The effect of immunomodulatory celecoxsib on the gene expression of inhibitory receptors in dendritic cells generated from monocyte cells.

Autoimmune diseases are characterized by irregular immune responses that disrupt self-tolerance. This research explores the effects of the immunomodulatory drug celecoxib on the expression of immune checkpoint receptors in monocyte-derived dendritic cells (DCs). Key receptors, including CTLA-4, VISTA, BTLA, PDL-1, B7H7, and LAG3, play critical roles in initiating and regulating immune responses and maintaining self-tolerance. Previous studies have highlighted the significance of immune checkpoints in preventing autoimmune conditions, with animal research supporting their effectiveness in immunotherapy. Our findings demonstrate that the upregulation of immune checkpoint receptors can enhance the inhibitory functions of DCs, thereby promoting self-tolerance. As a result, tolerogenic DCs present a promising therapeutic avenue for treating autoimmune diseases. Although these results are promising, further trials are required to validate this approach before it can be applied clinically. This study underscores the potential of targeting immune checkpoint receptors as a therapeutic strategy for autoimmune disorders.