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001-es BibID:	BIBFORM067428
Első szerző:	Elshabrawy, Hatem A.
Cím:	TLRs, future potential therapeutic targets for RA / Hatem A. Elshabrawy, Abdul E. Essani, Zoltán Szekanecz, David A. Fox, Shiva Shahrara
Dátum:	2017
ISSN:	1568-9972
Megjegyzések:	Toll like receptors (TLR)s have a central role in regulating innate immunity and in the last decade studies have begun to reveal their significance in potentiating autoimmune diseases such as rheumatoid arthritis (RA). Earlier investigations have highlighted the importance of TLR2 and TLR4 function in RA pathogenesis. In this review, we discuss the newer data that indicate roles for TLR5 and TLR7 in RA and its preclinical models. We evaluate the pathogenicity of TLRs in RA myeloid cells, synovial tissue fibroblasts, T cells, osteoclast progenitor cells and endothelial cells. These observations establish that ligation of TLRs can transform RA myeloid cells into M1 macrophages and that the inflammatory factors secreted from M1 and RA synovial tissue fibroblasts participate in TH-17 cell development. From the investigations conducted in RA preclinical models, we conclude that TLR-mediated inflammation can result in osteoclastic bone erosion by interconnecting the myeloid and TH-17 cell response to joint vascularization. In light of emerging unique aspects of TLR function, we summarize the novel approaches that are being tested to impair TLR activation in RA patients.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Rheumatoid arthritis (RA) Toll like receptors (TLR)s Inflammation Bone erosion M1 macrophages TH-17 cells
Megjelenés:	Autoimmunity Reviews 16 : 2 (2017), p. 103-113. -
További szerzők:	Essani, Abdul E. Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Fox, David A. Shahrara, Shiva
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM074059
Első szerző:	Van Raemdonck, Katrien
Cím:	Impact of obesity on autoimmune arthritis and its cardiovascular complications / Katrien Van Raemdonck, Sadiq Umar, Zoltán Szekanecz, Ryan K. Zomorrodi, Shiva Shahrara
Dátum:	2018
ISSN:	1568-9972
Megjegyzések:	Obesity can instigate and sustain a systemic low-grade inflammatory environment that can amplify autoimmunedisorders and their associated comorbidities. Metabolic changes and inflammatory factors produced by theadipose tissue have been reported to aggravate autoimmunity and predispose the patient to cardiovasculardisease (CVD) and metabolic comorbidities. Rheumatoid arthritis (RA) and psoriatic arthritis (PsA) are autoimmunearthritic diseases, often linked with altered body mass index (BMI). Severe joint inflammation and bonedestruction have a debilitating impact on the patient's life; there is also a staggering risk of cardiovascularmorbidity and mortality. Furthermore, these patients are at risk of developing metabolic symptoms, includinginsulin resistance resulting in type 2 diabetes mellitus (T2DM). In addition, arthritis severity, progression andresponse to therapy can be markedly affected by the patient's BMI. Hence, a complex integrative pathogenesisinterconnects autoimmunity with metabolic and cardiovascular disorders. This review aims to shed light on thenetwork that connects obesity with RA, PsA, systemic lupus erythematosus and Sj?gren's syndrome. We havefocused on clarifying the mechanism by which obesity affects different cell types, inflammatory factors andtraditional therapies in these autoimmune disorders. We conclude that to further optimize arthritis therapy andto prevent CVD, it is imperative to uncover the intricate relation between obesity and arthritis pathology.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Obesity Metabolic syndrome Cardiovascular disease Inflammation RA PsA
Megjelenés:	Autoimmunity Reviews. - 17 : 8 (2018), p. 821-835. -
További szerzők:	Umar, Sadiq Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Zomorrodi, Ryan K. Shahrara, Shiva
Pályázati támogatás:	TAMOP-4.2.4.A/2-11/1-2012-0001 TÁMOP GINOP-2.3.2-15-2016-00050 GINOP GINOP-2.3.2-15-2016-00015 GINOP
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