Kaul, Vandana ; Van Kaer, Luc ; Das, Gobardhan ; Das, Jyoti (2012) Prostanoid receptor 2 signaling protects T helper 2 cells from BALB/c mice against activation-induced cell death Journal of Biological Chemistry, 287 (30). pp. 25434-25439. ISSN 0021-9258
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Official URL: http://www.jbc.org/content/287/30/25434.abstract
Related URL: http://dx.doi.org/10.1074/jbc.C111.324707
Abstract
T helper 2 (Th2) cells play a central role in the progression of many diseases such as allergic airway inflammation, autoimmune diseases, and infections caused by intracellular pathogens. Consequently, animals such as BALB/c mice, which exhibit a propensity for generating Th2 responses, are susceptible to allergic airway inflammation, type-II autoimmune diseases, and various infections induced by intracellular pathogens, namely, Leishmania. In contrast, C3H/OuJ mice have a tendency for generating T helper 1 (Th1) responses and show resistance to these diseases. Here, we show that prostaglandin endoperoxide E2 selectively inhibits activation-induced cell death of Th2 cells by signaling through its receptor E-prostanoid receptor 2 (EP2). Consequently, Th2 cells derived from BALB/c mice expressed very high levels of EP2. On the other hand, Th2 cells derived from C3H/OuJ mice expressed very low levels of EP2, which failed to support the survival of Th2 cells. Furthermore, we found that this effect of EP2 on Th2 cells from BALB/c mice was executed by a granzyme B-mediated mechanism. EP2 belongs to a group of G-protein-coupled receptors that are amenable to therapeutic targeting. Our findings therefore identify EP2 as a promising target for small molecule-directed immunomodulation.
Item Type: | Article |
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Source: | Copyright of this article belongs to American Society for Biochemistry and Molecular Biology. |
Keywords: | Cell Death; Cytokine; Immunology; Prostaglandins; T Cell; T Cell Biology; Activation-Induced Cell Death; E Prostanoid Receptor EP2 |
ID Code: | 113302 |
Deposited On: | 07 Jun 2018 05:10 |
Last Modified: | 07 Jun 2018 05:10 |
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