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Altogether 28 patients with SSc underwent laboratory and complex vascular assessments before and after six months of 20 mg rosuvastatin treatment. Flow-mediated dilation (FMD) of the brachial artery, as well as carotid artery intima-media thickness (ccIMT), carotid-femoral and aorto-femoral pulse wave-velocity (PWV) were analyzed by ECG-synchronized ultrasound. Ankle-brachial index (ABI) was determined by Doppler, and forearm skin microcirculation was assessed by Laser Doppler perfusion monitoring. Brachial artery FMD significantly improved upon rosuvastatin therapy (2.2% ± 3.3% before versus 5.7% ± 3.9% after treatment, P = 0.0002). With regard to patient subsets, FMD significantly improved in the 21 lcSSc patients (from 2.1% to 5.6%, P = 0.001). In the seven dcSSc patients, we observed a tendency of improvement in FMD (from 3% to 6%, P = 0.25). Changes in PWV, ccIMT and ABI were not significant. Mean triglyceride (1.7 ± 0.97 versus 1.3 ± 0.46 mmol\u002Fl, P = 0.0004), total cholesterol (5.3 ± 1.6 mmol\u002Fl versus 4.2 ± 1.3 mmol\u002Fl, P = 0.0003), low density lipoprotein cholesterol (3.0 ± 1.3 versus 2.2 ± 1.0 mmol\u002Fl, P = 0.005) and C-reactive protein levels (CRP) (5.1 ± 5.2 versus 3.4 ± 2.7, P = 0.01) levels significantly decreased after rosuvastatin treatment. Mean C3, C4 and IC levels also decreased significantly as compared to pretreatment values. Six-month rosuvastatin therapy improves endothelial function and lowers CRP, C3, C4 and IC levels indicating possible favourable effects of this statin on the cardiovascular and immune system in SSc.",{"EN":163,"VI":164},"Rosuvastatin improves impaired endothelial function, lowers high sensitivity CRP, complement and immuncomplex production in patients with systemic sclerosis - a prospective case-series study","Rosuvastatin cải thiện chức năng nội mô bị suy giảm, làm giảm CRP độ nhạy cao, sự sản sinh bổ thể và phức hợp miễn dịch ở bệnh nhân xơ cứng bì hệ thống - một nghiên cứu loạt ca tiến cứu",{"VOID":166},"Czirjak L, Kumanovics G, Varju C, Nagy Z, Pakozdi A, Szekanecz Z, Szucs G: Survival and causes of death in 366 Hungarian patients with systemic sclerosis. Ann Rheum Dis. 2008, 67: 59-63. 10.1136\u002Fard.2006.066340.\nCzirjak L, Nagy Z, Szegedi G: Survival analysis of 118 patients with systemic sclerosis. J Intern Med. 1993, 234: 335-337. 10.1111\u002Fj.1365-2796.1993.tb00753.x.\nArias-Nunez MC, Llorca J, Vazquez-Rodriguez TR, Gomez-Acebo I, Miranda-Filloy JA, Martin J, Gonzalez-Juanatey C, Gonzalez-Gay MA: Systemic sclerosis in northwestern Spain: a 19-year epidemiologic study. Medicine (Baltimore). 2008, 87: 272-280. 10.1097\u002FMD.0b013e318189372f.\nCypiene A, Laucevicius A, Venalis A, Dadoniene J, Ryliskyte L, Petrulioniene Z, Kovaite M, Gintautas J: The impact of systemic sclerosis on arterial wall stiffness parameters and endothelial function. Clin Rheumatol. 2008, 27: 1517-1522. 10.1007\u002Fs10067-008-0958-1.\nSzucs G, Timar O, Szekanecz Z, Der H, Kerekes G, Szamosi S, Shoenfeld Y, Szegedi G, Soltesz P: Endothelial dysfunction precedes atherosclerosis in systemic sclerosis--relevance for prevention of vascular complications. 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Atherosclerosis. 2007, 194: e154-164. 10.1016\u002Fj.atherosclerosis.2006.12.001.\nPeters SA, Palmer MK, Grobbee DE, Crouse JR, O'Leary DH, Raichlen JS, Bots ML: C-reactive protein lowering with rosuvastatin in the METEOR study. J Intern Med. 2010, 268: 155-161. 10.1111\u002Fj.1365-2796.2010.02230.x.\nRidker PM: Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation. 2003, 107: 363-369. 10.1161\u002F01.CIR.0000053730.47739.3C.\nCorrado E, Rizzo M, Coppola G, Fattouch K, Novo G, Marturana I, Ferrara F, Novo S: An update on the role of markers of inflammation in atherosclerosis. J Atheroscler Thromb. 2010, 17: 1-11. 10.5551\u002Fjat.2600.\nHerrick AL, Illingworth K, Blann A, Hay CR, Hollis S, Jayson MI: Von Willebrand factor, thrombomodulin, thromboxane, beta-thromboglobulin and markers of fibrinolysis in primary Raynaud's phenomenon and systemic sclerosis. Ann Rheum Dis. 1996, 55: 122-127. 10.1136\u002Fard.55.2.122.\nChen M, Daha MR, Kallenberg CG: The complement system in systemic autoimmune disease. J Autoimmun. 2010, 34: J276-286. 10.1016\u002Fj.jaut.2009.11.014.",{"VOID":168},"10.1186\u002Far4285","PUBLICATION",[171],"VI","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Far4285",[174,190,205,219,233,249,263,276,289,302,315,328],{"id":175,"sortIndex":19,"researcher":18,"roles":176,"affiliations":178,"properties":187,"displayName":189,"givenName":18,"familyName":18},"5da6971d-5ae3-4a15-98cd-ff49f0647192",[177],"AUTHOR",[179],{"id":180,"sortIndex":19,"affiliation":181,"properties":18},"0975b202-0287-4c0c-a5d7-bbc3dcd477d9",{"id":180,"createTime":18,"updateTime":18,"relativeEntities":182,"slug":18,"properties":183,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":186,"statistic":18},[],{"title":184},{"VI":185},"Departments of Clinical Immunology and Angiology, Institute of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary",[],{"title":188},{"VI":189},"Orsolya Timár",{"id":191,"sortIndex":104,"researcher":18,"roles":192,"affiliations":193,"properties":202,"displayName":204,"givenName":18,"familyName":18},"0934f828-20fc-4757-9e22-7804cd173a48",[177],[194],{"id":195,"sortIndex":19,"affiliation":196,"properties":18},"34d158c4-6268-4e45-b8c6-ad349889b015",{"id":195,"createTime":18,"updateTime":18,"relativeEntities":197,"slug":18,"properties":198,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":201,"statistic":18},[],{"title":199},{"VI":200},"Department of Rheumatology, Institute of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary",[],{"title":203},{"VI":204},"Zoltán 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Improvement was observed in all efficacy endpoints, including ACR20\u002F50\u002F70 scores of 54%, 26% and 8%, respectively, and a reduction in CRP level by greater than 50% for approximately half the population. This improvement was sustainable throughout an extension phase (> 84 weeks) and was also independent of initial DMARD resistance (anti-tumour necrosis factor-alpha and\u002For methotrexate). A relatively high patient withdrawal rate (37%) required the use of last observation carried forward (LOCF) data imputation. Incidence of adverse events was high (95%), although the majority were of mild or moderate severity with a considerable decline in frequency observed after 12 weeks of treatment. Two nonfatal serious adverse events were reported. Dose-response analyses tentatively indicate that an initial dosing level of 6.0 mg\u002Fkg per day administered orally in two daily intakes is the most appropriate, based upon potency and tolerability trends. Treatment with masitinib improved DMARD-refractory active RA. Following an initial high incidence of mostly mild to moderate side effects during the first 12 weeks of treatment, masitinib appears to be generally well tolerated. This, together with evidence of a sustainable efficacy response, suggests that masitinib is suitable for long-term treatment regimens. Since this was the first study of masitinib in a nononcologic pathology, the relatively high patient withdrawal rate observed can be partly attributed to a highly cautious response to adverse events. There is sufficient compelling evidence to warrant further placebo-controlled investigation. 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JM: Rational use of new and existing disease-modifying agents in rheumatoid arthritis. 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Ann Rheum Dis. 2003, 62 (Suppl 2): ii30-ii33.",{"doi":732},{"id":18,"text":2374,"url":2375,"identifiers":2376},"Lee DM, Friend DS, Gurish MF, Benoist C, Mathis D, Brenner MB: Mast cells: a cellular link between autoantibodies and inflammatory arthritis. Science. 2002, 297: 1689-1692. 10.1126\u002Fscience.1073176.","https:\u002F\u002Fdoi.org\u002F10.1126\u002Fscience.1073176",{"mag":2377,"openalex":2378,"pm":2379,"doi":2380},"1982709334","W1982709334","12215644","10.1126\u002Fscience.1073176",{"id":18,"text":2382,"url":2383,"identifiers":2384},"Nigrovic PA, Binstadt BA, Monach PA, Johnsen A, Gurish M, Iwakura Y, Benoist C, Mathis D, Lee DM: Mast cells contribute to initiation of autoantibody-mediated arthritis via IL-1. Proc Natl Acad Sci USA. 2007, 104: 2325-2330. 10.1073\u002Fpnas.0610852103.","https:\u002F\u002Fdoi.org\u002F10.1073\u002Fpnas.0610852103",{"mag":2385,"pmc":2386,"openalex":2387,"pm":2388,"doi":2389},"2110578003","1892913","W2110578003","17277081","10.1073\u002Fpnas.0610852103",{"id":728,"text":2391,"url":730,"identifiers":2392},"Paniagua RT, Sharpe O, Ho PP, Chan SM, Chang A, Higgins JP, Tomooka BH, Thomas FM, Song JJ, Goodman SB, Lee DM, Genovese MC, Utz PJ, Steinman L, Robinson WH: Selective tyrosine kinase inhibition by imatinib mesylate for the treatment of autoimmune arthritis. J Clin Invest. 2006, 116: 2633-2642.",{"doi":732},{"id":18,"text":2394,"url":2395,"identifiers":2396},"Nigrovic PA, Lee DM: Synovial mast cells: role in acute and chronic arthritis. Immunol Rev. 2007, 217: 19-37. 10.1111\u002Fj.1600-065X.2007.00506.x.","https:\u002F\u002Fdoi.org\u002F10.1111\u002Fj.1600-065x.2007.00506.x",{"mag":2397,"openalex":2398,"pm":2399,"doi":2400},"2019554345","W2019554345","17498049","10.1111\u002Fj.1600-065x.2007.00506.x",{"id":18,"text":2402,"url":2403,"identifiers":2404},"Eklund KK: Mast cells in the pathogenesis of rheumatic diseases and as potential targets for anti-rheumatic therapy. Immunol Rev. 2007, 217: 38-52. 10.1111\u002Fj.1600-065X.2007.00504.x.","https:\u002F\u002Fdoi.org\u002F10.1111\u002Fj.1600-065x.2007.00504.x",{"mag":2405,"openalex":2406,"pm":2407,"doi":2408},"2037316274","W2037316274","17498050","10.1111\u002Fj.1600-065x.2007.00504.x",{"id":18,"text":2410,"url":2411,"identifiers":2412},"Juurikivi A, Sandler C, Lindstedt KA, Kovanen PT, Juutilainen T, Leskinen MJ, Mäki T, Eklund KK: Inhibition of c-kit tyrosine kinase by imatinib mesylate induces apoptosis in mast cells in rheumatoid synovia: a potential approach to the treatment of arthritis. Ann Rheum Dis. 2005, 64: 1126-1131. 10.1136\u002Fard.2004.029835.","https:\u002F\u002Fdoi.org\u002F10.1136\u002Fard.2004.029835",{"mag":2413,"pmc":2414,"openalex":2415,"pm":2416,"doi":2417},"2164150729","1755598","W2164150729","16014680","10.1136\u002Fard.2004.029835",{"id":2419,"text":2420,"url":2421,"identifiers":2422},"181ec1be-63cf-43f6-ac3b-0ef8da2a5275","Kobayashi Y, Okunishi H: Mast cells as a target of rheumatoid arthritis treatment. Jpn J Pharmacol. 2002, 90: 7-11. 10.1254\u002Fjjp.90.7.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0021519819300629",{"doi":2423},"10.1254\u002Fjjp.90.7",{"id":728,"text":2425,"url":730,"identifiers":2426},"Ceponis A, Konttinen YT, Takagi M, Xu JW, Sorsa T, Matucci-Cerinic M, Santavirta S, Bankl HC, Valent P: Expression of stem cell factor (SCF) and SCF receptor (c-kit) in synovial membrane in arthritis: correlation with synovial mast cell hyperplasia and inflammation. J Rheumatol. 1998, 25: 2304-2314.",{"doi":732},{"id":2428,"text":2429,"url":2430,"identifiers":2431},"3e9c08e8-be34-484c-965f-7cab6a97a647","Reber L, DaSilva CA, Frossard N: Stem cell factor and its receptor c-Kit as targets for inflammatory diseases. Eur J Pharmacol. 2006, 533: 327-340. 10.1016\u002Fj.ejphar.2005.12.067.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0014299905014007",{"doi":2432},"10.1016\u002Fj.ejphar.2005.12.067",{"id":18,"text":2434,"url":2435,"identifiers":2436},"Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF, Cooper NS, Healey LA, Kaplan SR, Liang MH, Luthra HS, Medsger TA, Mitchell DM, Neustadt DH, Pinals RS, Schaller JG, Sharp JT, Wilder RL, Hunder GG: The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum. 1988, 31: 315-324. 10.1002\u002Fart.1780310302.","https:\u002F\u002Fdoi.org\u002F10.1002\u002Fart.1780310302",{"mag":2437,"openalex":2438,"pm":2439,"doi":2440},"2152348310","W2152348310","3358796","10.1002\u002Fart.1780310302",{"id":18,"text":2442,"url":2443,"identifiers":2444},"Hochberg MC, Chang RW, Dwosh I, Lindsey S, Pincus T, Wolfe F: The American College of Rheumatology 1991 revised criteria for the classification of global functional status in rheumatoid arthritis. Arthritis Rheum. 1992, 35: 498-502. 10.1002\u002Fart.1780350502.","https:\u002F\u002Fdoi.org\u002F10.1002\u002Fart.1780350502",{"mag":2445,"openalex":2446,"pm":2447,"doi":2448},"2081734937","W2081734937","1575785","10.1002\u002Fart.1780350502",{"id":18,"text":2450,"url":2451,"identifiers":2452},"Felson DT, Anderson JJ, Boers M, Bombardier C, Furst D, Goldsmith C, Katz LM, Lightfoot R, Paulus H, Strand V, Tugwell P, Weinblatt M, Williams HJ, Wolfe F, Kieszak S: American College of Rheumatology: preliminary definition of improvement in rheumatoid arthritis. Arthritis Rheum. 1995, 38: 727-735. 10.1002\u002Fart.1780380602.","https:\u002F\u002Fpubmed.ncbi.nlm.nih.gov\u002F9122830",{"mag":2453,"openalex":2454,"pm":2455,"doi":2456},"2401069492","W2401069492","9122830","10.1002\u002Fart.1780380602",{"id":18,"text":2458,"url":2459,"identifiers":2460},"Prevoo MLL, van't Hof MA, Kuper HH, van Leeuwen MA, Putte van de LBA, van Riel PLCM: Modified disease activity scores that include twenty-eight-joint counts. Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum. 1995, 38: 44-48. 10.1002\u002Fart.1780380107.","https:\u002F\u002Fdoi.org\u002F10.1002\u002Fart.1780380107",{"mag":2461,"openalex":2462,"pm":2463,"doi":2464},"2110177517","W2110177517","7818570","10.1002\u002Fart.1780380107",{"id":18,"text":2466,"url":2467,"identifiers":2468},"Siegel JN, Zhen BG: Use of the American College of Rheumatology N (ACR-N) Index of Improvement in Rheumatoid Arthritis: argument in favor. Arthritis Rheum. 2005, 52: 1637-1641. 10.1002\u002Fart.21243.","https:\u002F\u002Fdoi.org\u002F10.1002\u002Fart.21243",{"openalex":2469,"pm":2470,"doi":2471},"W4243377522","15934067","10.1002\u002Fart.21243",{"id":2473,"text":2474,"url":2475,"identifiers":2476},"34897637-fc58-493b-b451-dfac1506d6da","Flendrie M, Vissers WHPM, Creemers MCW, de Jong EMGJ, Kerkhof van de PCM, van Riel PLCM: Dermatological conditions during TNF-α-blocking therapy in patients with rheumatoid arthritis: a prospective study. Arthritis Res Ther. 2005, 7: R666-R676. 10.1186\u002Far1724.","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Far1724",{"doi":2477},"10.1186\u002Far1724",{"id":2479,"text":2480,"url":2481,"identifiers":2482},"17af1e02-6de4-4867-b886-1894c5e9e276","Van Glabbeke M, Verweij J, Casali PG, Simes J, Le Cesne A, Reichardt P, Issels R, Judson IR, van Oosterom AT, Blay JY: Predicting toxicities for patients with advanced gastrointestinal stromal tumours treated with imatinib: a study of the European Organisation for Research and Treatment of Cancer, the Italian Sarcoma Group, and the Australasian Gastro-Intestinal Trials Group (EORTC-ISG-AGITG). Eur J Cancer. 2006, 42: 2277-2285. 10.1016\u002Fj.ejca.2006.03.029.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0959804906005156",{"doi":2483},"10.1016\u002Fj.ejca.2006.03.029",{"id":18,"text":2485,"url":2486,"identifiers":2487},"Kerkela R, Grazette L, Yacobi R, Iliescu C, Patten R, Beahm C, Walters B, Shevtsov S, Pesant S, Clubb FJ, Rosenzweig A, Salomon RN, Van Etten RA, Alroy J, Durand JB, Force T: Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Nat Med. 2006, 12: 908-916. 10.1038\u002Fnm1446.","http:\u002F\u002Fdx.doi.org\u002F10.1016\u002Fs0093-3619(08)70545-8",{"doi":2488},"10.1016\u002Fs0093-3619(08)70545-8",{"id":18,"text":2490,"url":2491,"identifiers":2492},"Fernandez A, Sanguino A, Peng Z, Ozturk E, Chen J, Crespo A, Wulf S, Shavrin A, Qin C, Ma J, Trent J, Lin Y, Han HD, Mangala LS, Bankson JA, Gelovani J, Samarel A, Bornmann W, Sood AK, Lopez-Berestein G: An anticancer C-Kit kinase inhibitor is reengineered to make it more active and less cardiotoxic. J Clin Invest. 2007, 117: 4044-4054. 10.1172\u002FJCI32373.","https:\u002F\u002Fdoi.org\u002F10.1172\u002Fjci32373",{"mag":2493,"pmc":2494,"openalex":2495,"pm":2496,"doi":2497},"2102050170","3812846","W2102050170","18060038","10.1172\u002Fjci32373",{"id":18,"text":2499,"url":1415,"identifiers":2500},"Edwards JC, Szczepanski L, Szechinski J, Filipowicz-Sosnowska A, Emery P, Close DR, Stevens RM, Shaw T: Efficacy of B-cell–targeted therapy with rituximab in patients with rheumatoid arthritis. N Engl J Med. 2004, 350: 2572-2581. 10.1056\u002FNEJMoa032534.",{"mag":1417,"openalex":1418,"pm":1419,"doi":1420},{"id":18,"text":2502,"url":2503,"identifiers":2504},"Kremer JM, Dougados M, Emery P, Durez P, Sibilia J, Shergy W, Steinfeld S, Tindall E, Becker JC, Li T, Nuamah IF, Aranda R, Moreland LW: Treatment of rheumatoid arthritis with the selective costimulation modulator abatacept: twelve-month results of a phase 2b, double-blind, randomized, placebo-controlled trial. Arthritis Rheum. 2005, 52: 2263-2271. 10.1002\u002Fart.21201.","http:\u002F\u002Fdx.doi.org\u002F10.1002\u002Fart.21201",{"doi":2505},"10.1002\u002Fart.21201",{"id":18,"text":2507,"url":2508,"identifiers":2509},"Putte van de LBA, Rau R, Breedveld FC, Kalden JR, Malaise MA, Schattenkirchner M, Emery P, Burmester GR, Zeidler H, Moutsopoulos HM, Beck K, Kupper H: Efficacy and safety of the fully human anti-TNF-α monoclonal antibody, adalimumab (D2E7), in DMARD-refractory patients with rheumatoid arthritis: a 12-week, phase II study. Ann Rheum Dis. 2003, 62: 1168-1177. 10.1136\u002Fard.2003.009563.","http:\u002F\u002Fdx.doi.org\u002F10.1136\u002Fard.2003.009563",{"doi":2510},"10.1136\u002Fard.2003.009563",{"id":18,"text":2512,"url":2513,"identifiers":2514},"Putte van de LBA, Atkins C, Malaise M, Sany J, Russell AS, van Riel PLCM, Settas L, Bijlsma JW, Todesco S, Dougados M, Nash P, Emery P, Walter N, Kaul M, Fischkoff S, Kupper H: Efficacy and safety of adalimumab as monotherapy in patients with rheumatoid arthritis for whom previous disease modifying antirheumatic drug treatment has failed. Ann Rheum Dis. 2004, 63: 508-516. 10.1136\u002Fard.2003.013052.","https:\u002F\u002Fdoi.org\u002F10.1136\u002Fard.2003.013052",{"mag":2515,"pmc":2516,"openalex":2517,"pm":2518,"doi":2519},"2133541603","1755008","W2133541603","15082480","10.1136\u002Fard.2003.013052",{"id":2521,"createTime":2522,"updateTime":2523,"relativeEntities":2524,"slug":2525,"properties":2526,"entityType":169,"verifyStatus":416,"verifyTime":2537,"verifyNote":418,"languages":18,"translateLanguages":18,"viewCount":104,"primaryUrl":2538,"fullTextUrl":18,"authors":2539,"publicationType":341,"publisherRelationship":2735,"citationCount":19,"citationInfo":2790,"publishDate":2793,"publishYear":2791,"citationAnalyzeStatus":1368,"lastCitationAnalyze":2794,"indexDatabases":2795,"openAccess":18,"references":18,"isForceReanalyzing":400},"ccb2819b-d73f-40c0-80e4-584cf04650f5","2024-01-28T02:26:46.981+00:00","2026-07-25T23:44:54.293+00:00",[],"Simultaneous-inhibition-of-JAK-and-SYK-kinases-ameliorates-chronic-and-destructive-arthritis-in-mice",{"abstract":2527,"title":2529,"gsPaper":2531,"references":2533,"doi":2535},{"EN":2528},"Despite the broad spectrum of antirheumatic drugs, RA is still not well controlled in up to 30-50 % of patients. Inhibition of JAK kinases by means of the pan-JAK inhibitor tofacitinib has demonstrated to be effective even in difficult-to-treat patients. Here, we discuss whether the efficacy of JAK inhibition can be improved by simultaneously inhibiting SYK kinase, since both kinases mediate complementary and non-redundant pathways in RA. Efficacy of dual JAK + SYK inhibition with selective small molecule inhibitors was evaluated in chronic G6PI-induced arthritis, a non-self-remitting and destructive arthritis model in mice. Clinical and histopathological scores, as well as cytokine and anti-G6PI antibody production were assessed in both preventive and curative protocols. Potential immunotoxicity was also evaluated in G6PI-induced arthritis and in a 28-day TDAR model, by analysing the effects of JAK + SYK inhibition on hematological parameters, lymphoid organs, leukocyte subsets and cell function. Simultaneous JAK + SYK inhibition completely prevented mice from developing arthritis. This therapeutic strategy was also very effective in ameliorating already established arthritis. Dual kinase inhibition immediately resulted in greatly decreased clinical and histopathological scores and led to disease remission in over 70 % of the animals. In contrast, single JAK inhibition and anti-TNF therapy (etanercept) were able to stop disease progression but not to revert it. Dual kinase inhibition decreased Treg and NK cell counts to the same extent as single JAK inhibition but overall cytotoxicity remained intact. Interestingly, treatment discontinuation rapidly reversed such immune cell reduction without compromising clinical efficacy, suggesting long-lasting curative effects. Dual kinase inhibition reduced the Th1\u002FTh17 cytokine cascade and the differentiation and function of joint cells, in particular osteoclasts and fibroblast-like synoviocytes. Concurrent JAK + SYK inhibition resulted in higher efficacy than single kinase inhibition and TNF blockade in a chronic and severe arthritis model. Thus, blockade of multiple immune signals with dual JAK + SYK inhibition represents a reasonable therapeutic strategy for RA, in particular in patients with inadequate responses to current treatments. Our data supports the multiplicity of events underlying this heterogeneous and complex disease.",{"EN":2530},"Simultaneous inhibition of JAK and SYK kinases ameliorates chronic and destructive arthritis in mice",{"VOID":2532},"[\"7636111619066046011\"]",{"VOID":2534},"Paula FS, Alves JD. Non-tumor necrosis factor-based biologic therapies for rheumatoid arthritis: present, future, and insights into pathogenesis. Biol Targets Therapy. 2014;8:1–12.\nHammaker D, Firestein GS. “Go upstream, young man”: lessons learned from the p38 saga. Ann Rheum Dis. 2010;69:77–82.\nFoster JG, Blunt MD, Carter E, Ward SG. Inhibition of PI3K signaling spurs New therapeutic opportunities in inflammatory\u002Fautoimmune diseases and hematological malignancies. Pharmacol Rev. 2012;64(4):1027–54.\nSmolen JS, Beaulieu A, Rubbert-Roth A, Ramos-Remus C, Rovensky J, Alecock E, et al. Effect of interleukin-6 receptor inhibition with tocilizumab in patients with rheumatoid arthritis (OPTION study): a double-blind, placebo-controlled, randomised trial. Lancet. 2008;371(9617):987–97.\nBaslund B, Tvede N, Danneskiold-Samsoe B, Larsson P, Panayi G, Petersen J, et al. Targeting interleukin-15 in patients with rheumatoid arthritis - a proof-of-concept study. Arthritis Rheum. 2005;52(9):2686–92.\nMilici AJ, Kudlacz EM, Audoly L, Zwillich S, Changelian P. Cartilage preservation by inhibition of Janus kinase 3 in two rodent models of rheumatoid arthritis. Arthritis Res Ther. 2008;10(1):R14. doi: 10.1186\u002Far2365. Epub 2008 Jan 30.\nFridman JS, Scherle PA, Collins R, Burn TC, Li YL, Li J, et al. Selective inhibition of JAK1 and JAK2 is efficacious in rodent models of arthritis: preclinical characterization of INCB028050. J Immunol. 2010;184(9):5298–307.\nvan Vollenhoven RF, Fleischmann R, Cohen S, Lee EB, Garcia Meijide JA, Wagner S, et al. Tofacitinib or adalimumab versus placebo in rheumatoid arthritis. N Engl J Med. 2012;367(6):508–19.\nFleischmann R, Kremer J, Cush J, Schulze-Koops H, Connell CA, Bradley JD, et al. Placebo-controlled trial of tofacitinib monotherapy in rheumatoid arthritis. N Engl J Med. 2012;367(6):495–507.\nvan der Heijde D, Tanaka Y, Fleischmann R, Keystone E, Kremer J, Zerbini C, et al. Tofacitinib (CP-690,550) in patients with rheumatoid arthritis receiving methotrexate: twelve-month data from a twenty-four-month phase III randomized radiographic study. Arthritis Rheum. 2013;65(3):559–70.\nCharles-Schoeman C, Burmester G, Nash P, Zerbini CA, Soma K, Kwok K, et al. Efficacy and safety of tofacitinib following inadequate response to conventional synthetic or biological disease-modifying antirheumatic drugs. Ann Rheum Dis. 2015; doi: 10.1136\u002Fannrheumdis-2014-207178. [Epub ahead of print].\nKremer JM, Bloom BJ, Breedveld FC, Coombs JH, Fletcher MP, Gruben D, et al. The safety and efficacy of a JAK inhibitor in patients with active rheumatoid arthritis results of a double-blind, placebo-controlled phase IIa trial of three dosage levels of CP-690,550 versus placebo. Arthritis Rheum. 2009;60(7):1895–905.\nBurmester GR, Blanco R, Charles-Schoeman C, Wollenhaupt J, Zerbini C, Benda B, et al. Tofacitinib (CP-690,550) in combination with methotrexate in patients with active rheumatoid arthritis with an inadequate response to tumour necrosis factor inhibitors: a randomised phase 3 trial. Lancet. 2013;381(9865):451–60.\nLee EB, Fleischmann R, Hall S, Wilkinson B, Bradley JD, Gruben D, et al. Tofacitinib versus Methotrexate in rheumatoid arthritis. New Engl J Med. 2014;370(25):2377–86.\nBajpai M, Chopra P, Dastidar SG, Ray A. Spleen tyrosine kinase: a novel target for therapeutic intervention of rheumatoid arthritis. Expert Opin Inv Drug. 2008;17(5):641–59.\nSada K, Takano T, Yanagi S, Yamamura H. Structure and function of Syk protein-tyrosine kinase. J Biochem-Tokyo. 2001;130(2):177–86.\nYanagi S, Inatome R, Ding JY, Kitaguchi H, Tybulewicz VLJ, Yamamura H. Syk expression in endothelial cells and their morphologic defects in embryonic Syk-deficient mice. Blood. 2001;98(9):2869–71.\nMocsai A, Humphrey MB, Van Ziffle JAG, Hu YM, Burghardt A, Spusta SC, et al. The immunomodulatory adapter proteins DAP12 and Fc receptor gamma-chain (FcR gamma) regulate development of functional osteoclasts through the Syk tyrosine kinase. Proc Natl Acad Sci U S A. 2004;101(16):6158–63.\nCoffey G, DeGuzman F, Inagaki M, Pak Y, Delaney SM, Ives D, et al. Specific inhibition of spleen tyrosine kinase suppresses leukocyte immune function and inflammation in animal models of rheumatoid arthritis. J Pharmacol Exp Ther. 2012;340(2):350–9.\nSchubert D, Maier B, Morawietz L, Krenn V, Kamradt T. Immunization with glucose-6-phosphate isomerase induces T cell-dependent peripheral polyarthritis in genetically unaltered mice. J Immunol. 2004;172(7):4503–9.\nFrey O, Reichel A, Bonhagen K, Morawietz L, Rauchhaus U, Kamradt T. Regulatory T cells control the transition from acute into chronic inflammation in glucose-6-phosphate isomerase-induced arthritis. Ann Rheum Dis. 2010;69(8):1511–8.\nPettit AR, Ji H, von Stechow D, Muller R, Goldring SR, Choi YW, et al. TRANCE\u002FRANKL knockout mice are protected from bone erosion in a serum transfer model of arthritis. Am J Pathol. 2001;159(5):1689–99.\nYang S, Hollister AM, Orchard EA, Chaudhery SI, Ostanin DV, Lokitz SJ, et al. Quantification of bone changes in a collagen-induced arthritis mouse model by reconstructed three dimensional micro-CT. Biol Proced Online. 2013;15:8. doi: 10.1186\u002F1480-9222-15-8. eCollection 2013.\nSchindelin J, Arganda-Carreras I, Frise E, Kaynig V, Longair M, Pietzsch T, et al. Fiji: an open-source platform for biological-image analysis. Nat Methods. 2012;9(7):676–82.\nDouni E, Rinotas V, Makrinou E, Zwerina J, Penninger JM, Eliopoulos E, et al. A RANKL G278R mutation causing osteopetrosis identifies a functional amino acid essential for trimer assembly in RANKL and TNF. Hum Mol Genet. 2012;21(4):784–98.\nMatsumoto I, Zhang H, Yasukochi T, Iwanami K, Tanaka Y, Inoue A, et al. Therapeutic effects of antibodies to tumor necrosis factor-alpha, interleukin-6 and cytotoxic T-lymphocyte antigen 4 immunoglobulin in mice with glucose-6-phosphate isomerase induced arthritis. Arthritis Res Ther. 2008;10(3):R66. doi: 10.1186\u002Far2437. Epub 2008 Jun 5.\nSaxne T, Palladino MA, Heinegard D, Talal N, Wollheim FA. Detection of tumor necrosis factor-alpha but not tumor necrosis factor-beta in rheumatoid-arthritis synovial-fluid and serum. Arthritis Rheum. 1988;31(8):1041–5.\nZiolkowska N, Koc A, Luszczykiewicz G, Ksiezopolska-Pietrzak K, Klimczak E, Chwalinska-Sadovska H, et al. High levels of IL-17 in rheumatoid arthritis patients: IL-15 triggers in vitro IL-17 production via cyclosporin A-sensitive mechanism. J Immunol. 2000;164(5):2832–8.\nHoyer BF, Mumtaz IM, Yoshida T, Hiepe F, Radbruch A. How to cope with pathogenic long-lived plasma cells in autoimmune diseases. Ann Rheum Dis. 2008;67 Suppl 3:iii87–89.\nGhoreschi K, Jesson MI, Li XO, Lee JL, Ghosh S, Alsup JW, et al. Modulation of innate and adaptive immune responses by tofacitinib (CP-690,550). J Immunol. 2011;186(7):4234–43.\nTownsend RM, Kliwinski C, Kukral D, Postelnek J, Krishnan B, Killar L, et al. Prophylactic administration of abatacept prevents disease induction and bone destruction in a rat model of collagen-induced arthritis. Ann Rheum Dis. 2005;64:439–9.\nZhong JX, Yang P, Muta K, Dong R, Marrero M, Gong FL, et al. Loss of Jak2 selectively suppresses DC-mediated innate immune response and protects mice from lethal dose of LPS-induced septic shock. PLoS One. 2010;5(3):e9593. doi: 10.1371\u002Fjournal.pone.0009593.\nHeine A, Held SAE, Daecke SN, Wallner S, Yajnanarayana SP, Kurts C, et al. The JAK-inhibitor ruxolitinib impairs dendritic cell function in vitro and in vivo. Blood. 2013;122(7):1192–202.\nSallusto F, Lanzavecchia A. Efficient presentation of soluble-antigen by cultured human dendritic cells is maintained by granulocyte-macrophage colony-stimulating factor plus interleukin-4 and down-regulated by tumor-necrosis-factor-alpha. J Exp Med. 1994;179(4):1109–18.\nJakus Z, Simon E, Balazs B, Mocsai A. Genetic Deficiency of Syk Protects Mice From Autoantibody-Induced Arthritis. Arthritis Rheum. 2010;62(7):1899–910.\nLeibundGut-Landmann S, Osorio F, Brown GD, Sousa CRE. Stimulation of dendritic cells via the dectin-1\u002FSyk pathway allows priming of cytotoxic T-cell responses. Blood. 2008;112(13):4971–80.\nWeinblatt ME, Kremer JM, Bankhurst AD, Bulpitt KJ, Fleischmann RM, Fox RI, et al. A trial of etanercept, a recombinant tumor necrosis factor receptor: Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate. New Engl J Med. 1999;340(4):253–9.\nLipsky PE, van der Heijde DMFM, St Clair EW, Furst DE, Breedveld FC, Kalden JR, et al. Infliximab and methotrexate in the treatment of rheumatoid arthritis. New Engl J Med. 2000;343(22):1594–602.\nClair EWS, van der Heijde DMFM, Smolen JS, Maini RN, Bathon JM, Emery P, et al. Combination of infliximab and methotrexate therapy for early rheumatoid arthritis - A randomized, controlled trial. Arthritis Rheum. 2004;50(11):3432–43.\nConklyn M, Andresen C, Changelian P, Kudlacz E. The JAK3 inhibitor CP-690550 selectively reduces NK and CD8 + cell numbers in cynomolgus monkey blood following chronic oral dosing. J Leukocyte Biol. 2004;76(6):1248–55.\nKudlacz E, Perry B, Sawyer P, Conklyn M, McCurdy S, Brissette W, et al. The novel JAK-3 inhibitor CP-690550 is a potent immunosuppressive agent in various murine models. Am J Transplant. 2004;4(1):51–7.\nNosaka T, vanDeursen J, Tripp RA, Thierfelder WE, Witthuhn BA, McMickle AP, et al. Defective lymphoid development in mice lacking Jak3. Blood. 1995;86(10):486–6.\nThomis DC, Gurniak CB, Tivol E, Sharpe AH, Berg LJ. Defects in B-lymphocyte maturation and T-lymphocyte activation in mice lacking Jak3. Science. 1995;270(5237):794–7.\nCao XQ, Shores EW, Huli J, Anver MR, Kelsall BL, Russell SM, et al. Defective lymphoid development in mice lacking expression of the common cytokine receptor-gamma chain. Immunity. 1995;2(3):223–38.\nRanson T, Vosshenrich CAJ, Corcuff E, Richard O, Muller W, Di Santo JP. IL-15 is an essential mediator of peripheral NK-cell homeostasis. Blood. 2003;101(12):4887–93.\nLio CWJQ, Hsieh CS. A two-step process for thymic regulatory T cell development. Immunity. 2008;28(1):100–11.\nBurchill MA, Yang JY, Vang KB, Moon JJ, Chu HH, Lio CWJ, et al. Linked T cell receptor and cytokine signaling govern the development of the regulatory T cell repertoire. Immunity. 2008;28(1):112–21.\nSewgobind VDKD, Quaedackers ME, van der Laan LJW, Kraaijeveld R, Korevaar SS, Chan G, et al. The Jak inhibitor CP-690,550 preserves the function of CD4 + CD25brightFoxP3 + regulatory T cells and inhibits effector T cells. Am J Transplant. 2010;10(8):1785–95.\nRosengren S, Corr M, Firestein GS, Boyle DL. The JAK inhibitor CP-690,550 (tofacitinib) inhibits TNF-induced chemokine expression in fibroblast-like synoviocytes: autocrine role of type I interferon. Ann Rheum Dis. 2012;71(3):440–7.\nKao CY, Chen Y, Thai P, Wachi S, Huang F, Kim C, et al. IL-17 markedly up-regulates beta-defensin-2 expression in human airway epithelium via JAK and NF-kappa B signaling pathways. J Immunol. 2004;173(5):3482–91.\nHuang F, Kao CY, Wachi S, Thai P, Ryu J, Wu R. Requirement for both JAK-Mediated PI3K signaling and ACT1\u002FTRAF6\u002FTAK1-dependent NF-kappa B activation by IL-17A in enhancing cytokine expression in human airway epithelial cells’. J Immunol. 2007;179(10):6504–13.\nLowin T, Straub RH. Integrins and their ligands in rheumatoid arthritis. Arthritis Res Ther. 2011;13(5):244. doi: 10.1186\u002Far3464. Epub 2011 Oct 28.\nPap T, van der Laan WH, Aupperle KR, Gay RE, Verheijen JH, Firestein GS, et al. Modulation of fibroblast-mediated cartilage degradation by articular chondrocytes in rheumatoid arthritis. Arthritis Rheum. 2000;43(11):2531–6.\nLi P, Schwarz EM, O'Keefe RJ, Ma L, Looney RJ, Ritchlin CT, et al. Systemic tumor necrosis factor alpha mediates an increase in peripheral CD11b(high) osteoclast precursors in tumor necrosis factor alpha-transgenic mice. Arthritis Rheum. 2004;50(1):265–76.\nYao ZQ, Li P, Zhang Q, Schwarz EM, Keng P, Arbini A, et al. Tumor necrosis factor-alpha increases circulating osteoclast precursor numbers by promoting their proliferation and differentiation in the bone marrow through up-regulation of c-Fms expression. J Biol Chem. 2006;281(17):11846–55.\nBoyle WJ, Simonet WS, Lacey DL. Osteoclast differentiation and activation. Nature. 2003;423(6937):337–42.\nTeitelbaum SL. The alpha(v)beta(3) integrin mediates osteoclastic bone resorption. J Bone Miner Res. 2000;15(4):819–9.\nTakayanagi H, Iizuka H, Juji T, Nakagawa T, Yamamoto A, Miyazaki T, et al. Involvement of receptor activator of nuclear factor kappa B ligand\u002Fosteoclast differentiation factor in osteoclastogenesis from synoviocytes in rheumatoid arthritis. Arthritis Rheum. 2000;43(2):259–69.\nYeo L, Toellner KM, Salmon M, Filer A, Buckley CD, Raza K, et al. Cytokine mRNA profiling identifies B cells as a major source of RANKL in rheumatoid arthritis. Ann Rheum Dis. 2011;70(11):2022–8.\nHauser AE, Debes GF, Arce S, Cassese G, Hamann A, Radbruch A, et al. Chemotactic responsiveness toward ligands for CXCR3 and CXCR4 is regulated on plasma blasts during the time course of a memory immune response. J Immunol. 2002;169(3):1277–82.\nTokoyoda K, Zehentmeier S, Chang HD, Radbruch A. Organization and maintenance of immunological memory by stroma niches. Eur J Immunol. 2009;39(8):2095–9.\nKondrack RM, Harbertson J, Tan JT, McBreen ME, Surh CD, Bradley LM. Interleukin 7 regulates the survival and generation of memory CD4 cells. J Exp Med. 2003;198(12):1797–806.\nBenson MJ, Dillon SR, Castigli E, Geha RS, Xu SL, Lam KP, et al. Cutting edge: The dependence of plasma cells and independence of memory B cells on BAFF and APRIL. 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