The lung is a gas exchange organ that contends with a large array of environmental factors, including allergens, infectious microbes and reactive oxygen species.  A number of innate immune mechanisms have evolved to rapidly respond to these elements, and can mediate lung inflammation and asthma, a heterogeneous disease with several distinct phenotypes.  While many form of asthma require adaptive Th2-driven immunity, several other forms can develop independently of adaptive immunity, and involve Type 2 as well as Type 3 innate lymphoid cells (ILCs), producing IL-5, IL-9, IL-13 or IL-17 and IL-22.  Type 2 ILCs respond during allergen exposure and influenza infection, and trigger airway hyperreactivity (AHR), a cardinal feature of asthma.  In contrast, in obesity, which is associated with a steroid resistant form of severe asthma, CCR6⁺ Type 3 ILC3s expand in the lungs in response to IL-1b produced via the NLRP3 pathway by lung macrophages.  Administration of IL-1b directly into the lungs of mice resulted in the expansion of lung ILC3s, and directly induced AHR.  Furthermore, blockade of IL-1b with an IL-1 receptor antagonist reduced the number of lung ILC3 cells and abolished obesity-induced AHR in mice.  Obesity-associated AHR was independent of adaptive immunity, as it occurred in obese Rag1^−/− mice, and was dependent on interleukin-17A (IL-17A) and the NLRP3 inflammasome, as it did not develop in obese Il17a^−/− or Nlrp3^−/− mice, respectively.These studies suggest an important role for Type 2 and Type 3 ILCs in different forms of allergic and non-allergic asthma.