The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/1/79/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 1, January 5, 1998 79-87

Article

Impairment of T and B Cell Development by Treatment with a Type I Interferon

Qun Lin*, Chen Dong*, and Max D. Cooper*,{ddagger}

From the * Division of Developmental and Clinical Immunology, the Department of Medicine, the Department of Pediatrics, and the Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama 35294; and the {ddagger} Howard Hughes Medical Institute, Birmingham, Alabama 35294

Type I interferons {alpha} and β, naturally produced regulators of cell growth and differentiation, have been shown to inhibit IL-7–induced growth and survival of B cell precursors in vitro. After confirming an inhibitory effect on B lymphopoiesis in an ex vivo assay, we treated newborn mice with an active IFN-{alpha}2/{alpha}1 hybrid molecule to assess its potential for regulating B and T cell development in vivo. Bone marrow and splenic cellularity was greatly reduced in the IFN-{alpha}2/{alpha}1–treated mice, and B lineage cells were reduced by >80%. The bone marrow progenitor population of CD43+B220+HSA– cells was unaffected, but development of the CD19+ pro–B cells and their B lineage progeny was severely impaired. Correspondingly, IL-7–responsive cells in the bone marrow were virtually eliminated by the interferon treatment. Thymus cellularity was also reduced by >80% in the treated mice. Phenotypic analysis of the residual thymocytes indicated that the inhibitory effect was exerted during the pro–T cell stage in differentiation. In IFN-{alpha}/β receptor–/– mice, T and B cell development were unaffected by the IFN-{alpha}2/{alpha}1 treatment. The data suggest that type I interferons can reversibly inhibit early T and B cell development by opposing the essential IL-7 response.

Address correspondence to Dr. Max D. Cooper, 378 WTI, University of Alabama at Birmingham, Birmingham, AL 35294-3300. Phone: 205-934-3370; Fax: 205-934-1875; E-mail: max.cooper{at}ccc.uab.edu. Chen Dong's present address is Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, FMB 430, 310 Cedar Street, New Haven, CT 06510.

1 Abbreviations used in this paper: DN, double negative; HSA, heat-stable antigen; IRF, interferon regulatory factor.


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