Dipeptidyl peptidase IV (DPP4) deficiency increases Th1-driven allergic contact dermatitis

Area of Science:

• Immunology
• Dermatology
• Allergy Research

Background:

• CD26, also known as dipeptidyl peptidase IV (DPP4), is implicated in immunological processes.
• Recent findings highlight its role in allergic lung responses.

Purpose of the Study:

• To investigate the impact of DPP4 on allergic skin responses.
• To examine CD26 expression in atopic dermatitis (AD) and its functional role in contact hypersensitivity models.

Main Methods:

• Analyzed skin biopsies from AD patients and healthy controls for CD26/DPP4 expression.
• Utilized CD26/DPP4-deficient and wild-type rats in contact hypersensitivity models (Th1 and Th2 dominant).
• Assessed inflammatory responses via histology, flow cytometry (FACS), and ELISA.

Main Results:

• CD26/DPP4 expression was elevated in lesional skin of AD patients and in both rat models.
• CD26/DPP4 deficiency reduced inflammation in Th2-driven responses but aggravated it in Th1-driven responses.
• Findings suggest a context-dependent role of CD26/DPP4 in skin inflammation, potentially linked to Th1/Th2 balance.

Conclusions:

• Upregulation of CD26 in atopic dermatitis is a novel finding, consistent with other inflammatory skin diseases.
• Tissue expression of CD26/DPP4 can be either beneficial or detrimental in immunological skin responses, depending on the Th1/Th2 balance.
• Results may have implications for diabetic patients on DPP4 inhibitors with co-existing eczematous skin conditions.