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IMMUNOCYTOCHEMICAL DETECTION OF SOME APOPTOSIS REGULATING PROTEINS (P53 AND BCL-2) IN PERIPHERAL BLOOD LYMPHOCYTES OF RHEUMATOID ARTHRITIS PATIENTS | ||
| IRAQI JOURNAL OF MEDICAL SCIENCES | ||
| Article 1, Volume 6, Issue 1, 2008, Pages 89-98 | ||
| Authors | ||
| Abdul-Razak H. Ahmad; Nidhal Abdul Mohymen; Haider Faisal Ghazi | ||
| Abstract | ||
| Background: There are several regulatory proteins involved in the control of lymphocyte apoptosis. Their impairment may play a role in the pathogenesis of several autoimmune diseases. Recent studies have reported impairment in the apoptosis of peripheral blood lymphocytes (PBLs) in patients with rheumatoid arthritis (RA). Objective: The aim of this study is to evaluate the cellular expression of P53 and BcI-2 proteins in the PBLs and their roles in the apoptotic process, and correlate their cellular expressions with the percent of peripheral T cell population. Methods: This study involved forty-six RA patients were examined and compared with 17 healthy control individuals of similar ages. Lymphocytes were separated from peripheral blood samples, the assessment of their cellular expression of CD3 and regulatory proteins p53 and Bcl-2 by immunocytochemistry staining method. Results: The results showed abundant accumulation of CD3 T lymphocytes in the peripheral circulation of RA patients in comparison with controls. A highly significant increased percentage of Bcl-2 protein expression in RA PBLs, compared to healthy control (p<0.001) while there was no such statistical difference regarding P53 expression in PBLs from both groups (p=0.278). The results of linear regression showed a significant correlation between the increased peripheral blood T lymphocytes and cellular percentage of Bcl-2 protein expression (p<0.001), while there was no such correlation with the percentage of P53 expression (p=0.587). Conclusion: in conclusion of these results, we found an increase in the peripheral blood T lymphocytes from patients with RA that could be resulted from the noticed up-regulation of cellular expression of Bcl-2 protein, rather than with changes in cellular expression of P53 protein. | ||
| Keywords | ||
| Rheumatoid arthritis; apoptosis; Bcl; immunocytochemistry | ||
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