Different T cells' distribution and activation degree of Th17 CD4+ cells in peripheral blood in patients with osteoarthritis, rheumatoid arthritis, and healthy donors …

A Lurati, A Laria, A Gatti, B Brando… - … Research and Reviews, 2015 - Taylor & Francis
A Lurati, A Laria, A Gatti, B Brando, M Scarpellini
Open Access Rheumatology: Research and Reviews, 2015Taylor & Francis
Objective To determine distribution of T cells and activation degree of Th CD4+ cells in
peripheral blood of patients with osteoarthritis (OA), rheumatoid arthritis (RA), and healthy
donors. Methods Patients with established diagnosis of RA according to American College
of Rheumatology/European League Against Rheumatism 2010 criteria, knee or hip OA
according to American College of Rheumatology criteria, and healthy blood donor
volunteers were eligible. Multi-channel flow cytometry and monoclonal antibodies against …
Objective
To determine distribution of T cells and activation degree of Th CD4+ cells in peripheral blood of patients with osteoarthritis (OA), rheumatoid arthritis (RA), and healthy donors.
Methods
Patients with established diagnosis of RA according to American College of Rheumatology/European League Against Rheumatism 2010 criteria, knee or hip OA according to American College of Rheumatology criteria, and healthy blood donor volunteers were eligible. Multi-channel flow cytometry and monoclonal antibodies against CD3, CD4, CD8, CCR6, CD38, CXCR3, and HLA DR were used to distinguish and evaluate T cells’ subpopulation.
Results
We analyzed blood samples of 15 patients with well-defined RA, 56 with hip or knee OA, and 20 healthy age matched controls. Blood samples from RA patients showed significantly higher counts of CD4+ CD38+ DR+ (activated CD4 T cells) and Th17 (CCR6+ CXCR3−) cells as compared to OA patients and control group (P<0.01). Furthermore the samples from the OA patients showed a higher percentage of activated CD4 T cells and Th17 cells as compared to control group (P<0.05). Interestingly there was no difference between Th1 (CD4+ CXCR3+ CCR6−) and Th2 (CD4+ CXCR3− CCR6−) between the three groups (P>0.1).
Conclusion
According to the latest view of OA disease pathogenesis, our preliminary results support the hypothesis that OA may also be a disease with an immunological/inflammatory involvement like RA. It seems that there is a quantitative but non-qualitative difference in Th17 cells’ profile, including the expression of activation markers, between RA and OA.
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