Background: Long non-coding RNAs (lncRNAs) are emerging regulators of pathophysiological processes in a variety of diseases including asthma. In this study, we reported the identification of lncRNA-AK007111 as an essential modulator of mast cell apoptosis and investigated its potential mechanism.
Methods: RNA-seq profiling and transcriptome sequencing technology were adopted to screen for differentially expressed genes. Transfection was done by small interfering RNAs (siRNAs) to down-regulate lncRNA-AK007111 and Modulator of apoptosis 1 (MOAP1). Starvation was used to induce apoptosis. The apoptotic rate was measured by flow cytometry. Western Blot was conducted to detect the expression of apoptosis-related proteins.
Results: LncRNA-AK007111 was highly expressed in IgE/Ag-mediated activation of mast cells. Down-regulation of LncRNA-AK007111 promoted apoptosis of mast cells. Down-regulation of MOAP1 attenuated apoptosis in mast cells induced by the down-regulation of lncRNA-AK007111.
Conclusion: LncRNA-AK007111 may be a potential regulator of mast cell apoptosis by interaction with MOAP1.
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http://dx.doi.org/10.1080/02770903.2025.2463974 | DOI Listing |
Ann Allergy Asthma Immunol
March 2025
University Hospital of Reims, Immunology Laboratory, Biology and Pathology Department, Reims, France; University of Reims Champagne-Ardenne, INSERM UMR 1250, Reims, France. Electronic address:
Tryptase is currently the most specific mast cell biomarker available in clinical laboratories. Tryptase levels in peripheral blood contribute to the diagnostic, prognostic and therapeutic evaluation of three clinical categories: (1) immediate hypersensitivity reactions including the life-threatening systemic form known as anaphylaxis, (2) clonal mast cell diseases and other myeloid malignancies, including as a biomarker for efficacy of chemotherapeutic agents targeting mast cell survival, and (3) hereditary α-tryptasemia (HαT), a genetic trait found in 4 - 8% of general population associated to increased risk of severe immediate hypersensitivity reactions. Rapidly evolving pathophysiology knowledge and management guidelines impact tryptase use in clinical practice, explaining the need for frequent updates.
View Article and Find Full Text PDFObjective: This study aimed to investigate the role of Raf kinase inhibitor protein (RKIP) in degranulation induced by echinococcal cyst fluid (EgCF) in bone marrow-derived mast cells (BMMCs).
Methods: Primary BMMCs were isolated and cultured from the femurs and tibias of RKIP gene knockout (KO) and wild-type (WT) C57BL/6 mice. EgCF-induced degranulation models were established for both groups.
J Immunol
February 2025
Herman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, United States.
Food allergy has had a rapid rise in prevalence, and thus it is important to identify approaches to limit the development of food allergy early in life. Because maternal dietary supplementation with α-tocopherol (α-T), an isoform of vitamin E, during pregnancy and nursing increases neonate plasma levels of α-T and can limit neonate development of other allergies, we hypothesized that α-T can limit development of food allergy. To assess this, male mice with mutations in their skin barrier genes (FT-/- mice) were mated with wild-type females that received a diet supplemented with α-tocopherol or a control diet.
View Article and Find Full Text PDFJ Immunol
March 2025
Department of Immunology, Institute of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Mast cells (MCs) play a central role in allergic immune responses. MC activation is regulated by several inhibitory immunoreceptors. The CD300 family members CD300a and CD300lf recognize phospholipid ligands and inhibit the FcεRI-mediated activating signal in MCs.
View Article and Find Full Text PDFJ Immunol
March 2025
Herman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, United States.
Food allergy can be life threatening and often develops early in life, especially in infants and children with atopic dermatitis. Food allergy is induced in neonatal mice with skin barrier mutations (Flaky Tail, FT+/- mice with filaggrin and mattrin gene mutations) by epicutaneous sensitization with co-exposures to the food allergen peanut extract (PNE), the environmental allergen Alternaria alternata (Alt), and detergent (4% SDS); oral PNE-challenge induces anaphylaxis. Sensitization in these neonates also induces eosinophil infiltration into the skin and elevates skin expression of eotaxins (CCL11 and CCL24).
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