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OX40-OX40L interactions: a promising therapeutic target for allergic diseases?
Yui-Hsi Wang, Yong-Jun Liu
Yui-Hsi Wang, Yong-Jun Liu
Published December 3, 2007
Citation Information: J Clin Invest. 2007;117(12):3655-3657. https://doi.org/10.1172/JCI34182.
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Commentary

OX40-OX40L interactions: a promising therapeutic target for allergic diseases?

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Abstract

Recent advances in understanding the cellular and molecular mechanisms of atopy have shed light on potential targets for the development of new therapies for allergic diseases. In this issue of the JCI, Seshasayee et al. provide direct in vivo evidence that OX40 has critical roles in allergic inflammation mediated by thymic stromal lymphopoietin (TSLP) (see the related article beginning on page 3868). Blockade of interactions between OX40 on Th2 cells and OX40 ligand (OX40L) on TSLP-activated DCs using an OX40L-specific monoclonal antibody, inhibited Th2 cell–mediated immune responses in both mouse and nonhuman primate models of allergic inflammation. The results point to potential therapeutic approaches to targeting the cellular and molecular mechanism underlying TSLP-mediated allergic inflammation.

Authors

Yui-Hsi Wang, Yong-Jun Liu

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Figure 1

Pathophysiology of TSLP in allergic inflammation.

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Pathophysiology of TSLP in allergic inflammation.
Insults from allergens ...
Insults from allergens or viruses trigger mucosal epithelial cells or skin cells (keratinocytes, fibroblasts, and mast cells) to produce TSLP. TSLP initiates the innate phase of allergic immune responses by activating immature DCs to produce the chemokines IL-8 and eotaxin-2, as well as the Th2-attracting chemokines thymus and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC), and by costimulating mast cells to produce IL-5 and IL-13, as well as GM-CSF and IL-6. TSLP-activated DCs mature and migrate into the draining lymph nodes to initiate the adaptive phase of allergic immune responses. TSLP-activated DCs express OX40L, which triggers the differentiation of allergen-specific naive CD4+ T cells into inflammatory Th2 cells that produce IL-4, IL-5, IL-13, and TNF-α but not IL-10. Inflammatory Th2 cells then migrate back to the site of inflammation because of the local production of TARC and MDC. The cytokines produced by the inflammatory Th2 cells (IL-4, IL-5, IL-13, and TNF-α) initiate allergic inflammation by triggering IgE and mucus production and eosinophilia. Figure modified with permission from J. Allergy Clin. Immunol. (25).

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