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Journal of Virology, August 1999, p. 7093-7095, Vol. 73, No. 8
Laboratory of
Immunopathology,1 National Institute of Allergy
and Infectious Diseases, National Institutes of Health, Bethesda,
Maryland 20892, and Department of Immunology and Infectious
Diseases,
Received 26 February 1999/Accepted 4 May 1999
The unique Gag polyprotein of the replication-defective virus
responsible for murine AIDS (MAIDS) induces B-cell activation, proliferation, and differentiation, including immunoglobulin class switch-recombination to immunoglobulin E (IgE). Secretion of IgE normally requires the serial induction of interleukin 4 (IL-4), engagement of the IL-4 receptor, activation of signal transducer and
activator of transcription (STAT) 6, and induction of I
0022-538X/99/$04.00+0
STAT6-Deficient Mice Exhibit Normal Induction of
Murine AIDS and Expression of Immunoglobulin E following Infection with
LP-BM5 Murine Leukemia Viruses
germline transcripts as a prelude to switching. Remarkably, expression of IgE is
equivalent in normal and IL-4-deficient mice with MAIDS (Morawetz et
al., J. Exp. Med. 184:1651-1661, 1996). To understand this anomaly, we
studied mice with a null mutation of STAT6. Lymphoproliferation and
immunodeficiency, the hallmarks of MAIDS, developed with comparable kinetics and degree in normal and mutant mice. In addition, serum IgE
levels were indistinguishable in mice of either genotype. We conclude
that B cells from mice with MAIDS activate unique IL-4- and
STAT6-independent signaling pathways for B-cell activation and differentiation.
*
Corresponding author. Mailing address: LIP, NIAID, NIH,
Building 7, Room 304, 9000 Rockville Pike, Bethesda, MD 20892-0760. Phone: (301) 496-6379. Fax: (301) 402-0077. E-mail:
hmorse{at}atlas.niaid.nih.gov.
Journal of Virology, August 1999, p. 7093-7095, Vol. 73, No. 8
0022-538X/99/$04.00+0
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