UC San Diego

Group 2 innate lymphoid cells (ILC2s) promote type 2 inflammation in pulmonary diseases through the release of cytokines. ILC2s are a subset ILCs that also includes ILC1s and ILC3s. In response to an allergen assault, the airway epithelium releases alarmin cytokines that activate ILC2s to robustly produce inflammatory type 2 cytokines. However, while the processes that cause ILC2 activation and potentiation of lung inflammation are well studied, mechanisms surrounding the suppression of ILC function during an allergen assault are poorly understood. To determine the role of the highly expressed RNA binding protein RNA Binding Motif 3 (RBM3) on ILC2s, we challenged rbm3-/- and wild type (WT) mice with the fungal allergen Alternaria alternata and observed changes in cytokine production using flow cytometry. Our data shows that rbm3-/- mice have increased production of the type 2 cytokines IL5, IL13, but also the ILC3 or Th17 cytokine IL17A, compared to WT mice. Flow cytometry revealed that the rbm3-/- ILCs had increased cytokine production specific to IL5, IL13, and IL17. These findings confirm that RBM3 directly regulates the function of ILCs upon activation by an allergen. Ultimately, RBM3 may serve a protective role in preventing excessive lung damage and inflammation in allergic airway diseases.