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Title: KLRG1 and its role in Rheumatoid Arthritis
Author: Thompson, Charlotte
ISNI:       0000 0004 7968 7254
Awarding Body: Cardiff University
Current Institution: Cardiff University
Date of Award: 2019
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Introduction: Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic joint inflammation. A homeostatic disequilibrium of the immune system is implicated in the failure of systemic tolerance. A part of this disequilibrium may be the rise of CD3+CD8+CD28- T cells in RA. Their role in the pathogenesis of RA remains unknown. Methods: Analysis of peripheral blood samples from RA patients using flow cytometry were compared to healthy controls (RA patients n=50, healthy controls n=25). Results: CD3+CD8+CD28- cells are higher in RA. Further subdivision of this group revealed that CD3+CD8+CD28- cells are higher in Early RA as well as Established RA. This subset of CD3+CD8+CD28- cells also correlated with disease duration in Early RA patients. The cell surface receptor KLRG1, is expressed by a high percentage of CD3+CD8+CD28- cells. As well as being associated with clinical and serological markers in RA, CD3+CD8+CD28-KLRG1+ cells are higher in the Early RA patients who had a poor response to therapy at six months. CD3+CD8+CD28-KLRG1+ cells were found to produce more IL-10 than KLRG1- cells. The percentage of CD3+CD8+CD28- and CD3+CD8+CD28-KLRG1+ cells is higher in CMV positive than CMV negative RA patients but CMV distribution is similar across the responders and non-responders to treatment in Early RA. CMV positive CD3+CD8+CD28-KLRG1+ cells produce more IL-10 than KLRG1- cells. Conclusion: The higher percentage of CD3+CD8+CD28-KLRG1+ cells is associated clinical and serological markers as well as poor response to treatment in Early RA patients. This reinforces the importance of this subtype of T regs in the course of RA. However, the precise reason is unclear and requires further investigation.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (M.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available