T_H17 cells and corticosteroid insensitivity in severe asthma

Area of Science:

• Immunology
• Pulmonology
• Pathology

Background:

• Asthma is classified into type 2 (T2) eosinophilic and non-T2 neutrophilic phenotypes.
• Non-T2 asthma and late-onset T2 asthma often exhibit poor response to standard anti-inflammatory therapies, leading to significant morbidity.
• Elevated T helper 17 (T_H17) cell responses are increasingly linked to non-T2 asthma and corticosteroid insensitivity.

Purpose of the Study:

• To review the pathological role of T_H17 cells in corticosteroid-insensitive severe asthma.
• To identify potential therapeutic targets for treating this specific asthma endotype.

Main Methods:

• Literature review focusing on T_H17 cell involvement in severe asthma.
• Analysis of immune responses and inflammatory pathways in corticosteroid-resistant asthma.
• Exploration of therapeutic strategies targeting T_H17-mediated inflammation.

Main Results:

• T_H17 cells, producing IL-17A and IL-17F, are implicated in neutrophilic inflammation and airway remodeling in severe asthma.
• These cells contribute to subsets of asthma that are insensitive to corticosteroid treatment.
• The T_H17 pathway represents a potential mechanism driving therapeutic failure in certain severe asthma cases.

Conclusions:

• T_H17 cells play a significant pathological role in corticosteroid insensitivity within severe asthma.
• Targeting T_H17 cells and their associated cytokines (IL-17A, IL-17F) presents a promising therapeutic avenue for severe, corticosteroid-resistant asthma.
• Further research into T_H17-targeted therapies is warranted for this challenging asthma endotype.