AB0128 Cxcl1, but not auto-antibodies or cd4+ccr6+ memory th cells within blood, is a marker to differentiate mice into collagen induced arthritispositive or negative prior to clinically manifest disease
2018
Background There is currently a knowledge gap on early pathogenesis prior to Rheumatoid Arthritis (RA) diagnosis. Additionally, current medication available for RA treatment has not been developed for prevention. Collagen induced arthritis (CIA) could aid in extending knowledge on early RA pathogenesis and testing the preventive effects of medicines. Objectives In this study we sought a marker that can differentiate mice prior to clinically manifest disease into their future CIA status with the aim to facilitate research into early disease processes and preventive treatment strategies. Methods Blood was obtained at time points prior (days 12 and 19) and after clinically manifest disease (days 27 and 35) during CIA. Antibodies against bovine and mouse collagen type II (mCII) were measured from plasma by ELISA. CD4+CCR6+ memory Th cells as well as other T cell types were determined in blood. Cytokines and chemokines were detected in plasma by Luminex. Mice were divided into CIA negative and CIA positive groups based on CIA score reached on day 35. Results Antibodies against mCII of the IgG2a isotype differed prior to clinically manifest disease but are not suitable as a differentiation marker. CD4+CCR6+ memory Th cells in blood differed only at day 35. The same holds for IL-6, TNFα and CXCL2. In contrast, CXCL1 differed prior to clinically manifest disease with an AUC significantly better (p=0.003) than random. Conclusions Here we identified CXCL1 as a marker that can differentiate mice prior to clinically manifest disease into CIA positive and CIA negative mice. This might help facilitate research into early disease processes and preventive pre-clinical treatment strategies. Disclosure of Interest None declared
Keywords:
- Correction
- Source
- Cite
- Save
- Machine Reading By IdeaReader
0
References
0
Citations
NaN
KQI