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.
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Authors | O Kanagawa, B A Vaupel, S Gayama, G Koehler, M Kopf |
Journal | Science (New York, N.Y.)
(Science)
Vol. 262
Issue 5131
Pg. 240-2
(Oct 08 1993)
ISSN: 0036-8075 [Print] United States |
PMID | 8211142
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- DNA Primers
- Gene Products, gag
- Interleukin-2
- RNA, Messenger
- RNA, Viral
- Interleukin-4
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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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