Helper T cells and chemokines in elderly asthma - Mechanisms of airway inflammation and remodeling: A review.

Elderly bronchial asthma is a heterogeneous, often non-atopic disorder characterized by airway inflammation and remodeling influenced by age-related immune dysregulation. This review aims to elucidate the roles of helper T cells (Th cells) and chemokine networks in driving elderly asthma and to emphasize implications for precise diagnosis and targeted therapy. We performed a narrative synthesis of studies from PubMed and Web of Science (January 2020-December 2025) utilizing the keywords "elderly asthma," "helper T cells," "chemokines," "airway inflammation," and "immunosenescence," focusing on human cohorts aged ≥65 years and aged animal models. The literature reveals that the pathogenesis of elderly asthma is characterized by an imbalance between T helper 1 (Th1) and T helper 2 (Th2) responses, enhanced T helper 17 (Th17) activity, and diminished regulatory T cell (Treg) function, changes that are exacerbated by immunosenescence. Key chemokine axes-including C-C motif chemokine ligand 11 (CCL11)/C-C chemokine receptor 3 (CCR3), C-X-C motif chemokine ligand 8 (CXCL8)/C-X-C chemokine receptor 1 (CXCR1) and C-X-C chemokine receptor 2 (CXCR2), C-C motif chemokine ligand 2 (CCL2)/C-C chemokine receptor 2 (CCR2), C-X3-C motif chemokine ligand 1 (CX3CL1)/C-X3-C chemokine receptor 1 (CX3CR1), and stromal cell-derived factor 1 (SDF-1)/C-X-C motif chemokine ligand 12 (CXCL12)/C-X-C chemokine receptor 4 (CXCR4)-facilitate the recruitment of eosinophils, neutrophils, and monocytes/macrophages, thereby sustaining airway inflammation and remodeling. Overall, Th-chemokine circuits represent actionable targets for biomarker-guided, personalized treatment; however, further mechanistic and clinical validation studies specific to the elderly population are crucial for effective translation into practice.