コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 for the most effective and safe treatment of inflammatory arthritis.
2 ndow into early events in the development of inflammatory arthritis.
3 es inflammation and prevents joint damage in inflammatory arthritis.
4 itivity analysis that excludes patients with inflammatory arthritis.
5 and higher disease activity in patients with inflammatory arthritis.
6 esults in a STING-dependent, TLR-independent inflammatory arthritis.
7 an be targeted to prevent the development of inflammatory arthritis.
8 event disease in a mouse model of autoimmune inflammatory arthritis.
9 pathway to dissect and eventually target in inflammatory arthritis.
10 tic monitoring of synovitis in patients with inflammatory arthritis.
11 ntermediate may diminish bone destruction in inflammatory arthritis.
12 n limiting joint and gut inflammation during inflammatory arthritis.
13 fer system, focused on the effector phase of inflammatory arthritis.
14 ining of joints that become activated during inflammatory arthritis.
15 iomarker of disease progression in mice with inflammatory arthritis.
16 sponse, one that is particularly relevant to inflammatory arthritis.
17 isease mechanisms operating in patients with inflammatory arthritis.
18 enhances bone damage and disease severity in inflammatory arthritis.
19 Gout is the most common type of inflammatory arthritis.
20 1alpha is a potential therapeutic target for inflammatory arthritis.
21 s and the periarticular osteolysis attending inflammatory arthritis.
22 a ubiquitously expressed self-Ag and induce inflammatory arthritis.
23 st time, that IL-22 has a protective role in inflammatory arthritis.
24 uring acute joint inflammation in a model of inflammatory arthritis.
25 te immune cells and osteoclasts (OCs) during inflammatory arthritis.
26 r virulence mechanism during early stages of inflammatory arthritis.
27 sfer of OCP with SKG CD4+ T cells diminished inflammatory arthritis.
28 ell-suppressive activity that is expanded in inflammatory arthritis.
29 may show promise as a therapeutic target in inflammatory arthritis.
30 roscopy may be indicative of the presence of inflammatory arthritis.
31 ne collagen-induced arthritis (CIA) model of inflammatory arthritis.
32 flammatory cytokines and induced an erosive, inflammatory arthritis.
33 apeutic agent for targeting PBEF activity in inflammatory arthritis.
34 t of complement during the effector phase of inflammatory arthritis.
35 thritis, and administration of PGRN reversed inflammatory arthritis.
36 f these patients had RA, and 13 did not have inflammatory arthritis.
37 processes, necessary for the development of inflammatory arthritis.
38 ages in a subset of patients with TNF-driven inflammatory arthritis.
39 of p21-mediated suppression of experimental inflammatory arthritis.
40 mutant mice compared to wild-type mice with inflammatory arthritis.
41 gs, depletion of platelets attenuated murine inflammatory arthritis.
42 sm in K/BxN serum-induced arthritis to drive inflammatory arthritis.
43 urately differentiate it from other forms of inflammatory arthritis.
44 odels of allograft rejection and destructive inflammatory arthritis.
45 , and is an attractive therapeutic target in inflammatory arthritis.
46 n in vivo model of TNF-alpha-induced chronic inflammatory arthritis.
47 rties and prevent bone erosions in models of inflammatory arthritis.
48 via enhancing innate cellular activation in inflammatory arthritis.
49 TNFalpha, and TNFRI PLAD (p60 PLAD) inhibits inflammatory arthritis.
50 s compared with CE guidance in patients with inflammatory arthritis.
51 e in the destruction of bone associated with inflammatory arthritis.
52 activation for the treatment of experimental inflammatory arthritis.
53 ents may represent an effective way to treat inflammatory arthritis.
54 ated virus (AAV) type 2 delivery system, for inflammatory arthritis.
55 ight be an alternative therapeutic target in inflammatory arthritis.
56 ial structural damage in these rat models of inflammatory arthritis.
57 g cells, are involved in the pathogenesis of inflammatory arthritis.
58 s was induced using the K/BxN mouse model of inflammatory arthritis.
59 igand-targeted nanotherapy, would ameliorate inflammatory arthritis.
60 uence the topography of erosion formation in inflammatory arthritis.
61 nsgenic mice were used as a model of chronic inflammatory arthritis.
62 matory in a murine model of antibody-induced inflammatory arthritis.
63 and exerts tissue-protective actions during inflammatory arthritis.
64 unexpected proinflammatory role of IL-33 in inflammatory arthritis.
65 rom antimicrobial defense to anaphylaxis and inflammatory arthritis.
66 otent imaging modality for the assessment of inflammatory arthritis.
67 expression of citrullinated autoantigens in inflammatory arthritis.
68 ynthesized via COX-1, in particular PGI2, to inflammatory arthritis.
69 ssion differed between RA and other forms of inflammatory arthritis.
70 RA patients or patients with other forms of inflammatory arthritis.
71 duction and exacerbation of autoimmunity and inflammatory arthritis.
72 s potential as a novel therapeutic target in inflammatory arthritis.
73 action to inflammation, and are resistant to inflammatory arthritis.
74 RA patients or patients with other forms of inflammatory arthritis.
75 lammatory and destructive tissue response in inflammatory arthritis.
76 sed to assess the natural history of erosive inflammatory arthritis.
77 /- 15.7 years, 10 male) anti-TNF therapy for inflammatory arthritis.
78 vitamin D plays an immunomodulatory role in inflammatory arthritis.
79 ial function for T-bet in DCs in controlling inflammatory arthritis.
80 ells produce GM-CSF in autoantibody-mediated inflammatory arthritis.
81 or the development of novel therapeutics for inflammatory arthritis.
82 duction, yet is not effective in suppressing inflammatory arthritis.
83 t into the joint in the K/BxN mouse model of inflammatory arthritis.
84 of apoptotic regulators in a mouse model of inflammatory arthritis.
85 nd exacerbation of joint inflammation during inflammatory arthritis.
86 ic efficacy and safety for the management of inflammatory arthritis.
87 hway underlies inflammation and pathology in inflammatory arthritis.
88 hown therapeutic efficacy in mouse models of inflammatory arthritis.
89 RA), we evaluated the role of PON1 in murine inflammatory arthritis.
90 o promote healthy behaviour in patients with inflammatory arthritis.
91 we hypothesized that ELMO1 loss would worsen inflammatory arthritis.
92 reduces disease severity in a mouse model of inflammatory arthritis.
93 ing anti-TNF therapy known to resolve TNF-Tg inflammatory arthritis.
94 gulator of tissue damage in a mouse model of inflammatory arthritis.
95 recruitment and are protected in 2 models of inflammatory arthritis.
96 rs for diagnosis and treatment evaluation of inflammatory arthritis.
97 t actions of atorvastatin and pravastatin in inflammatory arthritis.
98 N protected cartilage integrity in mice with inflammatory arthritis.
99 tients with new-onset and chronic autoimmune inflammatory arthritis.
100 progranulin in regulatory T cells restrains inflammatory arthritis.
101 ding inflammatory bowel disease, sepsis, and inflammatory arthritis.
102 e B4 (LTB4) in myeloid cells, which modulate inflammatory arthritis.
103 itions and autoimmune diseases, particularly inflammatory arthritis.
104 y provide an effective cell-free therapy for inflammatory arthritis.
105 ndidate for the treatment of bone erosion in inflammatory arthritis.
106 ion of endogenous SPMs during self-resolving inflammatory arthritis.
107 arthritis when compared with self-resolving inflammatory arthritis.
108 The circadian clock regulates inflammatory arthritis.
109 Unc5b are novel targets for the treatment of inflammatory arthritis.
110 useful therapeutic targets for treatment of inflammatory arthritis.
111 esent in the synovial fluid of patients with inflammatory arthritis.
112 d to predict transition from autoimmunity to inflammatory arthritis.
113 ced CXCL1, and it attenuated the severity of inflammatory arthritis.
114 e IL-27 receptor (IL-27R) after the onset of inflammatory arthritis.
115 and 12-LO in an in vivo model of autoimmune inflammatory arthritis.
116 were observed in IL-27R-deficient mice with inflammatory arthritis.
117 t against the induction of murine autoimmune inflammatory arthritis.
118 nated action of sPLA2-IIA and 12-LO promotes inflammatory arthritis.
119 for the stimulation of osteoclastogenesis in inflammatory arthritis.
120 ve colitis (12 203), Crohn's disease (7628), inflammatory arthritis (27 358), systemic autoimmune dis
121 and 111 control patients with other forms of inflammatory arthritis (82 with rheumatoid arthritis, 13
122 e markedly increased in SHIP1(-/-) mice with inflammatory arthritis, a condition characterized by inc
123 Ankylosing spondylitis (AS) is a chronic inflammatory arthritis affecting the spine in young adul
124 ion of this drug in the K/BxN mouse model of inflammatory arthritis after first crossing in a human C
125 n 100 genotyped and phenotyped patients with inflammatory arthritis, all of whom were naive to immuno
127 degraded DNA leads to both a STING-dependent inflammatory arthritis and additional Unc93b1-dependent
128 ic (TNF-Tg) murine model of RA develops both inflammatory arthritis and an ILD that mimics a cellular
130 asts are essential cells for bone erosion in inflammatory arthritis and are derived from cells in the
131 on in autoantibody-positive subjects without inflammatory arthritis and are similar to airways abnorm
132 prozumab, a humanized anti-HSP mAb in murine inflammatory arthritis and colitis, and its effects on c
133 iagnostic uncertainty in patients with early inflammatory arthritis and concerns about treatment of p
134 ut-associated as well as systemic, including inflammatory arthritis and experimental autoimmune encep
135 , we examined the effects of chronic erosive inflammatory arthritis and GC treatment on bone quality,
136 eloid-expressed TACE play a critical role in inflammatory arthritis and indicate that iRHOM2 is a pot
137 characterized by high-titer autoantibodies, inflammatory arthritis and interstitial lung disease.
139 cute inflammation, including antigen-induced inflammatory arthritis and lung injury, both involving a
141 e that CX(3) CR1 deficiency is protective in inflammatory arthritis and may have effects that extend
145 the target autoantigen in the K/BxN model of inflammatory arthritis and perhaps in some humans with a
146 loss in TNF-induced inflammatory osteolysis, inflammatory arthritis and post-ovariectomy models.
148 ate immune receptors for dsRNA in modulating inflammatory arthritis and provide additional support fo
149 articipate in the pathogenesis of autoimmune inflammatory arthritis and provide insights of potential
150 tic rats with celastrus/celastrol suppressed inflammatory arthritis and reduced bone and cartilage da
151 sents a severe pathological phenotype during inflammatory arthritis and results in joint pain and bon
152 NLRP3 inflammasome activation contributes to inflammatory arthritis and systemic inflammation not onl
153 ulate inflammation in disease states such as inflammatory arthritis and systemic lupus erythematosus.
154 aluated in the K/BxN serum transfer model of inflammatory arthritis, and clinical signs of arthritis,
155 f RA, psoriatic arthritis and other forms of inflammatory arthritis, and it enhances the effect of mo
156 ption occurs in postmenopausal osteoporosis, inflammatory arthritis, and metastasis of tumors to bone
157 on of the IRE1alpha gene protected mice from inflammatory arthritis, and treatment with the IRE1alpha
158 , however, do not suggest that patients with inflammatory arthritis are at increased risk of COVID-19
160 ed and sustained development of experimental inflammatory arthritis, associated with markedly increas
161 Mc(3)(-/-) mice displayed an exacerbated inflammatory arthritis, associated with prominent bone e
164 in limiting GM-CSF signaling not only during inflammatory arthritis but also in experimental allergic
165 matory responses in chronic lung disease and inflammatory arthritis but has not been investigated in
167 ses) were compared with 3 control groups: 1) inflammatory arthritis but not Lyme disease vaccine (art
169 with rheumatoid arthritis and other forms of inflammatory arthritis, but not in joint fluid from pati
170 -6 (IL-6) contributes to the pathogenesis of inflammatory arthritis, but the role, if any, of epigene
171 tibodies contribute to joint inflammation in inflammatory arthritis by triggering cellular fragment c
172 substantial morbidity and increased rates of inflammatory arthritis, cardiometabolic diseases, and me
174 Gout is one of the most common types of inflammatory arthritis, caused by the deposition of mono
175 By 2-4 weeks, these mice developed symmetric inflammatory arthritis, characterized by tissue swelling
176 ssociated with calcium pyrophosphate crystal inflammatory arthritis (chondrocalcinosis) and that SBS
178 body-positive subjects with airways disease, inflammatory arthritis classifiable as articular RA deve
180 the Pgia8 locus regulates antibody-mediated inflammatory arthritis differently in males and females.
181 its a strong association with the autoimmune inflammatory arthritis disorder ankylosing spondylitis (
182 We demonstrate that mice undergoing chronic inflammatory arthritis displayed osteoporosis resulting
183 can affect periodontal disease, presence of inflammatory arthritis does not appear to be one of them
184 This clock drives rhythmic repression of inflammatory arthritis during the night in mice, but mec
185 h17/1 cells from the joints of children with inflammatory arthritis express high levels of both Th17
187 19 constitutes a challenge for patients with inflammatory arthritis for several reasons, in particula
188 ndylitis (AS) is a common, highly heritable, inflammatory arthritis for which HLA-B*27 is the major g
189 ved clinical outcomes for many patients with inflammatory arthritis; for others, however, these agent
190 anti-rheumatic drug (DMARD) treatment in the inflammatory arthritis groups (i.e. RA and UA) and confi
193 Furthermore, studies using animal models of inflammatory arthritis have demonstrated critical roles
194 rding the role of chlamydiae in induction of inflammatory arthritis have increased our detailed under
197 trol MC-dependent diseases including asthma, inflammatory arthritis, heart disease, and multiple scle
198 ains inflammation and is therapeutic against inflammatory arthritis; however, the underlying immunolo
199 nts who will subsequently develop persistent inflammatory arthritis (i.e. RA and UA) from those with
211 g, inflammatory responses, and inhibition of inflammatory arthritis in the K/BxN serum transfer model
212 DNs strongly inhibited the effector phase of inflammatory arthritis in the K/BxN serum transfer syste
214 to the spontaneous development of autoimmune inflammatory arthritis in transgenic mice containing CD4
215 s of C5orf30 contributes to the pathology of inflammatory arthritis in vivo, because inhibition of C5
216 applied to individuals with undifferentiated inflammatory arthritis in whom at least 1 joint is deeme
217 er disease onset ameliorated the severity of inflammatory arthritis including arthritis indices, paw
218 K and provides follow-up care to people with inflammatory arthritis including treatment, monitoring,
219 a possible trigger for some forms of chronic inflammatory arthritis, including spondyloarthritis and
220 biome-based precision medicine approaches in inflammatory arthritis, including strategies for predict
221 hance C3 activation, is necessary to mediate inflammatory arthritis induced by adherent immune comple
222 products is necessary for resolution of the inflammatory arthritis induced by Borrelia infection, an
223 D/TNF mice that develop amyloid deposits and inflammatory arthritis induced by human TNF-alpha (huTNF
229 oanatomic basis for formation of erosions in inflammatory arthritis is incompletely understood but is
232 can-3 regulates MSC adhesion and efficacy in inflammatory arthritis, likely via induction of the AKT
233 rheumatoid arthritis (RA) and other forms of inflammatory arthritis, low-dose methotrexate therapy re
234 Loss of iRHOM2 largely protects mice from inflammatory arthritis, making iRHOM2 a potential drug t
235 mmatory bowel disease (IBD), sarcoidosis and inflammatory arthritis, making pharmacologic inhibition
236 the biological clock and pathways underlying inflammatory arthritis, mice were administered collagen
237 cy of CX(3) CR1 is protective in the chronic inflammatory arthritis model collagen-induced arthritis
238 In experiments using the K/BxN serum-induced inflammatory arthritis model, CXCR6(-/-) mice showed pro
244 patients with osteoarthritis or seronegative inflammatory arthritis, neither of which exhibited signi
245 In a mouse model of autoantibody-induced inflammatory arthritis, neutrophils infiltrate the joint
247 aRIII contributes to the pain resulting from inflammatory arthritis of the TMJ, and siRNA has the pot
248 unctional and histologic improvements in the inflammatory arthritis of TTP(-/-) mice when CCL3 was ab
249 itis (PsA) is a debilitating immune-mediated inflammatory arthritis of unknown pathogenesis commonly
250 with those from patients with other forms of inflammatory arthritis or compared with control macropha
251 m the joints of patients with other forms of inflammatory arthritis or with control macrophages.
252 cells, an effect that has been implicated in inflammatory arthritis, osteoporosis, obesity, and myopa
253 n age, 45 years) with untreated recent-onset inflammatory arthritis participated in this prospective
254 Ankylosing spondylitis is a common form of inflammatory arthritis predominantly affecting the spine
255 f major joint replacement, terminal illness, inflammatory arthritis, prosthetic leg, cognitive impair
256 ve for chronic calcium pyrophosphate crystal inflammatory arthritis (pseudogout, chondrocalcinosis).M
257 fore or after inducing the adjuvant model of inflammatory arthritis reduced chondrocyte apoptosis, pr
258 ances, a substantial number of patients with inflammatory arthritis remain resistant to current thera
260 -Flip-KO mice spontaneously develop erosive, inflammatory arthritis, resembling rheumatoid arthritis,
261 ) CL1) and has been shown to be important in inflammatory arthritis responses, largely due to its eff
262 ribute to the pathogenesis of three types of inflammatory arthritis: rheumatoid arthritis, spondyloar
265 ase activity and disability in patients with inflammatory arthritis such as rheumatoid arthritis.
266 fficult to differentiate from other forms of inflammatory arthritis such as spondyloarthritis and rhe
267 risk factor for cardiovascular diseases and inflammatory arthritis, such as hypertension and gout.
268 ne loss in many skeletal diseases, including inflammatory arthritis, such as rheumatoid arthritis (RA
272 r matrix of their articular cartilage during inflammatory arthritis than wild-type (WT) C57BL/6 mice,
273 rthritis (PsA), a condition characterized by inflammatory arthritis that affects joints or entheses.
274 highly reactive with the self-peptide induce inflammatory arthritis that affects male and female mice
275 treatment, with some patients developing an inflammatory arthritis that becomes refractory to antibi
276 of mice with Borrelia burgdorferi causes an inflammatory arthritis that peaks 3-4 wk postinfection a
277 f people with hyperuricemia develop gout, an inflammatory arthritis that results from deposition of m
278 eumatoid arthritis (RA) is a prototype of an inflammatory arthritis that results in focal loss of art
280 ive strategy for at least some patients with inflammatory arthritis, the mechanisms that determine wh
281 mast cells contribute to the pathogenesis of inflammatory arthritis through PAR-2 activation via rele
282 ice lacking Rhbdf2 were protected from K/BxN inflammatory arthritis to the same extent as mice lackin
283 g) or pravastatin (0.2 mg/kg)-to mice during inflammatory arthritis up-regulated systemic and tissue
284 s controls), 2) Lyme disease vaccine but not inflammatory arthritis (vaccine controls), and 3) neithe
285 ets can contribute to the pathophysiology of inflammatory arthritis via IL-1- containing microparticl
286 SphK1 plays a key role in hTNF-alpha-induced inflammatory arthritis via impacting synovial inflammati
289 vator with antigen as a strategy to suppress inflammatory arthritis was tested in an experimental mou
290 autoimmunity against fibrinogen can mediate inflammatory arthritis, we immunized a variety of common
292 have been implicated in the pathogenesis of inflammatory arthritis, we sought to define the phenotyp
293 tients (14 women; mean age, 53.3 years) with inflammatory arthritis were examined at three different
294 -dose IVIG (1-2 g/kg body weight) suppressed inflammatory arthritis when given prophylactically.
295 diseases, AP1189 was tested in experimental inflammatory arthritis, where this biased agonist afford
296 n PON1 transgene was associated with reduced inflammatory arthritis, which correlated strongly with h
297 The majority of mice spontaneously develop inflammatory arthritis, which is accompanied by an enhan
298 sts resulted in a more severe and persistent inflammatory arthritis, with minimal effect on bone and
299 e when initiated early in the development of inflammatory arthritis, with sustained B cell depletion
300 iRNA nanocomplexes potently suppressed early inflammatory arthritis without affecting p65 expression