Seminal CD38 Is a Pivotal Regulator for Fetomaternal Tolerance
Seminal CD38 is a pivotal regulator for fetomaternal tolerance Byung-Ju Kima,b, Yun-Min Choia,b, So-Young Raha,b, Dae-Ryoung Parka,b, Seon-Ah Parka, Yun-Jo Chunga, Seung-Moon Parkc, Jong Kwan Parkd, Kyu Yun Jange, and Uh-Hyun Kima,b,f,1 + aNational Creative Research Laboratory for Ca2 Signaling Network and Departments of bBiochemistry, dUrology, and ePathology, Chonbuk National University Medical School, Jeonju, 561-180, Korea; cDivision of Biotechnology, College of Environmental and Bioresource Sciences, Chonbuk National University, Iksan, 570-752, Korea; and fInstitute of Cardiovascular Research, Chonbuk National University, Jeonju, 561-180, Korea Edited by John J. Eppig, The Jackson Laboratory, Bar Harbor, ME, and approved December 22, 2014 (received for review July 16, 2014) A successful pregnancy depends on a complex process that estab- a variety of inflammatory diseases (20–23). For example, recombi- lishes fetomaternal tolerance. Seminal plasma is known to induce nant CD38 inhibits LPS-induced inflammatory signals in mouse maternal immune tolerance to paternal alloantigens, but the seminal macrophages and human DCs through an interaction with CD31 factors that regulate maternal immunity have yet to be characterized. (24, 25). Here, we show that a soluble form of CD38 (sCD38) released from In this study, we found that CD38 is truncated and released seminal vesicles to the seminal plasma plays a crucial role in inducing into the seminal plasma from seminal vesicles (SVs) as a soluble + + + tolerogenic dendritic cells and CD4 forkhead box P3 (Foxp3 )reg- form (sCD38) in humans and mice. This finding prompted us to ulatory T cells (Tregs), thereby enhancing maternal immune tolerance examine whether CD38 plays a role in maternal immune toler- and protecting the semiallogeneic fetus from resorption.
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