Salomeh Fouladi; Minoo Adib; Mansoor Salehi; Hadi Karimzadeh; Zahra Bakhshiani; Vajiheh Ostadi
Volume 6, Issue 1 , March 2009, , Pages 49-54
Abstract
Background: HLA-B*27 is strongly associated with ankylosing spondylitis (AS). It represents a family of alleles that differ among ethnic groups. Objective: The aim of this study was to determine the distribution of HLA-B*27 alleles in AS patients and healthy controls in Isfahan (Iran). Methods: Sixty ...
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Background: HLA-B*27 is strongly associated with ankylosing spondylitis (AS). It represents a family of alleles that differ among ethnic groups. Objective: The aim of this study was to determine the distribution of HLA-B*27 alleles in AS patients and healthy controls in Isfahan (Iran). Methods: Sixty AS patients and 430 healthy blood donors were selected. All subjects were HLA-B*27 positive by flow cytometry. HLAB* 27 subtypes were determined by PCR-SSP. Results: Forty patients (66.7%) and 17 controls (3.95%) were HLA-B*27 positive. Subtypes detected by PCR-SSP were B*2705, B*2702, B*2704 and B*2707. One patient was B*2702/B*2710. No significant difference was found in the distribution of these alleles between AS patients and controls. Conclusion: Although Caucasian subtypes are predominant among Iranians, this population is characterized by a combination of both specific Caucasian and Oriental subtypes. However such results should be interpreted carefully because of the small sample size in our investigation and definitive conclusion awaits more ethnicgroup studies.
Abbas Ali Pourazar; Alireza Andalib; Farzad Qreizy; Hadi Karimzadeh; Ahmad Ghavami-Nejad; Behshad Pournasr-Khakbaz
Volume 2, Issue 2 , June 2005, , Pages 91-96
Abstract
Background: Inappropriate activation or blockage of the inhibition of complement system could cause tissue damages in autoimmune diseases particularly rheumatoid arthritis (RA). Defect in complement component regulation may cause damages to tissues, on the other hand, or the damaged tissue might affect ...
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Background: Inappropriate activation or blockage of the inhibition of complement system could cause tissue damages in autoimmune diseases particularly rheumatoid arthritis (RA). Defect in complement component regulation may cause damages to tissues, on the other hand, or the damaged tissue might affect the unnecessary activation of complement components. Objective: To investigate the expression of CD55 and CD 59 complement regulatory proteins in RA patients. Subjects and Methods: Fifty proved rheumatoid arthritis patients participated in this study and their blood were collected for investigations. CD55 and CD59 molecules expression on the erythrocytes was assayed using primary monoclonal antibody and secondary FITC conjugated Ab, then the prepared samples were run with a FACSCalibur flowcytometer (Becton-Dickinson) and the obtained data was analyzed using a Cell Quest software package. To evaluate the complement function, CH50 was performed using patient sera. All experiments were done with a matched healthy volunteer group. Results: The mean fluorescence intensity for CD55 was 27.6 ± 13.4 arbitrary unit for patients and 68.5 ± 10.5 for healthy group. CD59 mean fluorescence intensity was 314 ± 83 in patient group and 508 ± 56 in healthy volunteers. In addition, there was a significant difference between CH50 in patients (54.5 ± 15.5) and in healthy group (110 ± 20). A significant correlation between CD55 and CD59 expansion on the patient erythrocytes was found (P = 0.00, r = 0.576). No association was found between CD59, or CD55 with CH50 (P > 0.05). Conclusion: The expression of CD55 and CD59 is down-regulated on erythrocytes of patients with RA. Change in expression of regulatory complement components in RA may be a useful key for the assessment of disease progression or in patients' follow-up.