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Mustard is widely used in a variety of foods/food products to enhance the flavor and nutritional value that subsequently raise the risk of hypersensitivity reactions. Mustard allergy has been reported for many years and is increasing gradually especially in the areas where its consumption is comparatively higher, and it may be considered among the most important food allergies. A number of relevant clinical studies focused on mustard-induced allergic manifestations are summarized in the current review. In addition, the knowledge regarding the immunological as well as biochemical characteristics of mustard allergens that have been known till date and their cross-reactivity with other food allergens have also been discussed here. Notably, mustard may also be present as a hidden allergen in foods; therefore, it is important to recognize food products that may contain mustard as it may pose potential risk for the allergic individuals. Additionally, the better understanding of the underlying mechanism in mustard allergy is a prerequisite for the development of specific therapeutic procedures. Conclusively, mustard sensitivity should be routinely tested in patients with idiopathic anaphylaxis for the safety of the allergic patients.

Abstract Fibroblasts are structural cells primarily involved in tissue remodeling, but recent single-cell RNA sequencing (RNA-seq) transcriptomic data have highlighted their potential to display molecules linked to inflammation. The factors that drive such inflammatory transcriptional signatures found in patients are not clear. LIGHT (TNFSF14) is a cytokine that we previously suggested may be central to lung diseases exhibiting fibrosis and inflammation, including asthma and interstitial lung disease. With bulk RNA-seq, we then investigated the transcriptional activity of LIGHT in human pulmonary fibroblasts compared with interleukin (IL)-13 and IL-17, two other cytokines linked to lung disease. While all 3 cytokines individually induced unique and overlapping gene transcripts, when fibroblasts were stimulated with LIGHT and IL-13 they upregulated more inflammatory transcripts including CCL2, CCL26, CXCL2, CXCL3, CXCL5, CXCL6, IL32, CSF2, VCAM1, ICAM1, IL18R1, IL1RL1, TNFRSF12A, TNFRSF4, TNFRSF8, ITGA2, ITGA4, and ITGAV, and when stimulated with LIGHT and IL-17, inflammatory transcripts included CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL8, IL32, IL33, CSF2, TSLP, IL1A, IL6, IL18, VCAM1, ICAM1, IL18R1, IL1RL1, TNFSF4, TNFRSF4, TNFRSF8, ITGA2, ITGA4, and ITGAV. Furthermore, multiple cell cycle–related transcripts were induced with these combinations. Providing potential disease significance, portions of the fibroblast transcriptional signatures induced in vitro were found to be present in subsets of fibroblasts defined by single-cell RNA-seq isolated from patients with interstitial lung disease. This study therefore highlights the synergistic activities of LIGHT with other classical cytokines to regulate transcription in pulmonary fibroblasts and infers the involvement of LIGHT in shaping fibroblast phenotypes observed in chronic lung disease.