Decreased Gene Expression of Epstein-Barr Virus-Induced Gene 3 (EBI-3) may Contribute to the Pathogenesis of Rheumatoid Arthritis.


Journal

Immunological investigations
ISSN: 1532-4311
Titre abrégé: Immunol Invest
Pays: England
ID NLM: 8504629

Informations de publication

Date de publication:
May 2019
Historique:
pubmed: 5 12 2018
medline: 21 8 2019
entrez: 5 12 2018
Statut: ppublish

Résumé

Interleukin-35 (IL-35) is a member of the IL-12 family of heterodimeric cytokines produced by regulatory T (Treg) cells. This immunosuppressive cytokine can prevent exaggerated inflammatory responses like those responsible for the development of rheumatoid arthritis (RA). This study aims to determine the correlation between the gene expression of Epstein-Barr virus-induced gene 3 (EBI-3) and IL-12A (p35) subunits of IL-35 in peripheral blood leukocytes with immunological and clinical parameters in RA patients. We recruited 47 patients with RA and 44 healthy subjects. The disease activity score-28 (DAS-28) was assessed by an expert rheumatologist and the plasma levels of neopterin and anti-cyclic citrullinated peptide (anti-CCP) was measured using ELISA method also Serum rheumatoid factor (RF) was assessed by the agglutination test. For the evaluation of IL-12A and EBI-3 gene expression, we used qPCR. We did not find any significant correlation between the gene expression of IL-35 subunits and DAS-28. There was a negative correlation between the plasma levels of neopterin and the gene expression of EBI-3 (p = 0.004). Inversely, we found a positive correlation between plasma level of anti-CCP and neopterin (p < 0.001) also between RF and DAS-28 (p = 0.001). Regarding the significant negative correlation between EBI-3 gene expression and plasma levels of neopterin, it can be concluded that the altered gene expression of EBI-3 may play a role in the pathogenesis of RA.

Sections du résumé

BACKGROUND BACKGROUND
Interleukin-35 (IL-35) is a member of the IL-12 family of heterodimeric cytokines produced by regulatory T (Treg) cells. This immunosuppressive cytokine can prevent exaggerated inflammatory responses like those responsible for the development of rheumatoid arthritis (RA). This study aims to determine the correlation between the gene expression of Epstein-Barr virus-induced gene 3 (EBI-3) and IL-12A (p35) subunits of IL-35 in peripheral blood leukocytes with immunological and clinical parameters in RA patients.
METHODS METHODS
We recruited 47 patients with RA and 44 healthy subjects. The disease activity score-28 (DAS-28) was assessed by an expert rheumatologist and the plasma levels of neopterin and anti-cyclic citrullinated peptide (anti-CCP) was measured using ELISA method also Serum rheumatoid factor (RF) was assessed by the agglutination test. For the evaluation of IL-12A and EBI-3 gene expression, we used qPCR.
RESULTS RESULTS
We did not find any significant correlation between the gene expression of IL-35 subunits and DAS-28. There was a negative correlation between the plasma levels of neopterin and the gene expression of EBI-3 (p = 0.004). Inversely, we found a positive correlation between plasma level of anti-CCP and neopterin (p < 0.001) also between RF and DAS-28 (p = 0.001).
CONCLUSION CONCLUSIONS
Regarding the significant negative correlation between EBI-3 gene expression and plasma levels of neopterin, it can be concluded that the altered gene expression of EBI-3 may play a role in the pathogenesis of RA.

Identifiants

pubmed: 30513021
doi: 10.1080/08820139.2018.1549066
doi:

Substances chimiques

Anti-Citrullinated Protein Antibodies 0
EBI3 protein, human 0
IL12A protein, human 0
Interleukin-12 Subunit p35 0
Interleukins 0
Minor Histocompatibility Antigens 0
Neopterin 670-65-5
Rheumatoid Factor 9009-79-4

Types de publication

Journal Article

Langues

eng

Pagination

367-377

Auteurs

Nasrin Iranshahi (N)

a Department of Immunology , Kermanshah University of Medical Sciences , Kermanshah , Iran.

Shirin Assar (S)

b Rheumatology in Clinical Research Development Center, Imam Reza Hospital , Kermanshah University of Medical Sciences , Kermanshah , Iran.

Seyed Mojtaba Amiri (SM)

c Department of Biostatistics and Epidemiology, School of Health , Kermanshah University of Medical Sciences , Kermanshah , Iran.

Parisa Zafari (P)

d Department of Immunology , Mazandaran University of Medical Sciences , Sari , Iran.

Adel Fekri (A)

a Department of Immunology , Kermanshah University of Medical Sciences , Kermanshah , Iran.

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Classifications MeSH