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Involvement of Interleukin-3 in Delayed-Type Hypersensitivity
Nicolas Mach,
Chris S. Lantz,
Stephen J. Galli,
Glen Reznikoff,
Martin Mihm,
Clayton Small,
Richard Granstein,
Stefan Beissert,
Michel Sadelain,
Richard C. Mulligan, and
Glenn Dranoff
From the Departments of Medicine, Dana-Farber Cancer Institute and
Harvard Medical School; the Departments of Pathology, Beth Israel
Deaconess Medical and Harvard Medical School; the Departments of
Pathology, Massachusetts General Hospital and Harvard Medical School;
Howard Hughes Medical Institute, Children's Hospital, and the
Department of Genetics, Harvard Medical School, Boston, MA; the
Department of Dermatology, Cornell University Medical College, New
York, NY; the Department of Dermatology, University of Munster,
Munster, Germany; and the Department of Human Genetics and Immunology
Program, Memorial Sloan-Kettering Cancer Center, New York, NY.
The in vivo functions of interleukin-3 (IL-3) were investigated by
generating IL-3-deficient mice. Although hematopoiesis was unimpaired
in homozygous mutant animals, contact hypersensitivity reactions were
compromised. IL-3 was required for efficient priming of hapten-specific
contact hypersensitivity responses, but was dispensable for
T-cell-dependent sensitization to tumor cells. These findings reveal a
critical role for IL-3 in some forms of delayed-type hypersensitivity.
Blood, Vol. 91 No. 3 (February 1), 1998:
pp. 778-783
© 1998 by The American Society of Hematology.
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