TH17 cells in asthma and inflammation

BackgroundThe chronic airway disease asthma causes significant burden to patients as well as the healthcare system with limited options for prevention or cure. Inadequate treatment strategies are most likely due to the complex heterogeneous nature of asthma. Furthermore, the severe asthma phenotype is characterized by the lack of a response to standard medication, namely, corticosteroids.Scope of ReviewIn the last several years it has been shown that the eosinophilic/atopic phenotype of asthma driven by TH2 mechanisms is not the only immunologic pathway contributing to disease. In fact, there has been evidence revealing that severe asthmatics in particular have neutrophilic inflammation, and this is associated with corticosteroid resistance. TH17 cells, a recently discovered lineage of T helper cells, play an important role in lung host defense against multiple pathogens via production of the cytokine IL‐17. IL‐17 promotes neutrophil production and chemotaxis via multiple factors.Major ConclusionsMouse and human studies provide robust evidence that TH17 cells and IL‐17 play a role in severe asthma and may contribute to corticosteroid resistance.General SignificanceAs we learn more about TH17 cells in severe asthma, the goal is to potentially target this pathway for treatment in the hope of significantly improving the quality of life for those children and adults affected with this disease. This article is part of a Special Issue entitled: Biochemistry of Asthma.

Research highlights
► Severe, steroid resistant asthma is often characterized by airway neutrophilia.
► While TH2 cells drive mild asthma, severe asthma may have a key TH17 component.
► Asthma models have shown a role for the TH17/IL‐17 in promoting airway disease.
► TH17 induced allergic airway disease is steroid resistant in mouse models.
► Human studies show elevated levels of IL‐17 in severe, steroid resistant asthmatics.