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Three key genes expression profiling in Egyptian rheumatoid arthritis patients
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Rheumatoid arthritis (RA) is a multi-system autoimmune disease with synovial joints involvement. The triad of autoimmunity, genetics, and environment is the key player in RA pathogenesis. We intended to investigate gene expression of C-C Chemokine Ligand 2 (CCL2), protein tyrosine phosphatase non-receptor type 22 (PTPN22), and Cytotoxic T-lymphocyte associated protein 4 (CTLA-4) in RA patients versus controls, and its correlation with the activity of the disease. The relative expression of PTPN22, CTLA-4, and CCL2 in the peripheral blood of 59 RA patients and 50 controls was determined using RT-PCR. There was a significantly higher median (inter-quartile range) expression of CTLA-4 and CCL2 in RA patients in comparison to controls (P<0.05). However, in RA patients, PTPN22 expression was significantly lower than in controls (P=0.0001). A weak significant correlation was detected between PTPN22 and either CTLA-4 or CCL2. Also, on comparing RA patients with moderate to severe disease activity versus those who have a mild disease activity, CCL2 was significantly over-expressed (P > 0.05). Thus, in Egyptian RA patients, there was a significant PTPN22 down-expression and greater expression of CTLA-4 and CCL2. Moreover, over-expression of CCL2 in RA patients with moderate-to-severe disease activity was significant. We conclude that these three key genes could become useful diagnostic markers for RA and CCL2 expression as a good prognostic tool for RA disease activity.
Egyptian Association of Immunologists
Title: Three key genes expression profiling in Egyptian rheumatoid arthritis patients
Description:
Rheumatoid arthritis (RA) is a multi-system autoimmune disease with synovial joints involvement.
The triad of autoimmunity, genetics, and environment is the key player in RA pathogenesis.
We intended to investigate gene expression of C-C Chemokine Ligand 2 (CCL2), protein tyrosine phosphatase non-receptor type 22 (PTPN22), and Cytotoxic T-lymphocyte associated protein 4 (CTLA-4) in RA patients versus controls, and its correlation with the activity of the disease.
The relative expression of PTPN22, CTLA-4, and CCL2 in the peripheral blood of 59 RA patients and 50 controls was determined using RT-PCR.
There was a significantly higher median (inter-quartile range) expression of CTLA-4 and CCL2 in RA patients in comparison to controls (P<0.
05).
However, in RA patients, PTPN22 expression was significantly lower than in controls (P=0.
0001).
A weak significant correlation was detected between PTPN22 and either CTLA-4 or CCL2.
Also, on comparing RA patients with moderate to severe disease activity versus those who have a mild disease activity, CCL2 was significantly over-expressed (P > 0.
05).
Thus, in Egyptian RA patients, there was a significant PTPN22 down-expression and greater expression of CTLA-4 and CCL2.
Moreover, over-expression of CCL2 in RA patients with moderate-to-severe disease activity was significant.
We conclude that these three key genes could become useful diagnostic markers for RA and CCL2 expression as a good prognostic tool for RA disease activity.
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