Abstract
Type II collagen (CII) protein is the main component of hyaline cartilage. The clinical importance of CII in arthritis, aging, and osteoarthritis is significant, but its ability to induce specific immune tolerance has not been extensively studied previously. We have recently proven that CII is capable of inducing Anterior Chamber Associated Immune Deviation (ACAID) when injected into the eye. Here, we hypothesized that ACAID-mediated tolerance could be induced in Balb/c mice that receive an intravenous administration of CII-induced in vitro-generated ocular-like antigen-presenting cells (APCs) or T regulatory cells (Tregs). Delayed hypersensitivity (DTH) assays were used to examine this hypothesis. In mice injected with CII-specific ACAID APCs, the specific regulatory activities resided in the spleen cells, splenic T cells, and ACAID CD8+ T cells, as proven by local adoptive transfer (LAT) assays. Conversely, there was a lack of regulatory activity in the CD4+ CD25+ T cell compartment of the recipient mice. Thus, ACAID CD8+ Tregs generated in vitro could be directly responsible for the expression of CII-driven ACAID-mediated tolerance and could be used as potential therapeutic tools in the treatment of CH-associated autoimmune diseases.
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