Angiogenic T cells are decreased in rheumatoid arthritis patients

Rodríguez‐Carrio, Javier; Alperi-López, Mercedes; López, Patricia; Alonso-Castro, Sara; Ballina-García, Francisco Javier

doi:10.1136/annrheumdis-2013-204250

Cited by 43 publications

(53 citation statements)

References 44 publications

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“…Moreover, our research revealed a DAS28-dependent Tang-MP shedding, thus linking DAS28 with impaired endothelial repair. Actually, the disease parameters positively associated with Tang-MP in this work were the same as has been found negatively associated with Tang frequency [21]. Consequently, Tang-MPs could be considered as a surrogate biomarker of endothelial damage and vascular repair failure.…”

Section: Discussionsupporting

confidence: 59%

“…Although no differences in the frequency of MPs derived from T-lymphocytes were detected, both frequency and absolute number of Tang-MPs were increased in RA patients. Interestingly, this increased Tang-MP formation could account for the decreased Tang cell counts previously reported in RA [21]. Moreover, our research revealed a DAS28-dependent Tang-MP shedding, thus linking DAS28 with impaired endothelial repair.…”

Section: Discussionmentioning

confidence: 50%

“…In addition, since we have recently proposed a role for angiogenic T-cells (Tang) in RA [21], we aimed to evaluate whether Tang-derived MPs can be found and if associations with clinical parameters could provide new insights on this T-cell subset. Finally, in vitro studies were performed to estimate the potential deleterious effect of RA-MPs on vascular endothelium.…”

Section: Introductionmentioning

confidence: 99%

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Altered profile of circulating microparticles in rheumatoid arthritis patients

et al. 2014

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Microparticles (MPs) could be considered biomarkers of cell damage and activation as well as novel signalling structures. Since rheumatoid arthritis (RA) is characterized by immune and endothelial activation, the main aim of the present study was to analyse MP counts in RA patients. Citrated-blood samples were obtained from 114 RA patients, 33 healthy controls (HC) and 72 individuals with marked cardiovascular (CV) risk without autoimmune manifestations (CVR). MPs were analysed in platelet-poor plasma (PPP) and different subsets were identified by their surface markers: platelet-(CD41 + ), endothelial-(CD146 + ), granulocyte-(CD66 + ), monocyte-(CD14 + ) and Tang-derived (CD3 + CD31 + ). Disease activity (DAS28), clinical and immunological parameters as well as traditional CV risk factors (diabetes, hypertension, dyslipidemia and obesity) were registered from clinical records and all data were integrated using Principal Component Analysis (PCA). Absolute MP number was increased in RA patients compared with HC and positively correlated with traditional CV risk factors, similar to that of CVR subjects. In addition, frequency of the different MP subsets was different in RA patients and significantly associated to disease features. Moreover, in vitro assays revealed that MPs isolated from RA patients were able to promote endothelial activation and exhibited detrimental effects on HMEC-I endothelial cell functionality. Circulating MPs from RA Q1 patients displayed quantitative and qualitative alterations that are the result of both disease-specific and traditional CV risk factors. Accordingly, this MP pool exhibited in vitro detrimental effects on endothelial cells, thus supporting their role as biomarkers of vascular damage.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 50%

Section: Introductionmentioning

confidence: 99%

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Altered profile of circulating microparticles in rheumatoid arthritis patients

et al. 2014

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“…Critical to endothelial function, repair, and neovascularization are endothelial progenitor cells (EPCs) and recently identified angiogenic T cells (T ang ). Relative to controls, EPCs and T ang are reduced in rheumatoid arthritis, with the lowest T ang counts noted among patients with comorbid cardiovascular disease 4748. Their connection to rheumatoid arthritis is further established through inverse associations with disease activity and improved EPC counts after treatment with TNF inhibitors 4748…”

Section: Mechanisms Linking Rheumatoid Arthritis and Cardiovascular Dmentioning

confidence: 99%

Increased cardiovascular risk in rheumatoid arthritis: mechanisms and implications

England

Thiele

Anderson

et al. 2018

BMJ

373

266

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Rheumatoid arthritis is a systemic autoimmune disease characterized by excess morbidity and mortality from cardiovascular disease. Mechanisms linking rheumatoid arthritis and cardiovascular disease include shared inflammatory mediators, post-translational modifications of peptides/proteins and subsequent immune responses, alterations in the composition and function of lipoproteins, increased oxidative stress, and endothelial dysfunction. Despite a growing understanding of these mechanisms and their complex interplay with conventional cardiovascular risk factors, optimal approaches of risk stratification, prevention, and treatment in the context of rheumatoid arthritis remain unknown. A multifaceted approach to reduce the burden posed by cardiovascular disease requires optimal management of traditional risk factors in addition to those intrinsic to rheumatoid arthritis such as increased disease activity. Treatments for rheumatoid arthritis seem to exert differential effects on cardiovascular risk as well as the mechanisms linking these conditions. More research is needed to establish whether preferential rheumatoid arthritis therapies exist in terms of prevention of cardiovascular disease. Ultimately, understanding the unique mechanisms for cardiovascular disease in rheumatoid arthritis will aid in risk stratification and the identification of novel targets for meaningful reduction of cardiovascular risk in this patient population.

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“…This observation is consistent with the hypothesis of an ANA-positive drug resistant RA phenotype. Further proof is brought by Rodriguez-Carrio et al (20), who observed that ANA positivity is associated with a lower count of angiogenic T cells, which are involved in endothelial repair, knowing that TNF-α blockers and rituximab are associated with an improvement on endothelial function (21,22). There is evidence of methotrexate resistance associated with ANA positivity (23) and therefore bDMARDs resistance associated with ANA positivity is plausible, but since they have different mechanisms of action, a prospective comparative study would provide further information.…”

Section: Discussionmentioning

confidence: 99%