B cells are required for induction of T cell abnormalities in a murine retrovirus-induced immunodeficiency syndrome

• Published in: The Journal of experimental medicine Vol. 171; no. 1; pp. 315 - 320
• Main Authors: CERNY, A, HUGIN, A. W, HARDY, R. R, HAYAKAWA, K, ZINKERNAGEL, R. M, MAKINO, M, MORSE, H. C. III
• Format: Journal Article
• Language: English
• Published: New York, NY Rockefeller University Press 1990; The Rockefeller University Press
• Subjects: AIDS/HIV; Animals; B-Lymphocytes - immunology; Biological and medical sciences; CD4 Antigens - analysis; CD4-Positive T-Lymphocytes - immunology; Cells, Cultured; Concanavalin A; Enzyme-Linked Immunosorbent Assay; Immunodeficiencies; Immunodeficiencies. Immunoglobulinopathies; Immunoglobulin M - analysis; Immunologic Deficiency Syndromes - immunology; Immunologic Deficiency Syndromes - microbiology; Immunopathology; Leukemia Virus, Murine; Lymphocyte Activation; Medical sciences; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; T-Lymphocytes, Cytotoxic - immunology; Tumor Virus Infections - microbiology; Cell proliferation; Flow cytometry; Immunopathology; Modification; Oncovirinae; Pathogenesis; Rodentia; Retroviridae; Helper cell; Activation; B-Lymphocyte; Immune deficiency; Host virus relation; Infection; Virus; Vertebrata; Mixed cell culture; Phenotype; Mammalia; Mouse; Type C oncovirus; Viral disease; Dependence; Murine leukemia virus
• ISSN: 0022-1007; 1540-9538
• DOI: 10.1084/jem.171.1.315

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.