The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/4/1305/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 8, April 20, 1998 1305-1313

Articles

Impaired Interleukin 4 Signaling in T Helper Type 1 Cells

Hua Huang and William E. Paul

From the Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-1892

Cluster of differentation (CD)4+ T helper cells (Th)1s fail to produce interleukin (IL)-4. Even if restimulated in the presence of IL-4, a condition that induces IL-4–producing capacity in naive CD4+ T cells, Th1s fail to become IL-4 producers. We report that Th1 cells have a major impairment in IL-4 signaling. When compared to both Th2s and naive T cells, they display a striking diminution in phosphorylation of Stat6. They also show reduced phosphorylation of Janus kinase (JAK)-3 and insulin receptor substrate (IRS)-2 when compared to Th2s. Stat6 and JAK-3 are present in equivalent amounts in Th1s and Th2s, but IRS-2 protein levels are much lower in Th1s than in Th2s. Altered sensitivity to IL-4, the major inducer of the Th2 phenotype, may explain the stability of the Th1 state.

Address correspondence to William E. Paul, LI, NIAID, NIH, Bldg. 10, Rm. llN3ll, 10 Center Dr., MSC 1892, Bethesda, MD 20892-1892. Phone: 301-496-5046; Fax: 301-496-0222; E-mail: wepaul{at}helix.nih.gov

H. Huang is a fellow of the Leukemia Society of America.

1 Abbreviations used in this paper: {gamma}c, common gamma chain; CD, cluster of differentiation; EMSA, electrophoretic mobility shift assay; GAS, gamma-activated sequence; IRS, insulin receptor substrate; JAK, Janus kinase; mRNA, messenger RNA.


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