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1 -HSD1 deletion exhibit increased severity of experimental arthritis.
2 Gal-1 in regulating T cell reactivity during experimental arthritis.
3 osteoblasts and osteocytes attenuates murine experimental arthritis.
4 her targets, seems to be sufficient to treat experimental arthritis.
5 potential to visualize joint inflammation in 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 immune response can be central regulators of experimental arthritis.
15 okines/cytokines leading to the evolution of experimental arthritis.
16 h the severity of the inflammation in murine experimental arthritis.
17 t role in the development and aggravation of experimental arthritis.
18 ce, earlier onset, and increased severity of experimental arthritis, accompanied by greater numbers o
19 athologic characteristics of T cell-mediated experimental arthritis and evaluated modulation of type
20 romising approach for tolerance induction in experimental arthritis and perhaps even in susceptible i
21 hate-isomerase-specific antibodies to induce experimental arthritis, and we injected control mice wit
22 eins are cytoprotective, and in clinical and experimental arthritis, anti-heat shock protein reactivi
24 as been shown to have therapeutic effects in experimental arthritis by inhibiting both bone turnover
25 of the NOD2/RIPK2 signaling in the onset of experimental arthritis by triggering an IL-17-dependent
26 resents an effective therapeutic strategy in experimental arthritis, by demonstrating that the exogen
27 0 to a single joint of rabbits and mice with experimental arthritis can suppress disease in both the
30 s in murine models of acute inflammation and experimental arthritis demonstrated that TSG-6 has a str
31 ediated signaling as a beneficial pathway in experimental arthritis; hence this receptor is a novel t
37 d neutropenia remained capable of inhibiting experimental arthritis, leaving joint tissues free of in
38 types present in the RA joint, as well as in experimental arthritis, may be responsible, in part, for
41 that HCG exerts a protective effect in this experimental arthritis model, through modulation of infl
43 ies support the role of TLR2 and 4 in RA and experimental arthritis models; however, the regulation a
45 e been shown to reduce joint inflammation in experimental arthritis, presumably by lowering the relea
47 PI-2458 exerts disease-modifying activity in experimental arthritis through its direct inhibition of
48 in vivo measurement of cell proliferation in experimental arthritis using (18)F-FLT PET is a promisin
49 nvasively in vivo during different stages of experimental arthritis using the PET proliferation trace
55 ssociated with increased disease severity in experimental arthritis, we tested for a potential repeat
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