scholarly journals The correlation of syndecan-4 with disease activity and serological characteristics of rheumatoid arthritis

2021 ◽  
Author(s):  
Juan Zhao ◽  
Xia Ye ◽  
Zhuoli Zhang
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Disease Activity ◽  
Rheumatoid Factor ◽  
Synovial Tissue ◽  
Synovial Fibroblasts ◽  
Healthy Controls ◽  
Immunosorbant Assay ◽  
Enzyme Linked Immunosorbant Assay

Abstract [Objectives]To investigate the expression of syndecan-4 in serum, synovial fluid (SF) and synovium in rheumatoid arthritis (RA) by comparing with osteoarthritis (OA) patients, and to analyze the correlation of syndecan-4 with disease activity of RA .[Methods]Syndecan-4 in sera of 60 RA patients, 20 OA patients, 20 healthy controls, and in paired SF of 23 RA patients were tested by enzyme linked immunosorbant assay (ELISA). The expressions of syndecan-4 in synovium of 5 RA patients and 5 OA patients were detected by immunohistochemistry. The expressions of syndecan-4 of cultured synovial fibroblasts from RA and OA patients were detected by immunofluorescence. The correlation between serum syndecan-4 concentration and disease activity were analyzed in 60 RA patients.[Results]The serum syndedcan-4 concentration was significantly higher in RA patients than in OA patients and healthy controls, and was higher in rheumatoid factor (RF)-positive RA patients than in RF-negative ones. Syndecan-4 concentration in SF of RA patients was comparable with OA patients. Syndecan-4 expression in synovial tissue was similar between RA and OA patients. The syndecan-4 concentration was significantly lower in synovial fluid than in serum, either in RA or in OA patients. The serum and SF syndecan-4 concentrations were both positively correlated with RA disease activity scores.[Conclusion]The serum syndecan-4 concentration is higher in RA patients than in OA patients, and significantly higher in RF-positive RA patients than in RF-negative ones. The serum and SF syndecan-4 concentrations were both positively correlated with disease activity of RA patients.

scholarly journals POS0388 INTERLEUKIN 40 (IL-40) IS UP-REGULATED IN RHEUMATOID ARTHRITIS (RA) AND ASSOCIATED WITH DISEASE ACTIVITY, LEVELS OF AUTOANTIBODIES AND CHEMOKINES

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 424.1-424
Author(s):  
A. Navrátilová ◽  
L. Andres Cerezo ◽  
H. Hulejova ◽  
V. Becvar ◽  
D. Tegzová ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
B Cells ◽  
Synovial Fluid ◽  
Disease Activity ◽  
B Cell ◽  
Synovial Tissue ◽  
Lupus Erythematosus ◽  
Synovial Fibroblasts ◽  
Clinical Activity

Background:Interleukin 40 (IL-40) is newly identified B cell - associated cytokine implicated in humoral immune responses and in B cell development. As B cells play a pivotal role in autoimmunity, we aimed to investigate the function of IL-40 in rheumatoid arthritis (RA).Objectives:The aim of our study was to determine the function of IL-40 in RA.Methods:IL-40 expression in the synovial tissue was determined by immunohistochemistry and immunofluorescence (n=4-5). IL-40 was analysed in the serum/synovial fluid of patients with RA (n=69), systemic lupus erythematosus (SLE; n=69), osteoarthritis (OA; n=44), and in healthy controls (HC; n=25). Given the association of IL-40 with B cells, we analysed the effect of rituximab therapy on the serum IL-40 in 19 patients with RA after 16 and 24 weeks of the therapy. The clinical activity of patients with RA was assessed according to the 28 joint count Disease Activity Score (DAS28). Levels of C-reactive protein (CRP) and autoantibodies were measured by routine laboratory techniques. In vitro experiments were performed in RA synovial fibroblasts (n=9). Levels of cytokines and inflammatory mediators were determined in serum, synovial fluid and supernatants using ELISA or multiplex immunoassay.Results:IL-40 was overexpressed in RA synovial tissue compared to OA, particularly by synovial fibroblasts and immune cells such as B and T lymphocytes, macrophages and neutrophils. The levels of IL-40 were significantly higher in the synovial fluid of RA patients compared to OA (33.2 (6.6-68.9) vs. 0.7 (0.1-2.4) ng/ml; p<0.0001). In addition, IL-40 was increased in the serum of RA patients compared to SLE, OA or HC (4.8 (1.7-24.9) vs. 1.4 (1.0-1.9), 1.6 (0.6-3.1) or 1.5 (0.7-2.7) ng/ml; p<0.0001 for all) and decreased after 16 (p<0.01) and 24 weeks (p<0.001) in a subgroup of rituximab treated patients with RA. IL-40 levels in RA patients correlated with autoantibodies rheumatoid factor (IgM) and anti-citrullinated protein antibody (ACPA) in the serum (p<0.0001 and p<0.01) as well as in the synovial fluid (p<0.0001 and p<0.001). IL-40 in RA synovial fluid was also significantly associated with DAS28 (p<0.05), synovial fluid leukocyte count (p<0.01), number of swollen joints (p<0.05) and neutrophil attractants IL-8 (p<0.01) and MIP-1α (p<0.01). RA synovial fibroblasts exposed to recombinant IL-40 increased secretion of IL-8 (p<0.01), MCP-1 (p<0.05) and MMP-13 (p<0.01) compared to unstimulated cells in in vitro conditions.Conclusion:Our results show for the first time that IL-40 is elevated in RA and decreases following B-cell depletion therapy. The association of IL-40 with autoantibodies and chemokines may imply its potential involvement in RA development. Moreover, IL-40 up-regulates the secretion of chemokines and MMP-13 by synovial fibroblasts, indicating its role in the regulation of inflammation and tissue destruction in RA.Acknowledgements:Supported by MHCR 023728 a SVV 260 523Disclosure of Interests:None declared

scholarly journals IL-40: A New B Cell-Associated Cytokine Up-Regulated in Rheumatoid Arthritis Decreases Following the Rituximab Therapy and Correlates With Disease Activity, Autoantibodies, and NETosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Adela Navrátilová ◽  
Lucie Andrés Cerezo ◽  
Hana Hulejová ◽  
Viktor Bečvář ◽  
Michal Tomčík ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Disease Activity ◽  
B Cell ◽  
Synovial Tissue ◽  
Lupus Erythematosus ◽  
Synovial Fibroblasts ◽  
Tissue Destruction ◽  
Humoral Immune ◽  
B Cell Homeostasis

BackgroundInterleukin 40 (IL-40) is a newly identified B cell-associated cytokine implicated in humoral immune responses and B cell homeostasis. As B cells play a pivotal role in autoimmunity, we investigated the function of IL-40 in rheumatoid arthritis (RA).MethodsIL-40 expression was determined in the synovial tissue from RA and osteoarthritis (OA) patients. IL-40 was analysed in the serum/synovial fluid of patients with RA (n=50), systemic lupus erythematosus (SLE, n=69), OA (n=44), and healthy controls (HC, n=50). We assessed the changes of IL-40 levels in RA patients following the B cell depletion by rituximab (n=29) or after the TNF inhibition by adalimumab (n=25). We examined the relationship between IL-40, disease activity, autoantibodies, cytokines, and NETosis markers. Effect of IL-40 on synovial fibroblasts was determined.ResultsIL-40 was overexpressed in RA synovial tissue, particularly by synovial lining and infiltrating immune cells. The levels of IL-40 were up-regulated in the synovial fluid of RA versus OA patients (p&lt;0.0001). Similarly, IL-40 was increased in the serum of RA patients compared to HC, OA, or SLE (p&lt;0.0001 for all) and decreased after 16 and 24 weeks (p&lt;0.01 and p&lt;0.01) following rituximab treatment. No significant effect of adalimumab on IL-40 was observed. IL-40 levels in RA patients correlated with rheumatoid factor-IgM and anti-cyclic citrullinated peptides (anti-CCP) in the serum (p&lt;0.0001 and p&lt;0.01), as well as in the synovial fluid (p&lt;0.0001 and p&lt;0.001). Synovial fluid IL-40 was also associated with disease activity score DAS28 (p&lt;0.05), synovial fluid leukocyte count (p&lt;0.01), neutrophil attractants IL-8 (p&lt;0.01), MIP-1α (p&lt;0.01), and markers of neutrophil extracellular traps externalization (NETosis) such as proteinase 3 (p&lt;0.0001) and neutrophil elastase (p&lt;0.0001). Synovial fibroblasts exposed to IL-40 increased the secretion of IL-8 (p&lt;0.01), MCP-1 (p&lt;0.05), and MMP-13 (p&lt;0.01) compared to the unstimulated cells.ConclusionsWe show the up-regulation of IL-40 in RA and its decrease following B cell depleting therapy. The association of IL-40 with autoantibodies, chemokines, and markers of NETosis may imply its potential involvement in RA development. Moreover, IL-40 up-regulates the secretion of chemokines and MMP-13 in synovial fibroblasts, indicating its role in the regulation of inflammation and tissue destruction in RA.

scholarly journals AB0111 THE COMPARISON OF SYNDECAN-4 LEVEL IN SERA, SYNOVIAL FLUID AND SYNOVIUM OF RHEUMATOID ARTHRITIS AND OSTEOARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1356.1-1356
Author(s):  
J. Zhao ◽  
X. Ye ◽  
Z. Zhang
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Migration ◽  
Synovial Fluid ◽  
Disease Activity ◽  
Immune Cell ◽  
Inflammatory Responses ◽  
Heparan Sulphate ◽  
Healthy Controls ◽  
Baseline Serum

Background:Syndecan-4, one of the members of heparan sulphate proteoglycans (HSPGs), has been shown to be involved in regulating inflammatory responses, angiogenesis, and cell migration. Its role has been proved in animal arthritis models, however not clearly elucidated in rheumatoid arthritis (RA) patientsObjectives:To investigate the role of Syndecan-4 in the pathogenesis of RA, by detecting Syndecan-4 expression in the serum, synovial fluid and synovium of RA patients and comparing with osteoarthritis (OA) patientsMethods:The concentrations of syndecan-4 in sera and synovial fluid of RA and osteoarthritis (OA) patients were detected by ELISA. The expression of syndecan-4 in synovium of RA and OA patients was detected by immunohistochemistry. In another cohort of 60 RA patients, the association analysis was performed. All the RA patients were with disease duration more than 6 months and with DAS28-CRP>3.2 although after csDMARDs (including MTX and/or leflunomide) treatment for more than 3 months. The RA patients were treated with tumour necrosis factor α (TNFα) inhibitor (TNFi) and MTX 10mg per week for 12 weeks. The correlations between sera Syndecan-4 and disease activity of RA as well as therapeutic response to TNFi were analyzed.Results:The serum Syndedcan-4 level of RA patients [637.1 (483.6-1069.6) pg/mL] was significantly higher than that of OA patients [345.0 (287.9-421.1) pg/mL] and healthy controls [195.6 (165.0-225.2) pg/mL](P<0.001, P<0.001, respectively). The serum concentration of Syndecan-4 is also higher in OA patients than that in healthy controls (P<0.001). It was also higher in RF-positive RA patients than in RF-negative ones [603.0 (100.0-8879.1) pg/mL vs 460.3 (178.7-2468.9) pg/mL, (p=0.026)]. The Syndedcan-4 level in synovial fluid and synovia were comparable between RA and OA patients. No correlation was found between serum Syndedcan-4 and disease activity of RA. TNFi treatment did not change the serum Syndecan-4 level significantly. The baseline serum Syndecan-4 did not show predictive value for TNFi response.Conclusion:Syndecan-4 can be expressed in the synovia of RA and OA patients. The serum Syndecan-4 is higher in RA patients than in OA patients and healthy controls, and significantly higher in sero-positive RA patients than in sero-negative ones. Syndecan-4 may participate in the pathogenesis of RA.References:[1]Leonova EI, Galzitskaya OV. Role of Syndecans in Lipid Metabolism and Human Diseases. Adv Exp Med Biol, 2015, 855: 241-58.[2]Xie J, Wang J, Li R, Dai Q, Yong Y, Zong B, et al. Syndecan-4 over-expression preserves cardiac function in a rat model of myocardial infarction. J Mol Cell Cardiol 2012; 53: 250-8.[3]Strand ME, Aronsen JM, Braathen B, Sjaastad I, Kvaløy H, Tønnessen T, et al. Shedding of syndecan-4 promotes immune cell recruitment and mitigates cardiac dysfunction after lipopolysaccharide challenge in mice. J Mol Cell Cardiol. 2015;88:133-44.[4]Endo T, Ito K, Morimoto J, Kanayama M, Ota D, Ikesue M, et al. Syndecan 4 Regulation of the Development of Autoimmune Arthritis in Mice by Modulating B Cell Migration and Germinal Center Formation. Arthritis Rheumatol. 2015; 67:2512-22.Disclosure of Interests:None declared

scholarly journals A thyroid hormone network exists in synovial fibroblasts of rheumatoid arthritis and osteoarthritis patients

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Anna-Sophia Pörings ◽  
Torsten Lowin ◽  
Bianca Dufner ◽  
Joachim Grifka ◽  
Rainer H. Straub
Keyword(s):  
Rheumatoid Arthritis ◽  
Gene Expression ◽  
Thyroid Hormone ◽  
Synovial Fluid ◽  
Thyroid Hormones ◽  
Synovial Tissue ◽  
Hormone Receptors ◽  
Synovial Fibroblasts ◽  
Hormone Levels ◽  
Thyroid Hormone Levels

Abstract While patients with rheumatoid arthritis (RA) sometimes demonstrate thyroidal illness, the role of thyroid hormones in inflamed synovial tissue is unknown. This is relevant because thyroid hormones stimulate immunity, and local cells can regulate thyroid hormone levels by deiodinases (DIO). The study followed the hypothesis that elements of a thyroid hormone network exist in synovial tissue. In 12 patients with RA and 32 with osteoarthritis (OA), we used serum, synovial fluid, synovial tissue, and synovial fibroblasts (SF) in order to characterize the local thyroid hormone network using ELISAs, immunohistochemistry, imaging methods, tissue superfusion studies, cell-based ELISAs, flow cytometry, and whole genome expression profiling. Serum/synovial fluid thyroid hormone levels were similar in RA and OA (inclusion criteria: no thyroidal illness). The degradation product termed reverse triiodothyronine (reverse T3) was much lower in serum compared to synovial fluid indicating biodegradation of thyroid hormones in the synovial environment. Superfusion experiments with synovial tissue also demonstrated biodegradation, particularly in RA. Cellular membrane transporters of thyroid hormones, DIOs, and thyroid hormone receptors were present in tissue and SF. Density of cells positive for degrading DIOs were higher in RA than OA. TNF increased protein expression of degrading DIOs in RASF and OASF. Gene expression studies of RASF revealed insignificant gene regulation by bioactive T3. RA and OA synovial tissue/SF show a local thyroid hormone network. Thyroid hormones undergo strong biodegradation in synovium. While bioactive T3 does not influence SF gene expression, SF seem to have a relay function for thyroid hormones.

scholarly journals Differential inflammation-mediated function of prokineticin 2 in the synovial fibroblasts of patients with rheumatoid arthritis compared to osteoarthritis

2021 ◽  
Author(s):  
Kentaro Noda ◽  
Bianca Dufner ◽  
Haruyasu Ito ◽  
Ken Yoshida ◽  
Gianfranco Balboni ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Synovial Tissue ◽  
Synovial Fibroblasts ◽  
Prokineticin 2 ◽  
Physiological Processes ◽  
Sickness Behaviors ◽  
Synovial Tissues ◽  
Fibroblast Like Synoviocytes

Abstract Prokineticin 2 (PK2) is a secreted protein involved in several pathological and physiological processes, including the regulation of inflammation, sickness behaviors, and the circadian rhythm. Recently, it was reported that PK2 is associated with the pathogenesis of collagen-induced arthritis in mice. However, whether PK2 influences the pathogenesis of rheumatoid arthritis (RA) or osteoarthritis (OA) remains unknown. In this study, we collected synovial tissue, plasma, synovial fluid, and fibroblast-like synoviocytes (FLS) from RA and OA patients to analyze the role of PK2 using immunohistochemistry, ELISAs, and tissue superfusion studies. PK2 and its receptors prokineticin receptor (PKR) 1 and 2 were expressed in RA and OA synovial tissues. PKR1 expression in RA synovial tissue was downregulated compared with OA synovial tissue. The PK2 concentration was higher in RA synovial fluid than in OA synovial fluid but similar between RA and OA plasma. PK2 suppressed the production of IL-6 from TNFα-prestimulated OA-FLS, and this effect was attenuated in TNFα-prestimulated RA-FLS. This phenomenon was accompanied by the upregulation of PKR1 in OA-FLS and the downregulation of PK2 and PKR1 in RA-FLS. This study provides a new model to explain some aspects underlying the chronicity of inflammation in RA.

scholarly journals Differential inflammation-mediated function of prokineticin 2 in the synovial fibroblasts of patients with rheumatoid arthritis compared with osteoarthritis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kentaro Noda ◽  
Bianca Dufner ◽  
Haruyasu Ito ◽  
Ken Yoshida ◽  
Gianfranco Balboni ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Synovial Tissue ◽  
Synovial Fibroblasts ◽  
Collagen Induced Arthritis ◽  
Prokineticin 2 ◽  
Physiological Processes ◽  
Sickness Behaviors ◽  
Synovial Tissues

AbstractProkineticin 2 (PK2) is a secreted protein involved in several pathological and physiological processes, including the regulation of inflammation, sickness behaviors, and circadian rhythms. Recently, it was reported that PK2 is associated with the pathogenesis of collagen-induced arthritis in mice. However, the role of PK2 in the pathogenesis of rheumatoid arthritis (RA) or osteoarthritis (OA) remains unknown. In this study, we collected synovial tissue, plasma, synovial fluid, and synovial fibroblasts (SF) from RA and OA patients to analyze the function of PK2 using immunohistochemistry, enzyme-linked immunosorbent assays, and tissue superfusion studies. PK2 and its receptors prokineticin receptor (PKR) 1 and 2 were expressed in RA and OA synovial tissues. PKR1 expression was downregulated in RA synovial tissue compared with OA synovial tissue. The PK2 concentration was higher in RA synovial fluid than in OA synovial fluid but similar between RA and OA plasma. PK2 suppressed the production of IL-6 from TNFα-prestimulated OA-SF, and this effect was attenuated in TNFα-prestimulated RA-SF. This phenomenon was accompanied by the upregulation of PKR1 in OA-SF. This study provides a new model to explain some aspects underlying the chronicity of inflammation in RA.

scholarly journals Splicing machinery is impaired in rheumatoid arthritis, associated with disease activity and modulated by anti-TNF therapy

2021 ◽  
pp. annrheumdis-2021-220308
Author(s):  
Alejandro Ibáñez-Costa ◽  
Carlos Perez-Sanchez ◽  
Alejandra María Patiño-Trives ◽  
Maria Luque-Tevar ◽  
Pilar Font ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Disease Activity ◽  
Synovial Fibroblasts ◽  
Data Set ◽  
Altered Expression ◽  
Healthy Donors ◽  
Inflammatory Profile ◽  
Splicing Machinery

ObjectivesTo characterise splicing machinery (SM) alterations in leucocytes of patients with rheumatoid arthritis (RA), and to assess its influence on their clinical profile and therapeutic response.MethodsLeucocyte subtypes from 129 patients with RA and 29 healthy donors (HD) were purified, and 45 selected SM elements (SME) were evaluated by quantitative PCR-array based on microfluidic technology (Fluidigm). Modulation by anti-tumour necrosis factor (TNF) therapy and underlying regulatory mechanisms were assessed.ResultsAn altered expression of several SME was found in RA leucocytes. Eight elements (SNRNP70, SNRNP200, U2AF2, RNU4ATAC, RBM3, RBM17, KHDRBS1 and SRSF10) were equally altered in all leucocytes subtypes. Logistic regressions revealed that this signature might: discriminate RA and HD, and anti-citrullinated protein antibodies (ACPAs) positivity; classify high-disease activity (disease activity score-28 (DAS28) >5.1); recognise radiological involvement; and identify patients showing atheroma plaques. Furthermore, this signature was altered in RA synovial fluid and ankle joints of K/BxN-arthritic mice. An available RNA-seq data set enabled to validate data and identified distinctive splicing events and splicing variants among patients with RA expressing high and low SME levels. 3 and 6 months anti-TNF therapy reversed their expression in parallel to the reduction of the inflammatory profile. In vitro, ACPAs modulated SME, at least partially, by Fc Receptor (FcR)-dependent mechanisms. Key inflammatory cytokines further altered SME. Lastly, induced SNRNP70-overexpression and KHDRBS1-overexpression reversed inflammation in lymphocytes, NETosis in neutrophils and adhesion in RA monocytes and influenced activity of RA synovial fibroblasts.ConclusionsOverall, we have characterised for the first time a signature comprising eight dysregulated SME in RA leucocytes from both peripheral blood and synovial fluid, linked to disease pathophysiology, modulated by ACPAs and reversed by anti-TNF therapy.

scholarly journals Progranulin Is Associated with Disease Activity in Patients with Rheumatoid Arthritis

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Lucie Andrés Cerezo ◽  
Markéta Kuklová ◽  
Hana Hulejová ◽  
Zdeňka Vernerová ◽  
Nikola Kaspříková ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Disease Activity ◽  
Health Assessment ◽  
Immunohistochemical Analysis ◽  
Healthy Controls ◽  
Reactive Protein ◽  
Synovial Tissues ◽  
Inflammatory Infiltrates ◽  
Fluid Levels

Objective. Progranulin (PGRN) is implicated in the pathogenesis of rheumatoid arthritis (RA). The aim of this study was to assess the relationship between PGRN and disease activity in RA.Methods.PGRN levels were evaluated in patients with RA (n=47) and OA (n=42) and healthy controls (n=41). Immunohistochemical analysis of PGRN in synovial tissues was performed. The association between PGRN and C-reactive protein (CRP), disease activity score (DAS28-CRP), and health assessment questionnaire (HAQ) was studied.Results. Circulating PGRN was elevated in patients with RA and OA compared to healthy controls (227.1±100.2and221.5±102.5versus128.1±34.7 ng/mL;P<0.001). Synovial fluid levels of PGRN were higher in patients with RA compared to OA (384.5±275.3versus241.4±165.2 ng/mL;P=0.002). PGRN expression was significantly upregulated in the synovial tissue of RA patients particularly in the inflammatory infiltrates. Serum PGRN levels correlated with DAS28 (r=0.327,P=0.049) and HAQ score (r=0.323,P=0.032), while synovial fluid PGRN correlated only with HAQ (r=0.310,P=0.043) in patients with RA. PGRN levels were not associated with CRP or autoantibodies.Conclusions. This study demonstrates increased PGRN expression at local sites of inflammation and association between PGRN levels, disease activity, and functional impairment in patients with RA.

Relationship of HLA-DRB1 Alleles and Rheumatoid Arthritis in West South of Iran

2017 ◽  
Vol 9 (03) ◽  
Author(s):  
Karim Mowla ◽  
Elham Rajaee M. D. ◽  
Mehrdad Dargahi-MalAmir M. D. ◽  
Neda Yousefinezhad ◽  
Maryam Jamali Hondori
Keyword(s):  
Rheumatoid Arthritis ◽  
Environmental Factors ◽  
Rheumatoid Factor ◽  
Dna Extraction ◽  
Wrist Joint ◽  
Blood Sampling ◽  
Healthy Controls ◽  
Relationship Of ◽  
Synovial Pannus

Background: Rheumatoid arthritis is a systemic multifactor disease that presented with symmetrical polyarthritis more preferably in small wrist joint and ankle. Synovial pannus cause destruction and deformities in joints. The main reason of this disease in unknown, but past researchesshowed that genetically factor play important role beside environmental factors in susceptibility to this entity. Method:100 patients with rheumatoid arthritis diagnosed upon ACR 2010 criteria enrolled study. 92 healthy patents also enrolled DNA studying. of both group was extracted through DNA extraction kits by blood sampling. HLA-DRB1 typing was done by PCR-SSP method. Results: There were no significant differences in HLADRB1 *04, HLADRB1*08 and HLADRB1*11 alleles presentation between patients and healthy controls. Only there were statically significant correlation between HLA-DRB1*08 and Rheumatoid factor positive patents. (P = 0.025).

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