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1 recruitment and are protected in 2 models of inflammatory arthritis.
2 rs for diagnosis and treatment evaluation of inflammatory arthritis.
3 e B4 (LTB4) in myeloid cells, which modulate inflammatory arthritis.
4 te immune cells and osteoclasts (OCs) during inflammatory arthritis.
5 sfer of OCP with SKG CD4+ T cells diminished inflammatory arthritis.
6 ell-suppressive activity that is expanded in inflammatory arthritis.
7 may show promise as a therapeutic target in inflammatory arthritis.
8 roscopy may be indicative of the presence of inflammatory arthritis.
9 ne collagen-induced arthritis (CIA) model of inflammatory arthritis.
10 flammatory cytokines and induced an erosive, inflammatory arthritis.
11 apeutic agent for targeting PBEF activity in inflammatory arthritis.
12 t of complement during the effector phase of inflammatory arthritis.
13 thritis, and administration of PGRN reversed inflammatory arthritis.
14 f these patients had RA, and 13 did not have inflammatory arthritis.
15 processes, necessary for the development of inflammatory arthritis.
16 ages in a subset of patients with TNF-driven inflammatory arthritis.
17 of p21-mediated suppression of experimental inflammatory arthritis.
18 mutant mice compared to wild-type mice with inflammatory arthritis.
19 gs, depletion of platelets attenuated murine inflammatory arthritis.
20 itions and autoimmune diseases, particularly inflammatory arthritis.
21 sm in K/BxN serum-induced arthritis to drive inflammatory arthritis.
22 urately differentiate it from other forms of inflammatory arthritis.
23 odels of allograft rejection and destructive inflammatory arthritis.
24 , and is an attractive therapeutic target in inflammatory arthritis.
25 n in vivo model of TNF-alpha-induced chronic inflammatory arthritis.
26 rties and prevent bone erosions in models of inflammatory arthritis.
27 via enhancing innate cellular activation in inflammatory arthritis.
28 TNFalpha, and TNFRI PLAD (p60 PLAD) inhibits inflammatory arthritis.
29 s compared with CE guidance in patients with inflammatory arthritis.
30 e in the destruction of bone associated with inflammatory arthritis.
31 activation for the treatment of experimental inflammatory arthritis.
32 ents may represent an effective way to treat inflammatory arthritis.
33 ated virus (AAV) type 2 delivery system, for inflammatory arthritis.
34 ight be an alternative therapeutic target in inflammatory arthritis.
35 ial structural damage in these rat models of inflammatory arthritis.
36 g cells, are involved in the pathogenesis of inflammatory arthritis.
37 y provide an effective cell-free therapy for inflammatory arthritis.
38 s was induced using the K/BxN mouse model of inflammatory arthritis.
39 igand-targeted nanotherapy, would ameliorate inflammatory arthritis.
40 uence the topography of erosion formation in inflammatory arthritis.
41 nsgenic mice were used as a model of chronic inflammatory arthritis.
42 matory in a murine model of antibody-induced inflammatory arthritis.
43 unexpected proinflammatory role of IL-33 in inflammatory arthritis.
44 rom antimicrobial defense to anaphylaxis and inflammatory arthritis.
45 otent imaging modality for the assessment of inflammatory arthritis.
46 expression of citrullinated autoantigens in inflammatory arthritis.
47 ynthesized via COX-1, in particular PGI2, to inflammatory arthritis.
48 ssion differed between RA and other forms of inflammatory arthritis.
49 RA patients or patients with other forms of inflammatory arthritis.
50 duction and exacerbation of autoimmunity and inflammatory arthritis.
51 s potential as a novel therapeutic target in inflammatory arthritis.
52 action to inflammation, and are resistant to inflammatory arthritis.
53 ndidate for the treatment of bone erosion in inflammatory arthritis.
54 RA patients or patients with other forms of inflammatory arthritis.
55 lammatory and destructive tissue response in inflammatory arthritis.
56 sed to assess the natural history of erosive inflammatory arthritis.
57 vitamin D plays an immunomodulatory role in inflammatory arthritis.
58 ion of endogenous SPMs during self-resolving inflammatory arthritis.
59 ial function for T-bet in DCs in controlling inflammatory arthritis.
60 or the development of novel therapeutics for inflammatory arthritis.
61 duction, yet is not effective in suppressing inflammatory arthritis.
62 t into the joint in the K/BxN mouse model of inflammatory arthritis.
63 of apoptotic regulators in a mouse model of inflammatory arthritis.
64 the lack of efficacy of IL-10 in suppressing inflammatory arthritis.
65 ations that are crucial for the induction of inflammatory arthritis.
66 y help optimize target-oriented treatment of inflammatory arthritis.
67 PS may be useful in the treatment of chronic inflammatory arthritis.
68 ynovial fluid and tissues is the hallmark of inflammatory arthritis.
69 arthritis when compared with self-resolving inflammatory arthritis.
70 even reverse the osteolysis associated with inflammatory arthritis.
71 thways play key roles in the pathogenesis of inflammatory arthritis.
72 proach to the alleviation of bone erosion in inflammatory arthritis.
73 h acute knee injuries or progressive chronic inflammatory arthritis.
74 r blockade-targeting treatment strategies in inflammatory arthritis.
75 an attractive target for treatment of human inflammatory arthritis.
76 reated with RANKL and following induction of inflammatory arthritis.
77 alone or in the cohort with undifferentiated inflammatory arthritis.
78 ultiple sclerosis, as well as a rat model of inflammatory arthritis.
79 essential for osteoclast differentiation in inflammatory arthritis.
80 The circadian clock regulates inflammatory arthritis.
81 inder osteoclastogenesis and bone erosion in inflammatory arthritis.
82 irrelevant specificity in the development of inflammatory arthritis.
83 rapeutic intervention for focal bone loss in inflammatory arthritis.
84 Unc5b are novel targets for the treatment of inflammatory arthritis.
85 useful therapeutic targets for treatment of inflammatory arthritis.
86 esent in the synovial fluid of patients with inflammatory arthritis.
87 ced CXCL1, and it attenuated the severity of inflammatory arthritis.
88 e IL-27 receptor (IL-27R) after the onset of inflammatory arthritis.
89 and 12-LO in an in vivo model of autoimmune inflammatory arthritis.
90 were observed in IL-27R-deficient mice with inflammatory arthritis.
91 t actions of atorvastatin and pravastatin in inflammatory arthritis.
92 t against the induction of murine autoimmune inflammatory arthritis.
93 nated action of sPLA2-IIA and 12-LO promotes inflammatory arthritis.
94 for the stimulation of osteoclastogenesis in inflammatory arthritis.
95 itivity analysis that excludes patients with inflammatory arthritis.
96 and higher disease activity in patients with inflammatory arthritis.
97 esults in a STING-dependent, TLR-independent inflammatory arthritis.
98 an be targeted to prevent the development of inflammatory arthritis.
99 N protected cartilage integrity in mice with inflammatory arthritis.
100 event disease in a mouse model of autoimmune inflammatory arthritis.
101 pathway to dissect and eventually target in inflammatory arthritis.
102 tic monitoring of synovitis in patients with inflammatory arthritis.
103 ntermediate may diminish bone destruction in inflammatory arthritis.
104 fer system, focused on the effector phase of inflammatory arthritis.
105 ining of joints that become activated during inflammatory arthritis.
106 tients with new-onset and chronic autoimmune inflammatory arthritis.
107 sponse, one that is particularly relevant to inflammatory arthritis.
108 progranulin in regulatory T cells restrains inflammatory arthritis.
109 isease mechanisms operating in patients with inflammatory arthritis.
110 enhances bone damage and disease severity in inflammatory arthritis.
111 Gout is the most common type of inflammatory arthritis.
112 1alpha is a potential therapeutic target for inflammatory arthritis.
113 ding inflammatory bowel disease, sepsis, and inflammatory arthritis.
114 s and the periarticular osteolysis attending inflammatory arthritis.
115 a ubiquitously expressed self-Ag and induce inflammatory arthritis.
116 st time, that IL-22 has a protective role in inflammatory arthritis.
117 uring acute joint inflammation in a model of inflammatory arthritis.
118 ve colitis (12 203), Crohn's disease (7628), inflammatory arthritis (27 358), systemic autoimmune dis
119 and 111 control patients with other forms of inflammatory arthritis (82 with rheumatoid arthritis, 13
120 e markedly increased in SHIP1(-/-) mice with inflammatory arthritis, a condition characterized by inc
121 Ankylosing spondylitis (AS) is a chronic inflammatory arthritis affecting the spine in young adul
122 ion of this drug in the K/BxN mouse model of inflammatory arthritis after first crossing in a human C
123 in vitro, MyD88(-/-) mice still developed an inflammatory arthritis after infection with B. burgdorfe
125 degraded DNA leads to both a STING-dependent inflammatory arthritis and additional Unc93b1-dependent
127 asts are essential cells for bone erosion in inflammatory arthritis and are derived from cells in the
128 on in autoantibody-positive subjects without inflammatory arthritis and are similar to airways abnorm
130 prozumab, a humanized anti-HSP mAb in murine inflammatory arthritis and colitis, and its effects on c
131 iagnostic uncertainty in patients with early inflammatory arthritis and concerns about treatment of p
132 fore, selective MKK3 deficiency can suppress inflammatory arthritis and cytokine production while Tol
133 demonstrate a nonredundant role for LTB4 in inflammatory arthritis and define a neutrophil mediator
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
140 e that CX(3) CR1 deficiency is protective in inflammatory arthritis and may have effects that extend
143 the target autoantigen in the K/BxN model of inflammatory arthritis and perhaps in some humans with a
144 loss in TNF-induced inflammatory osteolysis, inflammatory arthritis and post-ovariectomy models.
146 ate immune receptors for dsRNA in modulating inflammatory arthritis and provide additional support fo
147 articipate in the pathogenesis of autoimmune inflammatory arthritis and provide insights of potential
148 tic rats with celastrus/celastrol suppressed inflammatory arthritis and reduced bone and cartilage da
149 sents a severe pathological phenotype during inflammatory arthritis and results in joint pain and bon
150 ulate inflammation in disease states such as inflammatory arthritis and systemic lupus erythematosus.
151 philic inflammation, immune complex-mediated inflammatory arthritis and thioglycollate-induced perito
152 tion-induced osteolysis is a problem in both inflammatory arthritis and total joint arthroplasty.
153 s, 6/6 (100%) of patients with nonrheumatoid inflammatory arthritis, and 8/10 (80%) of osteoarthritis
154 aluated in the K/BxN serum transfer model of inflammatory arthritis, and clinical signs of arthritis,
155 ption occurs in postmenopausal osteoporosis, inflammatory arthritis, and metastasis of tumors to bone
156 on of the IRE1alpha gene protected mice from inflammatory arthritis, and treatment with the IRE1alpha
159 Fas-deficient mice showed enhanced systemic inflammatory arthritis associated with up-regulation of
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
162 etic joints at baseline, no known underlying inflammatory arthritis at baseline nor followup, and no
166 matory responses in chronic lung disease and inflammatory arthritis but has not been investigated in
168 ses) were compared with 3 control groups: 1) inflammatory arthritis but not Lyme disease vaccine (art
170 with rheumatoid arthritis and other forms of inflammatory arthritis, but not in joint fluid from pati
171 -6 (IL-6) contributes to the pathogenesis of inflammatory arthritis, but the role, if any, of epigene
172 rization of PIA as a murine model of chronic inflammatory arthritis by demonstrating cellular and hum
173 tibodies contribute to joint inflammation in inflammatory arthritis by triggering cellular fragment c
175 Gout is one of the most common types of inflammatory arthritis, caused by the deposition of mono
176 By 2-4 weeks, these mice developed symmetric inflammatory arthritis, characterized by tissue swelling
177 ssociated with calcium pyrophosphate crystal inflammatory arthritis (chondrocalcinosis) and that SBS
179 body-positive subjects with airways disease, inflammatory arthritis classifiable as articular RA deve
180 BALB/c(-/-)) spontaneously developed chronic inflammatory arthritis, DBA/1 IL-1Ra-deficient (DBA/1(-/
181 eping with this conclusion, mice with severe inflammatory arthritis develop profound osteoclastogenes
182 the Pgia8 locus regulates antibody-mediated inflammatory arthritis differently in males and females.
183 its a strong association with the autoimmune inflammatory arthritis disorder ankylosing spondylitis (
184 We demonstrate that mice undergoing chronic inflammatory arthritis displayed osteoporosis resulting
185 can affect periodontal disease, presence of inflammatory arthritis does not appear to be one of them
186 of fetal DNA in serum from women with RA and inflammatory arthritis during and after pregnancy to tes
187 h17/1 cells from the joints of children with inflammatory arthritis express high levels of both Th17
188 ndylitis (AS) is a common, highly heritable, inflammatory arthritis for which HLA-B*27 is the major g
191 Furthermore, studies using animal models of inflammatory arthritis have demonstrated critical roles
192 rding the role of chlamydiae in induction of inflammatory arthritis have increased our detailed under
195 trol MC-dependent diseases including asthma, inflammatory arthritis, heart disease, and multiple scle
196 ains inflammation and is therapeutic against inflammatory arthritis; however, the underlying immunolo
199 ma HK is a key mediator of acute and chronic inflammatory arthritis in genetically susceptible Lewis
207 r understanding of the underlying process of inflammatory arthritis in spondyloarthropathy and other
208 g, inflammatory responses, and inhibition of inflammatory arthritis in the K/BxN serum transfer model
209 DNs strongly inhibited the effector phase of inflammatory arthritis in the K/BxN serum transfer syste
211 to the spontaneous development of autoimmune inflammatory arthritis in transgenic mice containing CD4
212 s of C5orf30 contributes to the pathology of inflammatory arthritis in vivo, because inhibition of C5
213 applied to individuals with undifferentiated inflammatory arthritis in whom at least 1 joint is deeme
214 relevance of these observations, we induced inflammatory arthritis in wild-type mice and treated the
215 er disease onset ameliorated the severity of inflammatory arthritis including arthritis indices, paw
216 K and provides follow-up care to people with inflammatory arthritis including treatment, monitoring,
217 hance C3 activation, is necessary to mediate inflammatory arthritis induced by adherent immune comple
218 products is necessary for resolution of the inflammatory arthritis induced by Borrelia infection, an
219 D/TNF mice that develop amyloid deposits and inflammatory arthritis induced by human TNF-alpha (huTNF
223 oanatomic basis for formation of erosions in inflammatory arthritis is incompletely understood but is
226 Loss of iRHOM2 largely protects mice from inflammatory arthritis, making iRHOM2 a potential drug t
227 mmatory bowel disease (IBD), sarcoidosis and inflammatory arthritis, making pharmacologic inhibition
228 the biological clock and pathways underlying inflammatory arthritis, mice were administered collagen
229 cy of CX(3) CR1 is protective in the chronic inflammatory arthritis model collagen-induced arthritis
230 In experiments using the K/BxN serum-induced inflammatory arthritis model, CXCR6(-/-) mice showed pro
234 ng recruitment of leukocytes to the joint in inflammatory arthritis models are not fully understood.
237 patients with osteoarthritis or seronegative inflammatory arthritis, neither of which exhibited signi
238 In a mouse model of autoantibody-induced inflammatory arthritis, neutrophils infiltrate the joint
240 aRIII contributes to the pain resulting from inflammatory arthritis of the TMJ, and siRNA has the pot
241 unctional and histologic improvements in the inflammatory arthritis of TTP(-/-) mice when CCL3 was ab
242 with those from patients with other forms of inflammatory arthritis or compared with control macropha
243 mption may represent a novel risk factor for inflammatory arthritis or may act as a marker for a grou
244 m the joints of patients with other forms of inflammatory arthritis or with control macrophages.
245 cells, an effect that has been implicated in inflammatory arthritis, osteoporosis, obesity, and myopa
246 n age, 45 years) with untreated recent-onset inflammatory arthritis participated in this prospective
247 es in the future management of patients with inflammatory arthritis, particularly those with rheumato
248 Ankylosing spondylitis is a common form of inflammatory arthritis predominantly affecting the spine
249 f major joint replacement, terminal illness, inflammatory arthritis, prosthetic leg, cognitive impair
250 ve for chronic calcium pyrophosphate crystal inflammatory arthritis (pseudogout, chondrocalcinosis).M
251 fore or after inducing the adjuvant model of inflammatory arthritis reduced chondrocyte apoptosis, pr
252 ances, a substantial number of patients with inflammatory arthritis remain resistant to current thera
254 -Flip-KO mice spontaneously develop erosive, inflammatory arthritis, resembling rheumatoid arthritis,
255 ) CL1) and has been shown to be important in inflammatory arthritis responses, largely due to its eff
260 ase activity and disability in patients with inflammatory arthritis such as rheumatoid arthritis.
261 fficult to differentiate from other forms of inflammatory arthritis such as spondyloarthritis and rhe
262 risk factor for cardiovascular diseases and inflammatory arthritis, such as hypertension and gout.
264 imulates osteoclastogenesis in patients with inflammatory arthritis, suggesting that CD11b+ PBMCs cou
268 7 categories comprising 8 of 13 indications (inflammatory arthritis, tendon pathology, effusion, burs
269 r matrix of their articular cartilage during inflammatory arthritis than wild-type (WT) C57BL/6 mice,
270 highly reactive with the self-peptide induce inflammatory arthritis that affects male and female mice
271 treatment, with some patients developing an inflammatory arthritis that becomes refractory to antibi
272 f people with hyperuricemia develop gout, an inflammatory arthritis that results from deposition of m
273 eumatoid arthritis (RA) is a prototype of an inflammatory arthritis that results in focal loss of art
275 ive strategy for at least some patients with inflammatory arthritis, the mechanisms that determine wh
276 mast cells contribute to the pathogenesis of inflammatory arthritis through PAR-2 activation via rele
277 ice lacking Rhbdf2 were protected from K/BxN inflammatory arthritis to the same extent as mice lackin
278 mine the role of MPCs in the pathogenesis of inflammatory arthritis, together with their role in atte
279 g) or pravastatin (0.2 mg/kg)-to mice during inflammatory arthritis up-regulated systemic and tissue
280 s controls), 2) Lyme disease vaccine but not inflammatory arthritis (vaccine controls), and 3) neithe
281 ets can contribute to the pathophysiology of inflammatory arthritis via IL-1- containing microparticl
282 SphK1 plays a key role in hTNF-alpha-induced inflammatory arthritis via impacting synovial inflammati
288 vator with antigen as a strategy to suppress inflammatory arthritis was tested in an experimental mou
289 autoimmunity against fibrinogen can mediate inflammatory arthritis, we immunized a variety of common
291 have been implicated in the pathogenesis of inflammatory arthritis, we sought to define the phenotyp
292 To gain insight into IL-10 responses in inflammatory arthritis, we used microarray analysis to d
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 The majority of mice spontaneously develop inflammatory arthritis, which is accompanied by an enhan
297 infliximab, in comparison with patients with inflammatory arthritis who were not receiving infliximab
298 ioidomycosis was calculated in patients with inflammatory arthritis who were receiving treatment with
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
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