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The Influence of IgE-Enhancing and IgE-Suppressive T Cells Changes with Exposure to Inhaled Ovalbumin¹

Yafei Huang^*,, Niyun Jin^*,, Christina L. Roark^*,, M. Kemal Aydintug^*,, J. M. Wands^*,, Hua Huang^*,, Rebecca L. O'Brien^*, and Willi K. Born^2,*,

^* Integrated Department of Immunology, National Jewish Health, Denver, CO 80206; University of Colorado, Denver, CO 80206; and Department of Medicine, National Jewish Health, Denver, CO 80206

It has been reported that the IgE response to allergens is influenced by T cells. Intrigued by a study showing that airway challenge of mice with OVA induces in the spleen the development of T cells that suppress the primary IgE response to i.p.-injected OVA-alum, we investigated the T cells involved. We found that the induced IgE suppressors are contained within the V4⁺ subset of T cells of the spleen, that they express V5 and CD8, and that they depend on IFN- for their function. However, we also found that normal nonchallenged mice harbor IgE-enhancing T cells, which are contained within the larger V1⁺ subset of the spleen. In cell transfer experiments, airway challenge of the donors was required to induce the IgE suppressors among the V4⁺ cells. Moreover, this challenge simultaneously turned off the IgE enhancers among the V1⁺ cells. Thus, airway allergen challenge differentially affects two distinct subsets of T cells with nonoverlapping functional potentials, and the outcome is IgE suppression.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants AI40611 and HL65410 (to W.K.B.) and AI44920 and AI063400 (to R.L.O.).

² Address correspondence and reprint requests to Dr. Willi K. Born, Integrated Department of Immunology, National Jewish Health, 1400 Jackson Street, GB K409, Denver, CO 80206. E-mail address: bornw{at}njc.org

³ Abbreviations used in this paper: AHR, airway hyperresponsiveness; DC, dendritic cell.