Document Detail


Differential regulation of murine B cell Fc gamma RII expression by CD4+ T helper subsets.
MedLine Citation:
PMID:  2528589     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The murine B cell FcR for IgG (Fc gamma RII) is a membrane glycoprotein reported to mediate inhibition of B cell activation and differentiation. We show that IL-4 inhibits the enhanced expression of Fc gamma RII by LPS-stimulated B cells. This activity is completely reversed by anti-IL-4 mAb and is specific, in that multiple other lymphokines tested do not exert a similar effect. This effect of IL-4 is apparent by day 1 of culture, although maximal inhibition occurs on day 4 at a concentration of 500 U/ml. The IL-4-induced inhibition of enhanced Fc gamma RII expression by LPS stimulation observed on day 4 of culture is associated with a significant reduction in the steady state level of Fc gamma RII beta gene-specific mRNA. IFN-gamma which inhibits many of the effects of IL-4 on B cells, does not reverse the IL-4-induced inhibition of Fc gamma RII membrane expression nor the levels of beta gene-specific mRNA. Fc gamma RII expression is significantly increased in B cells stimulated with antigen-specific, CD4+ T cell clones of the Th1 type (i.e., IL-2 and IFN-gamma-producing). By contrast, three different Th2 clones (i.e., IL-4-producing) fail to stimulate an increase in Fc gamma RII levels. Anti-IL-4 mAb significantly enhanced Fc gamma RII expression by Th2-stimulated B cells indicating that IL-4 was the active, inhibitory, substance produced by the Th2 cells. Supernatants from stimulated Th2 clones inhibited the enhanced expression of Fc gamma RII by LPS-stimulated B cells and this activity was completely reversed by anti-IL-4 mAb. By contrast, supernatants from stimulated Th1 clones further enhanced Fc gamma RII expression by LPS-stimulated B cells. The differential regulation of B cell Fc gamma RII expression by Th subsets may play an important role in the regulation of humoral immunity by altering the sensitivity of B cells to IgG immune complex-mediated inhibition of B cell activation and differentiation in vivo.
Authors:
C M Snapper; J J Hooley; U Atasoy; F D Finkelman; W E Paul
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  143     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  1989 Oct 
Date Detail:
Created Date:  1989-10-20     Completed Date:  1989-10-20     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2133-41     Citation Subset:  AIM; IM    
Affiliation:
Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, Differentiation / genetics,  metabolism*
Antigens, Differentiation, T-Lymphocyte*
B-Lymphocytes / metabolism*
Binding, Competitive
Cell Line
Female
Genes, Immunoglobulin
Immunoglobulin G / metabolism*
Interferon-gamma / pharmacology
Interleukin-4
Interleukins / biosynthesis,  physiology
Kinetics
Lipopolysaccharides / pharmacology
Lymphocyte Activation
Membrane Proteins / metabolism
Mice
Mice, Inbred C3H
Mice, Inbred DBA
Phenotype
RNA, Messenger / metabolism
Receptors, Fc / genetics,  metabolism*
Receptors, IgG
T-Lymphocytes, Helper-Inducer / classification,  immunology*
Chemical
Reg. No./Substance:
0/Antigens, Differentiation; 0/Antigens, Differentiation, T-Lymphocyte; 0/Immunoglobulin G; 0/Interleukins; 0/Lipopolysaccharides; 0/Membrane Proteins; 0/RNA, Messenger; 0/Receptors, Fc; 0/Receptors, IgG; 207137-56-2/Interleukin-4; 82115-62-6/Interferon-gamma

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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