Abstract

Evidences point that complement activation plays a role in rheumatoid arthritis (RA). In this context, expression of the CReg was investigated on white cells from peripheral blood of 30 RA patients and 30 healthy controls. Using flow cytometric analyses the relative fluorescence intensities (MFI) of Cregs were determined. CD59 MFI was significantly increased in RA cells comparing to controls, respectively: lymphocytes 36.8 versus 27.07; monocytes 32.0 versus 21.37; and granulocytes: 84.6 versus 66.1 (p 0.05). Interestingly, no difference was observed on the MFI to CD55, CD46 and CD35 in these cells. These data indicate an overexpression of CD59 in all the peripheral blood cells of RA patients, perhaps due to an increased synthesis for compensatory mechanisms because of complement activation, inflammatory status or other factors associated with the disease.

Highlights

  • Rheumatoid Arthritis (RA) is an autoimmune disease that affects 1% of the adult human population with females affected three times more than males [1]

  • To evaluate the proportion and mean fluorescence intensity (MFI) of CD55, CD59, CD46 and CD35 cells in RA patients and healthy controls, CellQuest software was used and the cells were performed as previous work [12]

  • The CD59 MFI in RA cells was significantly increased compared to controls cells: granulocytes (84.60 vs. 66.10), monocytes (32.00 vs. 21.37) and lymphocytes (36.8 vs. 27.07) (Figure 1)

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Summary

Introduction

Rheumatoid Arthritis (RA) is an autoimmune disease that affects 1% of the adult human population with females affected three times more than males [1]. The complement system, when not regulated, can cause tissue damage This condition can be induced by pro-inflammatory mechanisms, such as cytokines and chemokines. These are usually up-regulated in RA, indicating that these patients are at increased risk to damage mediated by the complement system. Normal cells resist complement-mediated lysis by several mechanisms such as specific membrane-bound proteins. Examples of these are the decay accelerating factor (CD55), the membrane inhibitor of reactive lysis or protectin (CD59), the membrane cofactor protein (CD46) and the complement receptor type I (CD35) [4,5]

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