Inflammatory processes usually occur as a body response to deleterious exogenous factors and are regulated by immune responses. These inflammatory responses are stimulus-dependent and vary according to individual intrinsic factors. The imbalance between pro- and anti-inflammatory cytokines release mediated by adaptive immune response has been recognized as crucial to the development and progression of different lung diseases, such as asthma and chronic obstructive pulmonary disease (COPD). Clinical and experimental studies have described Th17/T regulatory (Treg) cells imbalance in both COPD and asthma progression. A failure in inflammatory control mediated by Treg cells seems to mitigate the Th17 response leading to development and progression of these respiratory diseases.
Th17 cells are a subset of activated CD4+T cells and are recognized by the release of pro-inflammatory interleukins such as IL-17 and IL-22. These interleukins induce mucus hypersecretion and airway hyperesponsiveness as well as the perpetuation of inflammatory process and lung tissue damage. In asthma and COPD, the increase of IL-17 expression has been extensively associated with structural and functional changes, leading to progression of these diseases. In addition, the IL-17 is described to be responsible for severe asthma by recruiting and activating neutrophils and eosinophils to the airways, and therefore perpetuating the inflammatory process. In contrast, Treg cells are responsible for maintaining immune homeostasis by inhibiting abnormal immune responses and suppressing inflammation. IL-10, an important immunomodulatory cytokine, may be released by different cell types, including Treg cells. Several experimental and clinical studies have demonstrated an association between the decrease in IL-10 release and obstruction development and progression in smokers with COPD probably due a failure in the Treg activity. Furthermore, evidence attested that Treg cell function recovery plays a pivotal role in the suppression of allergic inflammation in asthma.
In this Research Topic, we aim to present a collection of manuscripts evaluating the importance of Th7/Treg cells imbalance in asthma and COPD development and progression. We welcome studies regarding Th17 and Treg responses in both respiratory diseases, including the signaling pathways that lead these subtypes cells differentiation. We welcome Original Research, Method, Mini Review or other types of articles, focusing on, but not limited to, the following subtopics:
· Th17/Treg imbalance in asthma development and progression
· Th17 response in severe asthma
· Th17/Th2 response in asthma
· T reg failure activity in asthma
· Th17/Treg imbalance in COPD development and progression
· Th17 in COPD exacerbation
· Treg failure activity in COPD exacerbation
· Th17/Th1 in COPD
· Signaling pathways enrolled in Th17/Treg differentiation in asthma
· Signaling pathways enrolled in Th17/Treg differentiation in COPD