ILC2s are potent mucosal effector cells that participate in type 2 inflammatory responses. Stier et al. demonstrate that IL-33 negatively regulates CXCR4, mediating the egress of ILC2 lineage cells from the bone marrow for potential hematogenous trafficking.
Capsule Summary
GLP-1R signaling, an emerging anti-inflammatory therapeutic 59 target, 60 attenuated type 2-associated immunopathology in mice infected with a strain of RSV that was 61 isolated from a hospitalized infant with severe lower respiratory tract infection and bronchiolitis.
Purpose of Review: The purpose of this review is to describe the recent advances that have been made in understanding the protective role of PGE 2 in aspirin-exacerbated respiratory disease (AERD), known in Europe as non-steroidal anti-inflammatory drug (NSAID) exacerbated respiratory disease (N-ERD). Recent Findings: Decreased PGE 2 signaling through the EP 2 receptor in patients with AERD leads to an increase in leukotriene synthesis and signaling. Leukotriene signaling can directly activate group 2 innate lymphoid cells (ILC2) and mast cells, but it also increases production IL-33 and TSLP. These cytokines drive Th2 inflammation in a suspected feed-feed forward mechanism in patients with AERD. Summary: Recent discoveries concerning the role of PGE 2 in leukotriene synthesis and signaling in AERD, as well as downstream effects on ILC2 and mast cells, allow for a more comprehensive understanding of the pathogenesis of this disease. These discoveries also identify new paths of potential investigation and possible therapeutic targets for AERD.
phenome-wide association study (PheWAS); asthma; estrogen receptor α As adults, women have higher rates of asthma and allergic disease as well as increased asthma severity compared to men. 1 Pre or peri-menstrual worsening of asthma symptoms (PMA) were reported in 17% of women enrolled in the severe asthma research program, with 52% of these women with PMA having severe asthma. 2, 3 Further, use of birth control medications or hormone replacement therapy during peri or post-menopause was also linked to worsening of asthma in some women. 2,4 Mouse models of asthma showed estrogen signaling through estrogen receptor-alpha (ER-α), and not ER-β, increased allergic airway inflammation, mucus production, and/or airway hyperresponsiveness. 2,4 Collectively, these findings suggest a critical role for ER-α signaling in asthma pathogenesis.
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