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The Journal of Immunology, Vol 143, Issue 1 214-220, Copyright © 1989 by American Association of Immunologists

ARTICLES

Expression of I-A by macrophages from Bcgr and Bcgs mice. Transient expression of I-A is due to degradation of MHC class II glycoproteins

L Vespa and BS Zwilling
Department of Microbiology, College of Biological Sciences, Ohio State University, Columbus 43210.

Murine peritoneal macrophages from mice that are resistant to Mycobacterium bovis (strain BCG) can be induced to continuously express MHC class II (Ia) glycoproteins. In contrast, macrophages from BCG susceptible mice will only transiently express Ia. The purpose of this investigation was to determine the biochemical basis of continuous or transient Ia expression. We therefore compared Ia biosynthesis by macrophages from C.D2Bcgr mice to that by macrophages from congenic BALB/c.Bcgs mice. We show that macrophages from both strains of mice synthesize Ia initially and that very little synthesis occurs after 5 days of in vitro culture. No differences in the amount of Ia synthesized by the macrophages was apparent as determined by quantitative immunoprecipitation and by ELISA. Despite the lack of synthesis, macrophages from C.D2Bcgr mice continue to express Ia. The results of pulse-chase experiments indicate that macrophages from BALB/c.Bcgs mice degrade newly synthesized MHC class II glycoproteins whereas the majority of Ia remains associated with macrophages from the C.D2Bcgr mice. The addition of chloroquine to cultures of macrophages from BALB/c.Bcgs mice prevented the degradation and prolonged the expression of Ia. The results of this investigation show that there are no differences in the synthesis of Ia by macrophages from the two congenic strains of mice. The transient expression of Ia by macrophages from BALB/c.Bcgs mice is due to its degradation.


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W. Wojciechowski, J. DeSanctis, E. Skamene, and D. Radzioch
Attenuation of MHC Class II Expression in Macrophages Infected with Mycobacterium bovis Bacillus Calmette-Guerin Involves Class II Transactivator and Depends on the Nramp1 Gene
J. Immunol., September 1, 1999; 163(5): 2688 - 2696.
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