deletion of il-33r (st2) abrogates resistance to eae in balbc mice by enhancing polarization of apc to inflammatory phenotype删除il-33r(st2)废除balbc小鼠抗实验性自身免疫性脑脊髓炎提高极化apc炎性表型.pdfVIP

deletion of il-33r (st2) abrogates resistance to eae in balbc mice by enhancing polarization of apc to inflammatory phenotype删除il-33r(st2)废除balbc小鼠抗实验性自身免疫性脑脊髓炎提高极化apc炎性表型.pdf

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deletion of il-33r (st2) abrogates resistance to eae in balbc mice by enhancing polarization of apc to inflammatory phenotype删除il-33r(st2)废除balbc小鼠抗实验性自身免疫性脑脊髓炎提高极化apc炎性表型

Deletion of IL-33R (ST2) Abrogates Resistance to EAE in BALB/C Mice by Enhancing Polarization of APC to Inflammatory Phenotype Marija Milovanovic, Vladislav Volarevic, Biljana Ljujic, Gordana Radosavljevic, Ivan Jovanovic, Nebojsa Arsenijevic, Miodrag L. Lukic* Center for Molecular Medicine and Stem Cell Research, Faculty of Medical Sciences, University of Kragujevac, Kragujevac, Serbia Abstract The administration of interleukin 33 and deletion of IL-33 receptor, ST2 molecule, affects the induction of autoimmunity in different experimental models of human autoimmune diseases. The aim of this study was to analyze the effect of ST2 deletion on the induction of experimental autoimmune encephalomyelitis (EAE) in resistant BALB/c mice. Mice were immunized with MOG35–55 peptide or disease was induced by passive transfer of encephalitogenic singenic cells and EAE was clinically and histologically evaluated. Expression of intracellular inflammatory cytokines, markers of activation and chemokine receptors on lymphoid tissue and CNS infiltrating mononuclear cells was analyzed by flow cytometry. We report here that deletion of ST22/ 2 molecule abrogates resistance of BALB/c mice to EAE induction based on clinical and histopathological findings. Brain and spinal cord infiltrates of ST22/ 2 mice had significantly higher number of CD4+ T lymphocytes containing inflammatory cytokines compared to BALB/c WT mice. Adoptive transfer of ST22/ 2 primed lymphocytes induced clinical signs of the disease in ST22/ 2 as well as in WT mice. MOG35–55 restimulated ST22/ 2 CD4+ cells as well as ex vivo analyzed lymph node cells had higher expression of T-bet and IL-17, IFN-c, TNF-a and GM-CSF in comparison with WT CD4+ cells. ST22/ 2 mic

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