Bronchus-associated lymphoid tissue and immune-mediated respiratory diseases
Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald in Principles of Mucosal Immunology, 2020
There are several mechanisms that downregulate allergic inflammation. For example, allergen-specific Treg cells can downregulate the function of TH2 cells and other airway effector cells, such as ILC2s. These Treg cells are thought to be very important in regulating allergic diseases including asthma, and atopic individuals are thought to have a relative deficiency in these cells, either in terms of numbers or function of these cells. There are several subsets of Treg cells, including natural Treg cells, which develop in the thymus and are important in recognizing self-antigens and preventing autoimmunity, and Treg cells that develop in the periphery in response to nominal antigens and allergens including adaptive Treg cells and TR1 cells. TH1 cells have also been thought to inhibit the development of TH2 cells and may play a role in preventing the development of allergy. This may occur, for example, in nonallergic individuals, where allergen-specific TH2 cells may not develop or may be deleted, possibly due to suppression from IFN-γ secreted by TH1 cells.
Expression of Cell Adhesion Molecules in Allergic Disorders of the Eye
Bruce S. Bochner in Adhesion Molecules in Allergic Disease, 2020
Allergic conjunctivitis is a common disease characterized by typical clinical features caused both by mediator release (mainly histamine) from activated mast cells and by an inflammatory reaction consequent to cytokines released by inflammatory cells. The main event in allergic inflammation is the migration of inflammatory cells (such as eosinophils, neutrophils, lymphocytes and monocytes) to the site of the allergic reaction. This requires adhesion to the endothelium and, next, locomotion to the target tissue, each stage of the process depending on cell–cell and cell–matrix adhesion (1) (Fig. 1). Several mediators of the acute allergic reaction are able to induce/increase expression of selectins on endothelium and leukocytes, allowing leukocyte migration (“rolling-over”)· The further stages are firm adhesion, de-adhesion, and transmigration through the blood vessel wall to the site of inflammation; these are regulated by integrins (leukocyte function-associated antigen [LFA]-1, very late activation antigen [VLA]-4) and their ligands (interecellular adhesion molecule [ICAM]-1, vascular cell adhesion molecule [VCAM]-1) in addition to other unknown factors (2). Thus, β1 integrins and cytoadhesins allow cell–matrix adhesion (3). The growing importance of adhesion mechanisms prompted Meuer and colleagues to postulate that we can no longer evaluate inflammation by simply looking at the mononuclear cell infiltrate but instead we should consider many mediators and adhesion receptors, the “real parameters” of the inflammatory process (2).
In Vivo Models of Smooth Muscle Growth
Alastair G. Stewart in AIRWAY WALL REMODELLING in ASTHMA, 2020
A number of potentially interesting candidate growth-promoting substances have been identified by in vitro testing. Of particular interest are those associated with allergic inflammation since allergy is one of the best-characterised mechanisms by which asthma is induced. Thromboxane, endothelin, cysteinyl-leukotrienes, and histamine have been shown to have mitogenic activity.24–26 The evidence for the synthesis and release of these substances in asthma is solid. The precise mechanisms by which such bronchoconstrictive mediators stimulate smooth muscle proliferation in vitro appear to be complex and to involve interactions among them. For example, endothelin causes phospholipase A2 activation and thromboxane synthesis in cultured rabbit airway smooth muscle cells. Thromboxane, in turn, triggers cysteinyl-leukotriene synthesis.24 The mitogenic activity of endothelin seems to mediated by leukotriene and so is indirect.
Allergen immunotherapy: progress and future outlook
Published in Expert Review of Clinical Immunology, 2023
Lara Šošić, Marta Paolucci, Stephan Flory, Fadi Jebbawi, Thomas M. Kündig, Pål Johansen
Allergic inflammation can be classified as a hypersensitivity reaction to environmental antigens according to Coombs and Gell [28], orchestrated by IgE antibodies (type-1-hypersensitivity reaction) or T cells (type-4-hypersensitivity reaction); type 2 and type 3 reactions are orchestrated by IgG or IgM antibodies or by immune complexes that also involve immune complexes. IgE-dependent allergies are also called immediate-type allergic reactions, or anaphylactic hypersensitivity reactions, as the onset is generally in the first minutes after exposure [29]. Examples of immediate-type allergic reactions include allergic rhinoconjunctivitis (ARC), allergic asthma, and anaphylaxis. Type 4 or delayed-type allergic reactions, e.g. contact dermatitis (CD), can manifest several days after exposure, and is not to be confused with the late-phase, but IgE-mediated type-1 allergic reaction that can occur several hours after allergen exposure due to release of additional mediators from mast cells and basophils [29].
Updates in the diagnosis and practical management of allergic rhinitis
Published in Expert Review of Clinical Pharmacology, 2023
Chiara Trincianti, Maria Angela Tosca, Giorgio Ciprandi
Allergic rhinitis is the most frequent IgE-mediated disease and recognizes a type 2 phenotype characterized by eosinophilic infiltrate and allergen exposure-dependent inflammation [68]. Although it is well known, and several guidelines have established precise diagnostic criteria and treatment protocols, controlling allergic rhinitis is not optimal in most patients [69]. In this regard, an attracting issue concerns the availability of simple biomarkers measuring type 2 inflammation. That is, it is well known that allergic inflammation may be present despite symptoms, such as the concept of minimal persistent inflammation [70]. In other words, the possibility of documenting the presence and severity of type 2 inflammation can modulate the use of antiallergic treatments. In fact, patients prefer to take drugs on demand, but this approach could be inappropriate, mainly if inflammation persists also without overt symptoms. In this regard, a trivial blood cell count is recommended for getting a rough idea of the degree of type 2 inflammation [71]. However, it remains desirable to also have biomarkers that can predict the response to AIT and define the efficacy so that treatment can be discontinued judiciously.
Allergy accelerates the disease progression of chronic rhinosinusitis
Published in Acta Oto-Laryngologica, 2019
Keng-Chung Shen, Yi-Tsen Lin, Chih-Feng Lin, Chin-Hao Chang, Te-Huei Yeh
All these evidence indicated that allergy is an accelerating factor of the disease progression resulting in earlier urge for surgical intervention. Allergies and CRS inflammation may coexist and have a close relationship. Mechanistically, allergic inflammation of the nose changes the integrity of the nasal mucosa and damages the nasal ciliary function. Stasis of nasal secretion may block ostia drainage from the sinus and cause sinus infection [14]. The major allergen in our study was HDM. It has been reported that perennial allergies, especially HDM over seasonal allergens, may potentially contribute to the development of rhinosinusitis [9]. Different from other aeroallergens, exposure to the HDM allergen not only induces the immune reactions of epithelial cells but also impairs the mucosal integrity of the epithelial lining [8]. In our study, the mean age at the time of surgery in the allergic group was significantly younger than that of the non-allergic group. It implies that allergies in CRS patients have detrimental influence of the nasal mucosa because of allergic inflammation and accelerate the disease progression.