TNF Superfamily and ILC2 Activation in Asthma

被引：3

作者：

Matsuyama, Takahiro ^{[1
,2
]}

Salter, Brittany Marie ^{[1
]}

Emami Fard, Nahal ^{[1
]}

Machida, Kentaro ^{[2
]}

Sehmi, Roma ^{[1
]}

机构：

[1] McMaster Univ, Dept Med, Resp Res Grp, Hamilton, ON L8S 4L8, Canada

[2] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Pulm Med, Kagoshima 8908520, Japan

来源：

BIOMOLECULES | 2024年 / 14卷 / 03期

关键词：

airway autoimmune response; eosinophilic asthma; GITRL; group 2 innate lymphoid cell; OX40L; RANKL; TL1A; TNF; TNFSF; INNATE LYMPHOID-CELLS; TUMOR-NECROSIS-FACTOR; SYSTEMIC-LUPUS-ERYTHEMATOSUS; CD4(+) T-CELLS; CYTOKINE 1A TL1A; NASAL POLYPS; CHRONIC RHINOSINUSITIS; DECOY RECEPTOR-3; TYPE-2; IMMUNITY; ALLERGIC-ASTHMA;

D O I：

10.3390/biom14030294

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Eosinophilic asthma is the most prevalent and well-defined phenotype of asthma. Despite a majority of patients responding to corticosteroid therapy and T2 biologics, there remains a subset that have recurrent asthma exacerbations, highlighting a need for additional therapies to fully ameliorate airway eosinophilia. Group 2 innate lymphoid cells (ILC2) are considered key players in the pathogenesis of eosinophilic asthma through the production of copious amounts of type 2 cytokines, namely IL-5 and IL-13. ILC2 numbers are increased in the airways of asthmatics and with the greatest numbers of activated ILC2 detected in sputa from severe prednisone-dependent asthma with uncontrolled eosinophilia. Although epithelial-derived cytokines are important mediators of ILC2 activation, emerging evidence suggests that additional pathways stimulate ILC2 function. The tumor necrosis factor super family (TNFSF) and its receptors (TNFRSF) promote ILC2 activity. In this review, we discuss evidence supporting a relationship between ILC2 and TNFSF/TNFRSF axis in eosinophilic asthma and the role of this relationship in severe asthma with airway autoimmune responses.

引用

页数：19

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