Abstract
Abstract We have previously shown that neuroimmune semaphorin Sema4A regulates experimental allergic asthma severity and Treg cell number in vivo (Mucosal Immunol., 2012, 5:409). Later, a study from the Vignali laboratory (Nature, 2013, 501:252) demonstrated that Sema4 controls Treg cell function and survival acting through its Neuropilin 1 receptor. In our current study, we employed the human cell lines HuT78 and HuT102 to further investigate the contribution of Sema4A to Treg phenotypes. These cell lines were selected for phenotypic and functional assays as they variably express Treg cell markers including CD25 and Foxp3. Moreover, they both express high levels of Sema4A. Although we did not detect Neuropilin 1 on these cell lines, they both were found to express another Sema4A counter receptor, Plexin B1. Culture of these cell lines with soluble Sema4A led to downregulation of Plexin B1 and upregulation of Sema4A and CD25 expression with slightly increased yield of CD4+CD25+ and CD25+Foxp3+ cells. Our future research is aimed at defining the role of Sema4A-PlexinB1 signaling pathways in Treg cell stability and function. We will extend this study to Treg cells obtained from normal PBMC and from patients with autoimmune and cancerous conditions. This will help us to develop new Sema4A-based therapeutic measures to combat these diseases.
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