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Isolating Human Peripheral Blood Mononuclear Cells and CD4+ T cells from Sézary Syndrome Patients for Transcriptomic Profiling
Published on: October 14, 2021
Peripheral blood lymphocytes analysis detects CD100/SEMA4D alteration in systemic sclerosis patients
Alina Besliu1, Leontina Banica, Denisa Predeteanu
1Cellular Receptors Laboratory, Cantacuzino National Institute of Research and Development for Microbiology and Immunology, Bucharest, Romania.
Dysregulation of Semaphorin 4D (CD100) in T and B cells is linked to systemic sclerosis (SSc). Increased CD100 expression and soluble CD100 in SSc patients suggest its role in this autoimmune disease.
Area of Science:
- Immunology
- Autoimmunity
- Dermatology
Background:
- Systemic sclerosis (SSc) is an autoimmune disease with complex pathogenesis.
- The immune system, particularly T and B cell interactions, is implicated in SSc.
- Semaphorin 4D (CD100) and CD72 are key molecules in T and B cell cooperation and have been linked to autoimmunity.
Purpose of the Study:
- To investigate the expression levels of CD100 and CD72 on T and B cells in patients with SSc.
- To determine the potential role of CD100 and CD72 dysregulation in the pathogenesis of SSc.
Main Methods:
- Flow cytometry was used to analyze CD100 and CD72 expression on T and B cells.
- Serum levels of soluble CD100 were measured in SSc patients and healthy donors.
- Correlations between CD100/CD72 expression and clinical parameters of SSc were assessed.
Main Results:
- Systemic sclerosis patients exhibited increased percentages of CD100(high) T and B cells.
- Significantly elevated CD100 expression was observed on CD4(+) T cells in SSc.
- Soluble CD100 levels were frequently detected in the sera of SSc patients.
- CD100 dysregulations correlated with anti-Scl70 antibodies, disease type, skin thickening, disease duration, and inflammation.
Conclusions:
- Dysregulation of CD100 expression and release may contribute to the development and/or progression of systemic sclerosis.
- CD100's role in T and B cell cooperation highlights its potential involvement in SSc pathogenesis.
- Further research into CD100 pathways could offer new therapeutic targets for SSc.
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