IL-4 Signaling Attenuates γδ T Cell IL-17A Protein Expression

Melissa T. Harintho, BS, Dr. Dawn C. Newcomb Baker, PhD, Jacqueline-Yvonne Cephus, BS, Kasia Goleniewska, Dr. R. Stokes Peebles Jr., MD, FAAAAI



γδ T cells reside at the interface of epithelial-environmental interfaces such as the respiratory and gastrointestinal tracts. γδ T cells are potent producers of IL-17A which is important in antibacterial and antifungal immunity. Patients with asthma are at increased risk for invasive bacterial infections and bacterial pneumonia. There is an increase in CD4+ Th2 cells in the airway of asthma patients and Th2 cells produce IL-4. IL-4 negatively regulates IL-17A expression from CD4+ Th17 cells; however, the effect of IL-4 on IL-17A expression by γδ T cells is unknown. We therefore hypothesized that IL-4 attenuates γδ T cell IL-17A protein expression.



γδ T cells were purified from the spleens of BALB/c mice. To induce IL-17 protein expression, γδ T cells were cultured with IL-1β and IL-23 for 3 days in the presence or absence of IL-4 (10 ng/mL). IL-17A, IL-17F, and IL-22 protein expression was determined by ELISA.



We found that IL-4 significantly decreased IL-17A protein expression in γδ T cells (35.9± 1.6 ng/ml to 10.5± 0.4 ng/mL, p<0.05, n=5). We also looked at IL-17F and IL-22 protein expression and found that IL-4 significantly decreased protein expression of these IL-17 cytokine family members in γδ T cells (21.9± 2.5 ng/mL to 10.3± 0.5 ng/mL and 10.4± 0.2 ng/mL to 2.6± 0.03 ng/mL, p<0.05, n=5).



IL-4 inhibition of IL-17 cytokine family protein expression by γδ T cells is a possible explanation for why asthmatic patients are at higher risk for bacterial pneumonia.

abstract No: 

    • AAAAI 2014 (70th)