The Initiation of Th2 Immunity Towards Food Allergens

Abstract

In contrast with Th1 immune responses against pathogenic viruses and bacteria, the incipient events that generate Th2 responses remain less understood. One difficulty in the identification of universal operating principles stems from the diversity of entities against which cellular and molecular Th2 responses are produced. Such responses are launched against harmful macroscopic parasites and noxious substances, such as venoms, but also against largely innocuous allergens. This suggests that the established understanding about sense and recognition applied to Th1 responses may not be translatable to Th2 responses. This review will discuss processes and signals known to occur in Th2 responses, particularly in the context of food allergy. We propose that perturbations of homeostasis at barrier sites induced by external or internal subverters, which can activate or lower the threshold activation of the immune system, are the major requirement for allergic sensitization. Innate signals produced in the tissue under these conditions equip dendritic cells with a program that forms an adaptive Th2 response.

Clinical Psoriasiform Dermatitis Following Dupilumab Use for Autoeczematization Secondary to Chronic Stasis Dermatitis

“…Skin stretch in chronic stasis dermatitis results in chronic barrier dysfunction, which supports an altered epidermal microenvironment that is primed for induction of a Th2-immune response, as described by Ellenbogen et al [7,14]. In the setting of this primed microenvironment, sensitization to autologous skin proteins occurs and subsequently promotes autoeczematization [3,14]. Thus, dupilumab was considered a reasonable treatment for our patient.…”

“…We treated our patient with dupilumab because we hypothesized that autoeczematization is driven by a Th2-mediated immune process involving the cytokines IL-4 and IL-13 whose functions are inhibited by dupilumab [6,13]. Skin stretch in chronic stasis dermatitis results in chronic barrier dysfunction, which supports an altered epidermal microenvironment that is primed for induction of a Th2-immune response, as described by Ellenbogen et al [7,14]. In the setting of this primed microenvironment, sensitization to autologous skin proteins occurs and subsequently promotes autoeczematization [3,14].…”

A compendium answering over 140 questions on COVID-19 and SARS-CoV-2

“…It is well-established that epithelial barrier defects and/or damage favor the development of Th2 immunity. 272,273 Increased hygiene, in general, as well as overexposure to epithelial barrier opening molecules, such as detergents, can promote the onset of allergic disease. 274 To date, there is no evidence linking the COVID-19 protective measures (gloves, hand-sanitizers,etc. )…”

Lipids and Fatty Acids in Human Milk: Benefits and Analysis

“…Th1 cells present important functions in cellular immunity against intracellular bacteria and protozoa, while Th2 cells mediate the response against extracellular parasites, as helminths, and participate in allergies [44]. Th17 cells apparently perform against different classes of pathogens and autoimmune conditions [45], and Treg cells perform regulating the inflammation, autoimmunity, allergy, infection, and tumors.…”