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Th17 and associated pathways are implicated in tissue homeostasis and host protection.

Dutzan and colleagues demonstrated that Th17 cells that reside in the gingivia, the mucosal membrane surrounding teeth which is an important oral barrier, increase with age. This finding was not found in other barriers, or in the secondary lymphoid organs such as the lymph nodes or the spleen.

Oral Th17 numbers decreased when mice were weaned on a soft diet, and increased when the gingival membrane was physically damaged by mechanical abrasion every other day or when mice were on normal chow.

The development of oral Th17 cells was dependent on IL-6 and independent of commensal bacterial colonization. This was supported by the lack of Th17 development in mice lacking the IL-6 receptor, and the maintenance of oral, but not skin or GI-specific, Th17 cells in specific-pathogen-free (SPF) and germ-free (GF) mice.

In summary, this study has demonstrated that orally-resident T helper 17 (Th17) cells develop via a commensal colonization-independent mechanism which is driven by mechanical damage induced by chewing.