Interleukin (IL)-4-independent immunoglobulin class switch to immunoglobulin (Ig)E in the mouse. NLM AIDSLINE Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.

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Interleukin (IL)-4-independent immunoglobulin class switch to immunoglobulin (Ig)E in the mouse.

J Exp Med. 1996 Nov 1;184(5):1651-61. Unique Identifier : AIDSLINE MED/97079123
Morawetz RA; Gabriele L; Rizzo LV; Noben-Trauth N; Kuhn R; Rajewsky K; Muller W; Doherty TM; Finkelman F; Coffman RL; Morse HC 3rd; Laboratory of Immunopathology, National Institute of Allergy and; Infectious Diseases, National Institutes of Health, Bethesda,; Maryland 20892, USA.


Abstract: Immunoglobulin (Ig) class switching in B cells is regulated by stimuli transduced by cytokines and cell-cell contact. Among these stimuli, interleukin (IL)-4 has been considered an absolute prerequisite for class switching to IgE in the mouse. Here we report that IL-4-deficient (IL-4-/-) and wildtype mice had comparably elevated serum IgE levels during the course of a murine retrovirus-induced immunodeficiency syndrome, MAIDS. IgE switching in IL-4-/- mice was also induced by injection of anti-IgD antibody. Treatment with anti-IgD induced germline epsilon (g epsilon) transcripts with comparable efficiency in IL-4-/- mice and controls, but the levels of productive epsilon transcripts (p epsilon) were lower by a factor of 200 and serum IgE levels were lower by a factor of 300 in IL-4-/- mice as compared with controls. Induction of g epsilon after anti-IgD treatment of IL-4-/- mice was unaffected by simultaneous treatment with monoclonal antibodies to IL-4 and IL-4 receptor alpha chain. Infection of IL-4-/- mice with Nippostrongylus brasiliensis, a potent stimulus for IgE production, resulted in induction of g epsilon transcripts; however, p epsilon transcripts were barely detectable and serum IgE was not detected. These findings establish a novel IL-4-independent pathway for IgE switching in the mouse that is strongly activated in retroviral infection but weakly in nematode infection. This pathway appears to be dependent on distinct factors that separately control induction of g epsilon transcription and switch recombination to p epsilon.
Keywords: Animal Dinoprostone/BIOSYNTHESIS IgD/IMMUNOLOGY IgE/*BIOSYNTHESIS/GENETICS *Immunoglobulin Class Switching Interferon Type II/BIOSYNTHESIS Interleukin-4/*DEFICIENCY/GENETICS Mice Mice, Inbred C57BL Mice, Mutant Strains Murine Acquired Immunodeficiency Syndrome/*IMMUNOLOGY Recombination, Genetic RNA, Messenger/BIOSYNTHESIS Strongylida Infections/IMMUNOLOGY Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. JOURNAL ARTICLEKWDanimaldinoprostone/biosynthesisigd/immunologyige/KWDbiosynthesis/geneticsKWDimmunoglobulinclassswitchinginterferontypeii/biosynthesisinterleukin-4/KWDdeficiency/geneticsmicemice,inbredc57blmice,mutantstrainsmurineacquiredimmunodeficiencysyndrome/KWDimmunologyrecombination,geneticrna,messenger/biosynthesisstrongylidainfections/immunologysupport,non-uKWDsKWDgov'tsupport,uKWDsKWDgov't,pKWDhKWDsKWDjournalarticle
970228
M9721846

Copyright © 1997 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

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