scholarly journals A Kv1.3 channel-specific blocker alleviates neurological impairment through inhibiting T-cell activation in experimental autoimmune encephalomyelitis

2018 ◽  
Vol 24 (10) ◽  
pp. 967-977 ◽  
Author(s):  
Xiao-Lu Yuan ◽  
Yi-Peng Zhao ◽  
Jie Huang ◽  
Jun-Chen Liu ◽  
Wen-Qian Mao ◽  
...  
Keyword(s):  
T Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
T Cell Activation ◽  
Cell Activation ◽  
Neurological Impairment ◽  
Autoimmune Encephalomyelitis ◽  
Kv1.3 Channel ◽  
Experimental Autoimmune

scholarly journals The Innate Immune Receptor CD14 Mediates Lymphocyte Migration in EAE

2015 ◽  
Vol 37 (1) ◽  
pp. 269-275 ◽  
Author(s):  
Ramona Halmer ◽  
Laura Davies ◽  
Yang Liu ◽  
Klaus Fassbender ◽  
Silke Walter
Keyword(s):  
Multiple Sclerosis ◽  
T Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
T Cell Activation ◽  
Cell Activation ◽  
Innate Immune ◽  
Autoimmune Encephalomyelitis ◽  
Immune Receptors ◽  
Experimental Autoimmune

Background: Multiple sclerosis is the most common autoimmune disease of the central nervous system in young adults and histopathologically characterized by inflammation, demyelination and gliosis. It is considered as a CD4+ T cell-mediated disease, but also a disease-promoting role of the innate immune system has been proposed, based e.g. on the observation that innate immune receptors modulate disease severity of experimental autoimmune encephalomyelitis. Recent studies of our group provided first evidence for a key role of the innate immune LPS receptor (CD14) in pathophysiology of experimental autoimmune encephalomyelitis. CD14-deficient experimental autoimmune encephalomyelitis mice showed increased clinical symptoms and enhanced infiltration of monocytes and neutrophils in brain and spinal cord. Methods: In the current study, we further investigated the causes of the disease aggravation by CD14-deficiency and examined T cell activation, also focusing on the costimulatory molecules CTLA-4 and CD28, and T cell migration capacity over the blood brain barrier by FACS analysis, in vitro adhesion and transmigration assays. Results: In the results, we observed a significantly increased migration of CD14-deficient lymphocytes across an endothelial monolayer. In contrast, we did not see any differences in expression levels of TCR/CTLA-4 or TCR/CD28 and lymphocyte adhesion to endothelial cells from CD14-deficient compared to wildtype mice. Conclusion: The results demonstrate an important role of CD14 in migration of lymphocytes, and strengthen the importance of innate immune receptors in adaptive immune disorders, such as multiple sclerosis.

scholarly journals Tim-3 Relieves Experimental Autoimmune Encephalomyelitis by Suppressing MHC-II

2022 ◽  
Vol 12 ◽  
Author(s):  
Lili Tang ◽  
Ge Li ◽  
Yang Zheng ◽  
Chunmei Hou ◽  
Yang Gao ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
T Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
T Cell Activation ◽  
Immune Tolerance ◽  
Cell Activation ◽  
Autoimmune Encephalomyelitis ◽  
Mhc Ii ◽  
Experimental Autoimmune

Tim-3, an immune checkpoint inhibitor, is widely expressed on the immune cells and contributes to immune tolerance. However, the mechanisms by which Tim-3 induces immune tolerance remain to be determined. Major histocompatibility complex II (MHC-II) plays a key role in antigen presentation and CD4+T cell activation. Dysregulated expressions of Tim-3 and MHC-II are associated with the pathogenesis of many autoimmune diseases including multiple sclerosis. Here we demonstrated that, by suppressing MHC-II expression in macrophages via the STAT1/CIITA pathway, Tim-3 inhibits MHC-II-mediated autoantigen presentation and CD4+T cell activation. As a result, overexpression or blockade of Tim-3 signaling in mice with experimental autoimmune encephalomyelitis (EAE) inhibited or increased MHC-II expression respectively and finally altered clinical outcomes. We thus identified a new mechanism by which Tim-3 induces immune tolerance in vivo and regulating the Tim-3-MHC-II signaling pathway is expected to provide a new solution for multiple sclerosis treatment.

Andrographolide Interferes with T Cell Activation and Reduces Experimental Autoimmune Encephalomyelitis in the Mouse

2004 ◽  
Vol 312 (1) ◽  
pp. 366-372 ◽  
Author(s):  
Mirentxu I. Iruretagoyena ◽  
Jaime A. Tobar ◽  
Pablo A. González ◽  
Sofía E. Sepúlveda ◽  
Claudio A. Figueroa ◽  
...  
Keyword(s):  
T Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
T Cell Activation ◽  
Cell Activation ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune
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