Removal of CD5 on T cells alters their differentiation and cytokine production in an in vitro model investigating effects of P. gingivalis LPS on oral epithelial and immune cells.

Periodontal disease is a highly prevalent oral inflammatory disease that affects nearly half of adults 30 years or older in the United States. It is characterized byexcessive inflammation within the periodontal pockets typically in response to bacterial challenge and is characterized by inflamed gums, destruction of periodontal ligaments, alveolar bone loss, and tooth loss if left untreated. T cells are adaptive immune cells which play important roles in driving inflammation and alveolar bone loss during severe periodontitis. Additionally, several studies have reported associations between periodontal pathogens and chronic inflammation within the oral cavity to several systemic diseases, including inflammatory bowel disease, diabetes mellitus, cardiovascular diseases, cognitive decline and Alzheimer's disease, chronic obstructive pulmonary disease, and certain cancers. CD5 is a glycoprotein receptor found on the surface of T cells that serves as a coinhibitory receptor that attenuates TCR signaling, and its immunoregulatory role has yet to be investigated in the context of periodontitis. Here, we characterize the functional differences between CD5 knockout T cells and wildtype T cells, including T cell activation, differentiation, and cytokine production, in an in vitro model used to investigate the effects of P. gingivalis LPS on oral epithelial and immune cells. In this study we report that removal of CD5 increases T cell activation and effector/memory formation and increased CD4+ T cell Csf1 mRNA transcription while decreasing Rankl transcription. Together, these findings provide insights into the role of CD5 in modulating inflammation during periodontal disease.