Modulation of PBMC-decay accelerating factor (PBMC-DAF) and cytokines in rheumatoid arthritis

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• 作者：Roma Pahwa ; Uma Kumar ; Nibhriti Das
• 关键词：Rheumatoid arthritis ; Complement regulatory protein ; Cytokines ; DAF ; Circulating PBMCs ; DAS28
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：414
• 期：1-2
• 页码：85-94
• 全文大小：621 KB
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• 作者单位：Roma Pahwa (1)
  Uma Kumar (2)
  Nibhriti Das (1) (3)
  
  1. Department of Biochemistry, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, 110029, India
  2. Department of Medicine, All India Institute of Medical Sciences, New Delhi, India
  3. Lab Medicine & Biochemistry, Nayati Multi super speciality Hospital, Mathura, 281003, U.P, India
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Biochemistry
  Medical Biochemistry
  Oncology
  Cardiology
  
• 出版者：Springer Netherlands
• ISSN：1573-4919

文摘

Studies have suggested that abnormal expression of complement regulatory proteins and cytokines contribute significantly to the path-physiology of rheumatoid arthritis. In this context, Decay accelerating factor (DAF) a complement regulatory protein is gaining increased attention. With the notion that immune effecter mechanisms are all interlinked and circulating peripheral blood mononuclear cells (PBMCs) should have a role in a systemic disease like rheumatoid arthritis, we studied the modulation and significance of PBMC-DAF and cytokines in RA. Seventy-five RA patients and 75 healthy controls were recruited. Expression of DAF and cytokines (IFN-γ, IL-17A and IL-10) in the PBMCs of patients and controls was determined. Correlations among DAF, cytokines, and disease activity were evaluated by standard statistical methods. The effect of IFN-γ, IL-17A, and IL-10 on the expression of DAF in patients and controls was studied in vitro. Expression of PBMC-DAF declined in patients both at mRNA and surface level and correlated negatively with the disease activity. Expression of IFN-γ also declined in patients but correlated positively with DAF and negatively with disease activity. Expression of IL-17A and IL-10 was higher in patients. The levels correlated positively with disease activity and negatively with DAF both in patients and controls. In vitro studies indicated that IFN-γ up-regulated DAF expression in PBMCs, whereas IL-17A and IL-10 had negative effect on the same. The decline in the PBMC-DAF is a contributing factor in manifestations of RA. Cytokine environment contributes to this decline. These findings brought novel insights into the complement-cytokine axis in the path-physiology of RA.