunobiology, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural