Expression of CD4+CD25+T Regulatory Cells and Foxp3 in Peripheral Blood of Patients with Rheumatoid Arthritis Patient

2013 ◽  
Vol 709 ◽  
pp. 844-847
Author(s):  
Ke Xin Sun ◽  
Yan Li ◽  
Su Hong Guo ◽  
Yi Ju Hou
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cells ◽  
Peripheral Blood ◽  
T Regulatory Cells ◽  
Blood Monocytes ◽  
Foxp3 Mrna ◽  
Peripheral Blood Monocytes ◽  
Polymerase Chain ◽  
The Relationship ◽  
Normal Controls

To investigate the expression of CD4+CD25+T cells and the Foxp3 in peripheral blood of rheumatoid arthritis（RA），and to analyze the relationship between their activities and patho- genesis.The number of CD4+CD25+T lymphocytes in the peripheral blood and Foxp3 mRNA expression on peripheral blood monocytes of 48 RA patients and 35 normal controls were analyzed by three-color FACs analysis and reverse transcription-polymerase chain reaction（RT- PCR）．The expression of CD4+CD25+T cells RA patients in active group was significantly lower than that in remission group and healthy controls（P0.05）； The relationship between peripheral blood CD4+CD25+Tregcells as well as the Foxp3 mRNA and active renal score was negatively correlated. The expression of CD4+CD25+Tregcells and the Foxp3 mRNA of peripheral blood in RA patients is abnormal and it is correlated with pathogenesis and activity of RA.

scholarly journals Proteinase-activated receptor 2 expression on peripheral blood monocytes and T-cells in patients with rheumatoid arthritis

2016 ◽  
Vol 38 (2) ◽  
pp. 91-98 ◽  
Author(s):  
Samia H. Kandel ◽  
Wafaa M. Radwan ◽  
Heba A. Esaily ◽  
Shimaa F. Al-mahmoudy
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cells ◽  
Peripheral Blood ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes

scholarly journals Enhanced bacterial phagocytosis by peripheral blood monocytes in rheumatoid arthritis.

1984 ◽  
Vol 43 (3) ◽  
pp. 435-439 ◽  
Author(s):  
M M Steven ◽  
S E Lennie ◽  
R D Sturrock ◽  
C G Gemmell
Keyword(s):  
Rheumatoid Arthritis ◽  
Peripheral Blood ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes

scholarly journals Promotion of osteoclastogenesis by IL-26 in rheumatoid arthritis

2019 ◽  
Vol 21 (1) ◽  
Author(s):  
Kyung-Ann Lee ◽  
Kyoung-Woon Kim ◽  
Bo-Mi Kim ◽  
Ji-Yeon Won ◽  
Hong Ki Min ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Peripheral Blood ◽  
Osteoclast Differentiation ◽  
Joint Damage ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tartrate Resistant Acid Phosphatase ◽  
Dependent Manner ◽  
Receptor Subunit ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes

Abstract Background The inflammatory cascade in the rheumatoid arthritis (RA) synovium is modulated by a variety of cytokine and chemokine networks; however, the roles of IL-26, in RA pathogenesis, are poorly defined. Here, we investigated the functional role of interleukin-26 (IL)-26 in osteoclastogenesis in RA. Methods We analyzed levels of IL-20 receptor subunit A (IL-20RA), CD55, and receptor activator of nuclear factor kappaB (NF-κB) ligand (RANKL) in RA fibroblast-like synoviocytes (FLSs) using confocal microscopy. Recombinant human IL-26-induced RANKL expression in RA-FLSs was examined using real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA). Human peripheral blood monocytes were cultured with macrophage colony-stimulating factor (M-CSF) and IL-26, after which osteoclastogenesis was evaluated by counting the number of tartrate-resistant acid phosphatase-positive multinucleated cells. Additionally, osteoclastogenesis was evaluated by monocytes co-cultured with IL-26-prestimulated FLSs. Results The expression of IL-20RA in RA-FLSs was higher than that in osteoarthritis-FLSs. Additionally, in IL-26-pretreated RA-FLSs, the expression of IL-20RA (but not IL-10 receptor subunit B) and RANKL increased in a dose-dependent manner, with IL-26-induced RANKL expression reduced by IL-20RA knockdown. Moreover, IL-26-induced RANKL expression was significantly downregulated by inhibition of signal transducer and activator of transcription 1, mitogen-activated protein kinase, and NF-κB signaling. Furthermore, IL-26 promoted osteoclast differentiation from peripheral blood monocytes in the presence of low dose of RANKL, with IL-26 exerting an additive effect. Furthermore, co-culture of IL-26-pretreated RA-FLSs with peripheral blood monocytes also increased osteoclast differentiation in the absence of addition of RANKL. Conclusions IL-26 regulated osteoclastogenesis in RA through increased RANKL expression in FLSs and direct stimulation of osteoclast differentiation. These results suggest the IL-26/IL-20RA/RANKL axis as a potential therapeutic target for addressing RA-related joint damage.

NF-κB Activation in Peripheral Blood Monocytes/Macrophages and T Cells during Acute Kawasaki Disease

2001 ◽  
Vol 99 (3) ◽  
pp. 373-377 ◽  
Author(s):  
Takashi Ichiyama ◽  
Tomomi Yoshitomi ◽  
Miki Nishikawa ◽  
Motoki Fujiwara ◽  
Tomoyo Matsubara ◽  
...  
Keyword(s):  
T Cells ◽  
Kawasaki Disease ◽  
Peripheral Blood ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
Acute Kawasaki Disease

Abstract 488: Dipeptidyl Peptidase-4 Links Metabolic Regulation With Innate Immune Signaling

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Jixin Zhong ◽  
Xiaoquan Rao ◽  
Steve Oghumu ◽  
Jeffrey Deiuliis ◽  
Abhay Satoskar ◽  
...  
Keyword(s):  
T Cells ◽  
Peripheral Blood ◽  
Immune Cell ◽  
Human Peripheral Blood ◽  
Adaptor Protein ◽  
Dipeptidyl Peptidase ◽  
Oral Glucose ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
Dipeptidyl Peptidase 4

Objective: Dipeptidyl peptidase-4 (DPP4) is well known for its ability to modulate post-prandial blood glucose by inactivation of incretin hormones. DPP4 is highly expressed on innate and adaptive immune cell populations and is recognized to be regulated upon inflammatory activation. We investigated the role of myeloid DPP4 in post-prandial glucose regulation and a role for TLR4-MyD88 in humans and mice. Methods and Results: We evaluated DPP4 expression on circulating immune cells in patients with atherosclerosis (ATH, n=20) and compared them with healthy controls without atherosclerosis using flow cytometry. ATH patients had increased DPP4 expression on peripheral blood monocytes (4.22 ± 0.44 vs. 5.76 ± 0.44, in control vs. ATH, p=0.037) as well as CD4+ T cells (27.46 ± 2.67 vs. 48.06 ± 1.96, control vs. ATH, p<0.0001). More importantly, DPP4 expression on T cells and monocytes correlated with plasma non HDL-Cholesterol level (R2=0.153, p=0.036 and R2=0.244, 0.012 respectively). Stimulation with LPS increased DPP4 expression on human peripheral blood monocytes by ~4-fold. DPP4 up-regulation by LPS was abrogated by Toll-like receptor-4 (TLR4) knockdown using siRNA. Bone marrow monocytes deficient for MyD88, an adaptor protein for TLR signaling, displayed reduced expression of DPP4. Consistent with these findings, MyD88-/- mice also showed improved post-prandial glycemia in response to oral glucose challenge, a phenotype seen in DPP4-/- mice. Conclusions: Our results suggest a previously unrecognized role for TLR4-MyD88 as a critical regulator of DPP4 expression and post-prandial glucose control.

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