The degree of CD4+ T cell autoreactivity determines cellular pathways underlying inflammatory arthritis.

ABSTRACT: Although therapies targeting distinct cellular pathways (e.g., anticytokine versus anti-B cell therapy) have been found to be an effective strategy for at least some patients with inflammatory arthritis, the mechanisms that determine which pathways promote arthritis development are poorly understood. We have used a transgenic mouse model to examine how variations in the CD4(+) T cell response to a surrogate self-peptide can affect the cellular pathways that are required for arthritis development. CD4(+) T cells that are highly reactive with the self-peptide induce inflammatory arthritis that affects male and female mice equally. Arthritis develops by a B cell-independent mechanism, although it can be suppressed by an anti-TNF treatment, which prevented the accumulation of effector CD4(+) T

SUBMITTER: Perng OA 

PROVIDER: S-EPMC3974175 | biostudies-literature | 2014 Apr

REPOSITORIES: biostudies-literature