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1 t role in the development and aggravation of experimental arthritis.
2 -HSD1 deletion exhibit increased severity of experimental arthritis.
3 Gal-1 in regulating T cell reactivity during experimental arthritis.
4 osteoblasts and osteocytes attenuates murine experimental arthritis.
5 her targets, seems to be sufficient to treat experimental arthritis.
6 in synovial vascular permeability in murine experimental arthritis.
7 levels of interleukin-17 in the joint during experimental arthritis.
8 the role of NOD1 and NOD2 on development of experimental arthritis.
9 bility of mast cells to contribute to murine experimental arthritis.
10 adverse roles in inflammatory disorders like experimental arthritis.
11 ontrolling the resolution of inflammation in experimental arthritis.
12 lls during the initiation and progression of experimental arthritis.
13 um-induced models of immune complex-mediated experimental arthritis.
14 potential to visualize joint inflammation in experimental arthritis.
15 immune response can be central regulators of experimental arthritis.
16 okines/cytokines leading to the evolution of experimental arthritis.
17 phagy in LECs modulates T cell activation in experimental arthritis.
18 h the severity of the inflammation in murine experimental arthritis.
19 ce, earlier onset, and increased severity of experimental arthritis, accompanied by greater numbers o
20 athologic characteristics of T cell-mediated experimental arthritis and evaluated modulation of type
21 romising approach for tolerance induction in experimental arthritis and perhaps even in susceptible i
22 s with distinct functional subsets in murine experimental arthritis and remission stages in human RA.
23 hate-isomerase-specific antibodies to induce experimental arthritis, and we injected control mice wit
24 eins are cytoprotective, and in clinical and experimental arthritis, anti-heat shock protein reactivi
26 as been shown to have therapeutic effects in experimental arthritis by inhibiting both bone turnover
27 of the NOD2/RIPK2 signaling in the onset of experimental arthritis by triggering an IL-17-dependent
28 resents an effective therapeutic strategy in experimental arthritis, by demonstrating that the exogen
29 0 to a single joint of rabbits and mice with experimental arthritis can suppress disease in both the
32 s in murine models of acute inflammation and experimental arthritis demonstrated that TSG-6 has a str
33 ediated signaling as a beneficial pathway in experimental arthritis; hence this receptor is a novel t
35 inistration of SR-A accelerates the onset of experimental arthritis in mice, whereas inhibition of SR
40 d neutropenia remained capable of inhibiting experimental arthritis, leaving joint tissues free of in
41 types present in the RA joint, as well as in experimental arthritis, may be responsible, in part, for
44 that HCG exerts a protective effect in this experimental arthritis model, through modulation of infl
45 ether with compelling data from in vitro and experimental arthritis models demonstrating its pro-infl
47 ies support the role of TLR2 and 4 in RA and experimental arthritis models; however, the regulation a
49 e been shown to reduce joint inflammation in experimental arthritis, presumably by lowering the relea
50 ults in increased severity and chronicity of experimental arthritis, reduced total numbers of Treg ce
52 based single-cell RNA-sequencing analyses in experimental arthritis show that FAP signal reduction re
53 PI-2458 exerts disease-modifying activity in experimental arthritis through its direct inhibition of
54 in vivo measurement of cell proliferation in experimental arthritis using (18)F-FLT PET is a promisin
55 nvasively in vivo during different stages of experimental arthritis using the PET proliferation trace
61 ssociated with increased disease severity in experimental arthritis, we tested for a potential repeat