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Group 3 Innate Lymphoid Cells: A Potential Therapeutic Target for Steroid Resistant Asthma.
Clin Rev Allergy Immunol
December 2024
Division of Allergy and Clinical Immunology, The Johns Hopkins Asthma & Allergy Center, Johns Hopkins University School of Medicine, 5501 Hopkins Bayview Circle, Room 3B.71, Baltimore, MD, 21224, USA.
Asthma is a chronic airway inflammatory disease that affects millions globally. Although glucocorticoids are a mainstay of asthma treatment, a subset of patients show resistance to these therapies, resulting in poor disease control and increased morbidity. The complex mechanisms underlying steroid-resistant asthma (SRA) involve Th1 and Th17 lymphocyte activity, neutrophil recruitment, and NLRP3 inflammasome activation.
View Article and Find Full Text PDFCMV IgG in the blood is not associated with hepatitis but correlates with poor outcomes in immunotherapy treated melanoma patients.
Cancer Immunol Immunother
January 2025
Department of Dermatology and National Center for Tumor Diseases (NCT), Medical Faculty Heidelberg, NCT Heidelberg, a partnership between DKFZ and University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany.
Cytomegalovirus (CMV) infection or reactivation in immune-compromised individuals can lead to a wide range of severe complications including hepatitis. However, its relation with immune checkpoint inhibitors (ICIs) induced hepatitis (ICI-hepatitis) and tumor responses in advanced melanoma patients remains unclear. Hundred and ninety metastatic cutaneous melanoma patients (mCM) who received ICI treatment, with CMV IgG or IgM information available at baseline, were included in the study (Cohort 1).
View Article and Find Full Text PDF[Recent progress in the treatment of non-T2 asthma].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
December 2024
Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Guilin Medical College, Guilin 541000, China *Corresponding author, E-mail:
Non-T2 asthma, also known as non-eosinophilic asthma or low T2 asthma, does not have markers of type 2 inflammation and is often associated with hormone insensitivity and severe asthma. This article reviews the progress in drug therapy for non-T2 asthma.
View Article and Find Full Text PDFThe Role of WNT5a and TGF-β1 in Airway Remodelling and Severe Asthma.
Allergy
January 2025
Department of Respiratory Sciences, College of Life Sciences, and NIHR Biomedical Research Centre (Respiratory Theme), Glenfield Hospital, Leicester, UK.
Background: Airway remodelling is a feature of severe asthma with airway epithelial damage observed frequently. We evaluated the role of WNT5a and TGF-β in asthmatic airway biopsies and in sputum and bronchial brushings assessed their role in remodelling.
Methods: WNT5a and TGF-β protein expression were assessed in the lamina propria epithelium of people with asthma (GINA 1-3, n-8 and GINA 4-5, n-14) and healthy subjects (n-9), alongside relevant remodelling markers.
A randomized comparison of bencycloquidium bromide, mometasone furoate and a combination for persistent allergic rhinitis.
J Allergy Clin Immunol Pract
December 2024
Department of Allergy, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China; Department of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China; Beijing Laboratory of Allergic Diseases and Beijing Key Laboratory of Nasal Diseases, Beijing Institute of Otolaryngology, Beijing 100005, China. Electronic address:
Background: Moderate to severe persistent allergic rhinitis (AR) poses a substantial socioeconomic burden.
Objectives: We aimed to establish the superiority of bencycloquidium bromide (BCQB) nasal spray and BCQB combined with mometasone furoate nasal spray (MFNS) over MFNS alone in adults with moderate-to-severe persistent AR.
Methods: In this multicentre, randomised controlled clinical trial (NCT05038202), adults with moderate-to-severe persistent AR were randomly assigned to receive the BCQB, MFNS, or a combination treatment, for 4-week periods.
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