Sentence examples for mouse arthritis models from inspiring English sources

In this context, cell lysis could be responsible for the release of NAMPT in the extracellular compartment thus accounting for the increased NAMPT concentration found in the serum and tissues of RA patients and in mouse arthritis models ([13] [15] and our results).

Another non-invasive technique, thermal signature analysis, has been used to analyze rat rather than mouse arthritis models [ 21].

Our results in this report using mouse arthritis models are consistent with these results, suggesting that these genes are commonly involved in the pathogenesis at the elicitation phase.

In this study, we used both H4R-deficient mice and a specific H4R antagonist, JNJ 28307474, to investigate the involvement of the H4R in mouse arthritis models.

Moreover, blocking c-Fms inhibits macrophage infiltration, TNFα production by macrophages, and OC formation and activation in several mouse arthritis models [ 12, 45], and reduces TNFα-induced inflammatory arthritis [ 11], suggesting a therapeutic benefit in RA treatment.

In mouse arthritis models, FcγRIII deficient hosts exhibit resistance to collagen type II induced arthritis and anti-glucose-6-phosphate isomerase (GPI) antibody induced arthritis [ 2, 3], suggesting that FcγRIII is indispensible in autoantibody dependent arthritis.

Although MMP-2 may promote cartilage degradation, it suppresses the development of inflammatory joint disease in a mouse arthritis model [ 44].

T-5224 inhibited the expressinhibitedF-α and other cytokinexpressionuse arthritis mofel [ 5], suggesting it may andotheribit LPS-inducytokines productinn.

Here we showed that lymphocyte DRD2 activation alleviates both imbalance of T-helper (Th 17/T-regulatory (Th 17/T-regulatoryflamed sympTreg in a mouse arthritis model of RA.

To clarify the immunoregulatory role of HDAi in a mouse arthritis model, we examined the effect of an HDAi (TSA) on SKG mice, a T cell-mediated model of chronic arthritis.

The CAIA mouse arthritis model has demonstrated that anti-CII can initiate acute polyarthritis associated with PMN activation leading to endothelial cell adhesion and recruitment of these PMN to inflamed tissue.