IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Vargas, F D
Right arrow Articles by Kongshavn, P A
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Vargas, F D
Right arrow Articles by Kongshavn, P A

 Previous Article  |  Next Article 

Infect Immun. 1984 April; 44(1): 162-167

Trypanosoma musculi infection in B-cell-deficient mice.

F D Vargas, P Viens and P A Kongshavn

ABSTRACT

The course of infection with Trypanosoma musculi was assessed in mice deprived of B-lymphocytes by administration, from birth, of rabbit antiserum to mouse immunoglobulin M (IgM). Initial control of parasitemia leading to the first crisis and establishment of the plateau phase was unaffected by lack of B-lymphocyte function, although multiplicative forms persisted throughout the infection in anti-IgM-treated mice, instead of disappearing after the first crisis as in intact mice. Elimination of trypanosomes after the second crisis was not observed in anti-IgM-treated mice, which maintained high numbers of parasites in the blood and peritoneal cavity, resulting in some mortality. A temporary reduction in parasitemia was achieved in anti-IgM-treated mice by transfusion of immune plasma. Immunodepression, as measured by splenic mitogen responsiveness, and splenomegaly were both observed in anti-IgM-treated as well as in intact mice, indicating that these features of murine trypanosomiasis are independent of B-lymphocyte function. Since in T. musculi infection parasitemia can be controlled initially but not eliminated in mice lacking B-cell function, the only crucial protection provided by antibody would appear to be in curing the infection after the second crisis.


Infect Immun. 1984 April; 44(1): 162-167







Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 1984 by the American Society for Microbiology. All rights reserved.