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Impaired calcium influx underlies skewed T helper cell differentiation in children with IgE-mediated food allergies.
Allergy
September 2024
Department of Allergy and Immunology, The Children's Hospital at Westmead, Westmead, New South Wales, Australia.
Background: Reasons for Th2 skewing in IgE-mediated food allergies remains unclear. Clinical observations suggest impaired T cell activation may drive Th2 responses evidenced by increased atopic manifestations in liver transplant patients on tacrolimus (a calcineurin inhibitor). We aimed to assess differentiation potential, T cell activation and calcium influx of naïve CD4 T cells in children with IgE-mediated food allergies.
View Article and Find Full Text PDFAdvances and novel developments in mechanisms of allergic inflammation.
Allergy
December 2020
Sean N. Parker Center for Allergy and Asthma Research at Stanford University, Stanford University, Stanford, CA, USA.
In the past decade, research in the molecular and cellular underpinnings of basic and clinical immunology has significantly advanced our understanding of allergic disorders, allowing scientists and clinicians to diagnose and treat disorders such as asthma, allergic and nonallergic rhinitis, and food allergy. In this review, we discuss several significant recent developments in basic and clinical research as well as important future research directions in allergic inflammation. Certain key regulatory cytokines, genes and molecules have recently been shown to play key roles in allergic disorders.
View Article and Find Full Text PDFImmunoglobulin E sialylation regulates allergic responses.
Immunol Cell Biol
September 2020
Division of Infectious Diseases, Department of Medicine, Stanford University, Stanford, CA, USA.
Shade et al. demonstrate that people with peanut allergies produce IgE antibodies that are enriched for sialic acid-containing glycoforms. The sialylated IgE triggered significantly more degranulation by basophils and mast cells, suggesting intrinsic functional differences between IgEs from allergic and nonallergic subjects.
View Article and Find Full Text PDFIL-33 Is a Cell-Intrinsic Regulator of Fitness during Early B Cell Development.
J Immunol
September 2019
Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232;
IL-33 is an IL-1 family member protein that is a potent driver of inflammatory responses in both allergic and nonallergic disease. This proinflammatory effect is mediated primarily by extracellular release of IL-33 from stromal cells and binding of the C-terminal domain of IL-33 to its receptor ST2 on targets such as CD4 Th2 cells, ILC2, and mast cells. Notably, IL-33 has a distinct N-terminal domain that mediates nuclear localization and chromatin binding.
View Article and Find Full Text PDFFemale and male mouse lung group 2 innate lymphoid cells differ in gene expression profiles and cytokine production.
PLoS One
December 2019
Terry Fox Laboratory, British Columbia Cancer, Vancouver, British Columbia, Canada.
Epidemiological studies have shown sex differences in prevalence of non-allergic asthma. Recent reports demonstrated negative effects of androgen signaling on group 2 innate lymphoid cells (ILC2s), explaining a potential mechanism behind sex bias in asthma prevalence. To further understand sex-related differences in ILC2 functions and ILC2 intrinsic or lung environmental mechanisms behind it, we have investigated the effects of sex and age on lung ILC2 function, the amounts of ILC2-activating cytokines in the lung and gene expression profiles of male and female ILC2s.
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