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Contribution of B cell subsets to delayed development of MAIDS in xid mice.

Authors
Tang, Y; Kim, WK; Holmes, KL; Hugin, AW; Kenny, JJ; Chattopadhyay, SK; Hartley, JW; Morse, HC 3rd
Citation
Cellular immunology, 165(1):1-6, 1995
Journal Title
Cellular immunology
ISSN
0008-87491090-2163
Abstract
C57BL/6 (B6) mice develop a syndrome of progressive lymphoproliferation and immunodeficiency, murine AIDS (MAIDS), when infected with an etiologic replication-defective virus termed BM5def. Induction of MAIDS requires the presence of CD4+ T cells and B cells. B6 mice with altered conventional B cell function and a deficit in CD5+ B cells due to the xid mutation develop disease with a greatly prolonged latency. The association of this mutation with resistance to MAIDS was confirmed in studies of P.xid mice. To test the hypothesis that conventional B cells are required for rapid induction of disease, B6.xid mice were injected with spleen cells from nude mice or were given bone marrow from aged donors. Both sets of recipients developed advanced disease by 10 weeks post infection, suggesting that resistance to MAIDS in xid mutants may be due to effects of B cells other than the CD5+ subset.
MeSH terms
AnimalsAntigens, CD/geneticsAntigens, CD5B-Lymphocyte Subsets/*immunology/*transplantationBone Marrow Transplantation/*immunologyFlow CytometryImmunologic Deficiency Syndromes/geneticsMiceMice, Inbred C57BLMice, Mutant StrainsMice, TransgenicMurine Acquired Immunodeficiency Syndrome/genetics/*immunology/*physiopathologyMutation/geneticsProtein-Tyrosine Kinases/geneticsX Chromosome/genetics
DOI
10.1006/cimm.1995.1179
PMID
7545546
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
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