scholarly journals The role of CTLA-4 in tolerance induction and T cell differentiation in experimental autoimmune encephalomyelitis: i.p. antigen administration

1999 ◽  
Vol 11 (12) ◽  
pp. 1881-1888 ◽  
Author(s):  
Robert B. Ratts ◽  
Lachelle R. Arredondo ◽  
Patrice Bittner ◽  
Peter J. Perrin ◽  
Amy E. Lovett-Racke ◽  
...  
Author(s):  
Tayebeh Nowras ◽  
Mohammad Fereidouni ◽  
Hamidreza Safari ◽  
Mohsen Naseri

Multiple sclerosis (MS) is one of the autoimmune diseases that affects the central nervous system (CNS) and causes myelin loss and axonal damage. Recent studies have shown the important role of autoreactive T cells in the pathogenesis of MS. One of the plants in the Astersa family, which has therapeutic benefits, is Artemisia dracunculus L. or Tarragon. In this study, the role of aqueous extract of Tarragon in suppressing Th1 and Th17 cell differentiation and ameliorating experimental autoimmune encephalomyelitis (EAE) was investigated. EAE was induced in C57BL/6 female mice by Hook kit MOG35-55/CFA Emulsion PTX and one group was treated with Tarragon at a dose of 500 mg/kg. Mice were euthanized on day 33 post-immunization, spleens were removed for assessing Th1, Th17 and Treg cells by flow cytometry. We provided evidence that Tarragon (500 mg/kg) significantly ameliorated clinical scores of EAE. We did not observe significant alterations in T cell differentiation to Th1, Th17 or Treg in the spleen of mice during EAE. This is the first experimental evidence showing that administration of aqueous extract of Tarragon reduces the severity of EAE, but the protective effect of Tarragon is independent of alteration in T cells in the spleen. These results suggest other mechanisms for the effectiveness of this extract in improving the EAE process.


1999 ◽  
Vol 11 (12) ◽  
pp. 1889-1896 ◽  
Author(s):  
Robert B. Ratts ◽  
Lachelle R. Arredondo ◽  
Patrice Bittner ◽  
Peter J. Perrin ◽  
Amy E. Lovett-Racke ◽  
...  

Biosystems ◽  
2013 ◽  
Vol 112 (2) ◽  
pp. 107-121 ◽  
Author(s):  
Richard B. Greaves ◽  
Mark Read ◽  
Jon Timmis ◽  
Paul S. Andrews ◽  
James A. Butler ◽  
...  

2015 ◽  
Vol 37 (1) ◽  
pp. 269-275 ◽  
Author(s):  
Ramona Halmer ◽  
Laura Davies ◽  
Yang Liu ◽  
Klaus Fassbender ◽  
Silke Walter

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.


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