Childhood multiple sclerosis: Clinical features and demonstration of changes in T cell subsets with disease activity

1982 ◽  
Vol 11 (5) ◽  
pp. 463-468 ◽  
Author(s):  
Stephen L. Hauser ◽  
Michael J. Bresnan ◽  
Ellis L. Reinherz ◽  
Howard L. Weiner
Immunology ◽  
2017 ◽  
Vol 154 (2) ◽  
pp. 239-252 ◽  
Author(s):  
Thais B. Ferreira ◽  
Joana Hygino ◽  
Ana Cristina Wing ◽  
Taissa M. Kasahara ◽  
Priscila M. Sacramento ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jiao Sun ◽  
Yameng Sui ◽  
Yunqing Wang ◽  
Lijun Song ◽  
Dong Li ◽  
...  

AbstractGalectin-9 (Gal-9) is a multifunctional immunomodulatory factor highly expressed in RA. This study aimed to investigate the expression of Gal-9 and its correlation with disease activity and therapeutic response in RA patients. Active RA patients were enrolled and treated with tacrolimus (TAC) alone or in combination therapy for 12 weeks in a prospective cohort study. Clinical and immunological parameters were recorded at baseline and week 12. We measured Gal-9 expression in different T cell subsets and in plasma. The disease activity of RA patients decreased after treatment. At baseline, the Gal-9 expression percentage was higher in the group with severe disease than in mild or moderate groups. After treatment, the Gal-9 expression in CD3+, CD4+, CD8+ and CD4-CD8− cell subsets decreased, as well as Gal-9 mean fluorescence intensity in CD3+, CD4+ and CD8+ T cells. Similarly, plasma Gal-9 levels were lower at week 12 than at baseline. Good responders showed significantly lower Gal-9 expression on CD3+ and CD4+ T cell subsets and lower plasma Gal-9 levels than poor responders. Gal-9 expression positively correlates with disease activity in RA patients. Gal-9 can be regarded as a new biomarker for evaluating RA activity and therapeutic effect, including TAC.


2018 ◽  
Vol 20 (1) ◽  
Author(s):  
Jonathan Aldridge ◽  
Jayesh M. Pandya ◽  
Linda Meurs ◽  
Kerstin Andersson ◽  
Inger Nordström ◽  
...  

2009 ◽  
Vol 131 ◽  
pp. S70
Author(s):  
Finn Sellebjerg ◽  
Martin Krakauer ◽  
Dan Hesse ◽  
Henrik Lund ◽  
Signe Limborg ◽  
...  

1999 ◽  
Vol 45 (2) ◽  
pp. 247-250 ◽  
Author(s):  
Burkhard Becher ◽  
Paul S. Giacomini ◽  
Daniel Pelletier ◽  
Ellie McCrea ◽  
Alexandre Prat ◽  
...  

Author(s):  
M. A. Bach ◽  
E. Tournier-Lasserve

2020 ◽  
Vol 117 (35) ◽  
pp. 21546-21556 ◽  
Author(s):  
Lisa Ann Gerdes ◽  
Claudia Janoschka ◽  
Maria Eveslage ◽  
Bianca Mannig ◽  
Timo Wirth ◽  
...  

The tremendous heterogeneity of the human population presents a major obstacle in understanding how autoimmune diseases like multiple sclerosis (MS) contribute to variations in human peripheral immune signatures. To minimize heterogeneity, we made use of a unique cohort of 43 monozygotic twin pairs clinically discordant for MS and searched for disease-related peripheral immune signatures in a systems biology approach covering a broad range of adaptive and innate immune populations on the protein level. Despite disease discordance, the immune signatures of MS-affected and unaffected cotwins were remarkably similar. Twinship alone contributed 56% of the immune variation, whereas MS explained 1 to 2% of the immune variance. Notably, distinct traits in CD4+effector T cell subsets emerged when we focused on a subgroup of twins with signs of subclinical, prodromal MS in the clinically healthy cotwin. Some of these early-disease immune traits were confirmed in a second independent cohort of untreated early relapsing-remitting MS patients. Early involvement of effector T cell subsets thus points to a key role of T cells in MS disease initiation.


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