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Journal of Experimental Medicine, Vol 171, 315-320, Copyright © 1990 by Rockefeller University Press
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A Cerny, AW Hugin, RR Hardy, K Hayakawa, RM Zinkernagel, M Makino and HC Morse 3d
Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.
The role of B cells in induction of phenotypic and functional abnormalities of T cells in a murine retrovirus-induced immunodeficiency syndrome, MAIDS, was evaluated in mice depleted of mature B cells from birth with anti-IgM antibodies (mu-suppressed) and infected at 4 wk of age. Multicolor FACS analyses of CD4+ T cell subsets showed that development of phenotypic abnormalities of these cells at 9 wk after infection was completely inhibited by mu- suppression. Furthermore, induction of impaired proliferative responses to Con A and alloantigens and CTL responses to alloantigens was fully blocked in antibody-treated animals. The extent of virus replication was comparable in spleens of untreated and mu-suppressed mice. Retroviral induction of T cell dysfunction in MAIDS is thus dependent on the presence of B cells, and high level virus expression in mice without B cells has little or no effect on T cell function.
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