Determining the Effects of Obesity and Type 2 Diabetes on CCR6+ Epidermal γδ T Cell Number and Function in Inflammatory Disease and Wound Healing

---

Presentation Time: 03:15 PM - 04:30 PM
Poster Board Number: B602
Abstract ID: 4187

Presenting Author:
Emma Engel , Research Assistant at California State Univ., San Marcos

Abstract:

 A maladaptive healing cascade causes chronic wounds. γδ T cells are affected, the dysregulation of which causes a reduction of cytokines and growth hormones. We are studying the Chemokine Receptor 6 (CCR6)/Chemokine Ligand 20 (CCL20) axis and how it functions in the wounds of obese and diabetic mice. When keratinocytes are stressed by wounding or psoriasis, CCL20 is released and interacts with CCR6 on Dermal T cells to recruit them to the epidermis. Epidermal T cells and their role in this axis are not as well understood. Upon wounding, it was found that a subset of epidermal γδ T cells express CCR6 within 24 hours, and it is downregulated by 72 hours. The role of the CCR6 epidermal γδ T cells express was also investigated. Epidermal γδ T cells, when co stimulated with CCL20 and anti-CD3, generate IL-17A, suggesting that CCR6 plays a role in TH17 responses during inflammation. Animals and humans with obesity and diabetes both exhibit elevated IL-17, so obese and diabetic mice were examined during wound healing and psoriasis.  

During keratinocyte stress, epidermal gd T cells experienced significantly elevated levels of CCR6 and IL-17 in obese and diabetic mice. This shows that in chronic diseases like type 2 diabetes, resident T cell IL-17 responses are amplified. In better understanding the mechanisms used by resident T cells during their inflammatory responses to keratinocyte stress, a targeted therapy can be developed to help treat chronic wounds and psoriasis.