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Susanne J. Szabo^*, Anand S. Dighe^*, Ueli Gubler, and Kenneth M. Murphy^*

From the ^* Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110; and the Department of Inflammation/Autoimmune Diseases Hoffmann La-Roche Inc., Nutley, New Jersey 07110

The developmental commitment to a T helper 1 (Th1)- or Th2-type response can significantly influence host immunity to pathogens. Extinction of the IL-12 signaling pathway during early Th2 development provides a mechanism that allows stable phenotype commitment. In this report we demonstrate that extinction of IL-12 signaling in early Th2 cells results from a selective loss of IL-12 receptor (IL-12R) β2 subunit expression. To determine the basis for this selective loss, we examined IL-12R β2 subunit expression during Th cell development in response to T cell treatment with different cytokines. IL-12R β2 is not expressed by naive resting CD4⁺ T cells, but is induced upon antigen activation through the T cell receptor. Importantly, IL-4 and IFN- were found to significantly modify IL-12 receptor β2 expression after T cell activation. IL-4 inhibited IL-12R β2 expression leading to the loss of IL-12 signaling, providing an important point of regulation to promote commitment to the Th2 pathway. IFN- treatment of early developing Th2 cells maintained IL-12R β2 expression and restored the ability of these cells to functionally respond to IL-12, but did not directly inhibit IL-4 or induce IFN- production. Thus, IFN- may prevent early Th cells from premature commitment to the Th2 pathway. Controlling the expression of the IL-12R β2 subunit could be an important therapeutic target for the redirection of ongoing Th cell responses.

¹ Abbreviation used in this paper: IL-2R, IL-12 receptor.

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• IM, S.-H., BARCHAN, D., MAITI, P. K., RAVEH, L., SOUROUJON, M. C., FUCHS, S. (2001). Suppression of experimental myasthenia gravis, a B cell-mediated autoimmune disease, by blockade of IL-18. FASEB J. 15: 2140-2148 [Abstract] [Full Text]  
• Siegmund, B., Fantuzzi, G., Rieder, F., Gamboni-Robertson, F., Lehr, H.-A., Hartmann, G., Dinarello, C. A., Endres, S., Eigler, A. (2001). Neutralization of interleukin-18 reduces severity in murine colitis and intestinal IFN-gamma and TNF-alpha production. Am. J. Physiol. Regul. Integr. Comp. Physiol. 281: R1264-R1273 [Abstract] [Full Text]  
• Tran, G. T., Carter, N., He, X. Y., Spicer, T. S., Plain, K. M., Nicolls, M., Hall, B. M., Hodgkinson, S. J. (2001). Reversal of experimental allergic encephalomyelitis with non-mitogenic, non-depleting anti-CD3 mAb therapy with a preferential effect on Th1 cells that is augmented by IL-4. Int Immunol 13: 1109-1120 [Abstract] [Full Text]  
• Costa, G. L., Sandora, M. R., Nakajima, A., Nguyen, E. V., Taylor-Edwards, C., Slavin, A. J., Contag, C. H., Fathman, C. G., Benson, J. M. (2001). Adoptive Immunotherapy of Experimental Autoimmune Encephalomyelitis Via T Cell Delivery of the IL-12 p40 Subunit. J. Immunol. 167: 2379-2387 [Abstract] [Full Text]  
• Nakahira, M., Tomura, M., Iwasaki, M., Ahn, H.-J., Bian, Y., Hamaoka, T., Ohta, T., Kurimoto, M., Fujiwara, H. (2001). An Absolute Requirement for STAT4 and a Role for IFN-{gamma} as an Amplifying Factor in IL-12 Induction of the Functional IL-18 Receptor Complex. J. Immunol. 167: 1306-1312 [Abstract] [Full Text]  
• Nawijn, M. C., Dingjan, G. M., Ferreira, R., Lambrecht, B. N., Karis, A., Grosveld, F., Savelkoul, H., Hendriks, R. W. (2001). Enforced Expression of GATA-3 in Transgenic Mice Inhibits Th1 Differentiation and Induces the Formation of a T1/ST2-Expressing Th2-Committed T Cell Compartment In Vivo. J. Immunol. 167: 724-732 [Abstract] [Full Text]  
• Cottrez, F., Groux, H. (2001). Regulation of TGF-{{beta}} Response During T Cell Activation Is Modulated by IL-10. J. Immunol. 167: 773-778 [Abstract] [Full Text]  
• Kim, J., Uyemura, K., Van Dyke, M. K., Legaspi, A. J., Rea, T. H., Shuai, K., Modlin, R. L. (2001). A Role for IL-12 Receptor Expression and Signal Transduction in Host Defense in Leprosy. J. Immunol. 167: 779-786 [Abstract] [Full Text]  
• Nutku, E., Zhuang, Q., Soussi-Gounni, A., Aris, F., Mazer, B. D., Hamid, Q. (2001). Functional Expression of IL-12 Receptor by Human Eosinophils: IL-12 Promotes Eosinophil Apoptosis. J. Immunol. 167: 1039-1046 [Abstract] [Full Text]  
• von der Weid, T., Bulliard, C., Schiffrin, E. J. (2001). Induction by a Lactic Acid Bacterium of a Population of CD4+ T Cells with Low Proliferative Capacity That Produce Transforming Growth Factor {beta} and Interleukin-10. CVI 8: 695-701 [Abstract] [Full Text]  
• Gorbachev, A. V., DiIulio, N. A., Fairchild, R. L. (2001). IL-12 Augments CD8+ T Cell Development for Contact Hypersensitivity Responses and Circumvents Anti-CD154 Antibody-Mediated Inhibition. J. Immunol. 167: 156-162 [Abstract] [Full Text]  
• Grohmann, U., Belladonna, M. L., Vacca, C., Bianchi, R., Fallarino, F., Orabona, C., Fioretti, M. C., Puccetti, P. (2001). Positive Regulatory Role of IL-12 in Macrophages and Modulation by IFN-{{gamma}}. J. Immunol. 167: 221-227 [Abstract] [Full Text]  
• Nishikomori, R., Gurunathan, S., Nishikomori, K., Strober, W. (2001). BALB/c Mice Bearing a Transgenic IL-12 Receptor {{beta}}2 Gene Exhibit a Nonhealing Phenotype to Leishmania major Infection Despite Intact IL-12 Signaling. J. Immunol. 166: 6776-6783 [Abstract] [Full Text]  
• Peng, Y., Falck-Pedersen, E., Elkon, K. B. (2001). Variation in Adenovirus Transgene Expression between BALB/c and C57BL/6 Mice Is Associated with Differences in Interleukin-12 and Gamma Interferon Production and NK Cell Activation. J. Virol. 75: 4540-4550 [Abstract] [Full Text]  
• Kieper, W. C., Prlic, M., Schmidt, C. S., Mescher, M. F., Jameson, S. C. (2001). IL-12 Enhances CD8 T Cell Homeostatic Expansion. J. Immunol. 166: 5515-5521 [Abstract] [Full Text]  

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