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Resistance of mice deficient in IL-4 to retrovirus-induced immunodeficiency syndrome (MAIDS)

Abstract
The murine acquired immunodeficiency syndrome (MAIDS) is induced by a defective murine leukemia virus and has many symptoms similar to those found in patients infected with the human immunodeficiency virus. The presence of both B cells and CD4+ T cells is critical for the development of the disease. Furthermore, a Th2 cytokine response dominates during the progression of the disease. When interleukin-4 (IL-4)-deficient mice that are defective in Th2 cytokine responses were infected, there was no lethality, and the development of the T cell abnormalities associated with MAIDS was delayed. These data suggest that IL-4 or a Th2 response is involved in the development of retrovirus-induced immunodeficiency in mice.
AuthorsO Kanagawa, B A Vaupel, S Gayama, G Koehler, M Kopf
JournalScience (New York, N.Y.) (Science) Vol. 262 Issue 5131 Pg. 240-2 (Oct 08 1993) ISSN: 0036-8075 [Print] United States
PMID8211142 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • DNA Primers
  • Gene Products, gag
  • Interleukin-2
  • RNA, Messenger
  • RNA, Viral
  • Interleukin-4
Topics
  • Animals
  • Base Sequence
  • DNA Primers
  • Gene Products, gag (genetics)
  • Immunity, Innate
  • Interleukin-2 (biosynthesis)
  • Interleukin-4 (biosynthesis, deficiency, genetics, immunology)
  • Leukemia Virus, Murine (genetics)
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred Strains
  • Molecular Sequence Data
  • Murine Acquired Immunodeficiency Syndrome (immunology)
  • RNA, Messenger (analysis, genetics)
  • RNA, Viral (analysis, genetics)
  • T-Lymphocytes, Helper-Inducer (immunology)

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