Human PBMCs were isolated by Ficoll-Paque density gradient centrifugation from blood of health volunteer donors. The immune cells and MSCs were cultured in transwell system. LC3-II was detected by Western Blot

so as to measure autophagic flux. Monocytes transfected with LC3-GFP were treated in different co-cultured system respectively and then LC3+ spots were quantified by fluorescent microscopy. The Microarray was done by CapitalBio Corporation. Results: The hMSChireg induce an almost complete inhibition of IFN-γ secretion of PHA stimulated PBMCs whereas the residual ones induce only partial inhibition (5% vs 39% change in IFN-γ secretion STA-9090 mw at 1 : 20 ratio to PBMC). Also, hMSChireg can suppress TNF-α production to a much lower level than their counterpoint (41% vs 79% change in IFN-γ secretion at 1 : 20 ratio to PBMC). hMSChireg decrease the expression of IFN-γ and TNF-α more effectively (2% vs 19%, 5% vs 19%). In addition, hMSChireg

can induce Treg more effectively than the other part of MSCs (5.4% vs 3.3%), hMSChireg treated monocytes up-regulate their LC3-II gene expression while the effect of their counterpoint is weaker. hMSChireg more significantly enhance autophagy of macrophage (4.20 vs. 1.56 LC3+ spots/cell). gene expression profiles are generated from both hMSChireg and residual MSCs which show that the levels of COX-2, IL-1α, IL-1β, IL-6, IL-8 and IDO1 are significantly up-regulated in hMSChireg with an increased ability to secrete PGE2. Conclusion: MSChireg, as a unique subpopulation of MSC, more effectively suppress Th1 polarization of CD4+ T cells and induce Treg and at same time more significantly enhance Temsirolimus price autophagy. This indicates that MSChireg may not only contribute to inhibit excess inflammatory but also ameliorate the defective innate immunity in IBD. However, according to our previous data and others’ reports, even under inflammatory conditions only a proportion of MSC can be detected in the intestine, suggesting that additional mechanisms of immune suppression may be active. In addition,

enhancing binding of MSChireg enhances their migration to the inflamed colon and in turn may also be expected to potentiate their immunosuppressive HSP90 effects in vivo. So we hypothesize that MSChireg could lead to a more rapid clinical response and a dose reduction of cells, which could have profound effects on current treatment development programs. Key Word(s): 1. IBD; 2. MSC; 3. immunoregulatory; 4. in vitro; Presenting Author: LEI LIU Additional Authors: XIAOLAN ZHANG Corresponding Author: XIAOLAN ZHANG Affiliations: The Second Hospital of Hebei Medical University Objective: T helper (TH) 1 and TH17 cytokines have been reported to be involved in the genesis and maintenance of inflammatory bowel disease (IBD). Mesenchymal stem cells (MSCs) were described to suppress effector T-cell responses and have therapeutic effects in some immune disorders.