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Zoabi, Y.;  Levi-Schaffer, F.;  Eliashar, R. Mast Cells’ Role in Allergic Rhinitis. Encyclopedia. Available online: https://encyclopedia.pub/entry/39122 (accessed on 26 December 2025).
Zoabi Y,  Levi-Schaffer F,  Eliashar R. Mast Cells’ Role in Allergic Rhinitis. Encyclopedia. Available at: https://encyclopedia.pub/entry/39122. Accessed December 26, 2025.
Zoabi, Yara, Francesca Levi-Schaffer, Ron Eliashar. "Mast Cells’ Role in Allergic Rhinitis" Encyclopedia, https://encyclopedia.pub/entry/39122 (accessed December 26, 2025).
Zoabi, Y.,  Levi-Schaffer, F., & Eliashar, R. (2022, December 22). Mast Cells’ Role in Allergic Rhinitis. In Encyclopedia. https://encyclopedia.pub/entry/39122
Zoabi, Yara, et al. "Mast Cells’ Role in Allergic Rhinitis." Encyclopedia. Web. 22 December, 2022.
Mast Cells’ Role in Allergic Rhinitis
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This entry is adapted from the peer-reviewed paper 10.3390/biomedicines10102486

Allergic rhinitis (AR) is a common rhinopathy that affects up to 30% of the adult population. It is defined as an inflammation of the nasal mucosa, develops in allergic individuals, and is detected mostly by a positive skin-prick test. Mast cells (MCs) are innate immune system effector cells that play a pivotal role in innate immunity and modulating adaptive immunity, rendering them as key cells of allergic inflammation and thus of allergic diseases. MCs are typically located in body surfaces exposed to the external environment such as the nasal mucosa. Due to their location in the nasal mucosa, they are in the first line of defense against inhaled substances such as allergens. Immunoglobulin E (IgE)-dependent activation of MCs in the nasal mucosa following exposure to allergens in a sensitized individual is a cardinal mechanism in the pathophysiology of AR.

allergy allergic rhinitis rhinosinusitis mast cells

1. Introduction

Allergic rhinitis (AR) is a common allergic inflammatory rhinopathy that affects up 20 to 30% of adults and up to 40% of children worldwide [1]. Rhinitis is defined as inflammation of the lining of the nose; AR is the most widespread form of noninfectious rhinitis. Similar to other allergic diseases, AR is a result of an inordinate response of the immune system of a sensitized individual to innocuous substances known as allergens. [1][2].
AR is classically characterized by ongoing symptoms of rhinorrhea, nasal congestion and blockage, sneezing, and/or itching of the nose. These symptoms may significantly impact the patients’ quality of life, often interfering with sleep and contributing to poor academic and work performance [1].
Diagnosis of AR is usually made clinically when an individual experiences one or more of the hallmark symptoms mentioned above in response to allergen exposure. AR is classified as seasonal when the symptoms are experienced seasonally (i.e., pollen season) and perennial when the symptoms are experienced year-round. Another classification method is based on the length and recurrence of the symptoms. Intermittent AR (IAR) is defined as symptoms persisting for less than 4 days/week or less than 4 weeks, while persistent AR (PAR) is defined as symptoms lasting for more than 4 days/week for at least 4 weeks [3].
To confirm the diagnosis, sensitization to allergens is assessed by an allergy skin-prick test or an in vitro antigen-specific immunoglobulin E (IgE) test. Clinical allergy is evidenced by active symptoms upon allergen exposure in a sensitized individual. A unique condition is local allergic rhinitis, which is characterized by local IgE production in the nasal tissues whilst systemic allergy testing is negative [3].
Management of AR symptoms starts with allergen (i.e., house dust mite, animal dander, pollen, etc.) avoidance. AR symptoms are mainly controlled via pharmacotherapeutic agents. These include antihistamines, intranasal corticosteroids, leukotriene receptor antagonists (LTRAs), cromolyn sodium, biologics, and immunotherapy [4].
Exposure to inhaled allergens in a sensitized individual starts the cascade leading to the AR symptoms via activation of mast cells (MCs) lining the nasal mucosa through crosslinking of antigens to a specific IgE antibody bound to the surface of MCs, resulting in the release of MC mediators. The latter contribute to the immediate allergic response and to further recruitment and infiltration of immune cells to the site of inflammation, including eosinophils, B cells, and T cells. The primary T-cell response in AR is mediated by T-helper (Th2) cells. Th2 cells secrete cytokines such as interlukin-4 (IL-4) and interlukin-13 (IL-13), which drive further IgE production. This milieu of inflammatory cells and mediators contributes to the late and chronic phase response of allergic inflammation [5][6].
In addition to AR, MCs’ role is established in the pathogenesis of frequent comorbidities characterized by allergic inflammation such as atopic dermatitis (AD) and allergic asthma. To promote allergic inflammation, MCs interact with other inflammatory cells via soluble mediators and cell–cell contact. One of these interactions occurs through the allergic effector unit (AEU), where CD48 on MCs crosstalk with a 2B4 receptor on eosinophils, promoting an inflammatory outcome [7][8][9].
A differential diagnosis of AR includes other types of sinonasal diseases because symptoms may overlap. In fact, more than one type of rhinitis may coexist at the same time [3]. An example is rhinosinusitis, another rhinopathy that involves inflammation of the paranasal sinuses and is characterized by the presence of postnasal drip, facial pressure, and a reduction or loss in the ability to smell [1][10]. Chronic rhino sinusitis (CRS) is defined as the persistent symptoms of nasal obstruction, rhinorrhea, hyposmia, and facial pain for more than 12 weeks in combination with inflammatory signs confirmed by nasal endoscopy or by a computed tomography scan. Phenotypically, CRS is divided into two groups based on the presence or absence of nasal polyps: CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP) [3][10][11]. Emerging evidence further divides CRS into different endotypes within each phenotypic category to better adjust treatment and management protocols [12]. The endotype of CRSwNP in most patients is of the Type 2 inflammation and typically shows tissue eosinophils and MCs [10], a common feature bridging CRSwNP and AR.
Another condition associated with CRSwNP is aspirin-induced respiratory disease (AERD), which is defined as a triad of adult onset asthma, CRSwNP, and anaphylactic response to COX-1 inhibitors (i.e., NSAIDs). Activation of MCs by classical (IgE-mediated) and nonclassical pathways is crucial in the pathophysiology of AERD due to the secretion of a diverse array of inflammatory mediators that activate different Type 2 inflammatory pathways involved in AERD pathogenesis [13].
As demonstrated above, MCs are essential players in the development of allergic diseases, including AR.

2. Mast Cells’ Role in Allergic Inflammation

The allergic reaction consists of an early phase mediated by the release of inflammatory mediators from preformed granules of MCs and a late phase characterized by the influx of inflammatory cells, which are mostly modulated by MCs and their secreted mediators [10][11].
MCs are located in the major body surfaces exposed to the external environment. This includes the skin, where connective tissue MCs are primarily found; the epithelium of the gastrointestinal tract; and the respiratory tract, where mainly mucosal MCs are found. The content of the preformed granules divides MCs into two phenotypic subtypes: mucosal MCs producing only tryptase and connective tissue MCs producing tryptase, chymase, and carboxypeptidase [14].
Due to their strategic positioning in the exposed body linings and the stored granules laden with preformed mediators, MCs may respond to invading stimuli more rapidly than other tissue-resident immune cells [14][15], thus playing a cardinal role as the host’s first-line of defense against invading organisms [16].
FcεRI is a high-affinity IgE receptor found on the surface of MCs and basophils. Allergen crosslinking of the IgE-bound FcεRI receptors results in the release of preformed and newly synthesized mediators in a phasic fashion. A few seconds after activation, MCs degranulate and release the stored content of the preformed granules, which contain histamine, heparin, proteases, and TNFα [14].
In addition, arachidonic acid is freed from membrane phospholipids and de novo synthesized arachidonic acid–lipid metabolites—mainly prostaglandin D2, leukotriene LTC4/D4/E4, and LTB4—are also promptly released as part of the immediate MC response. [17][18] Later, a vast array of cytokines, chemokines, and growth factors are synthesized and released [14][16]. After degranulation, MCs can resynthesize their preformed mediators.
MCs promote the trafficking of immune cells to the site of infection or inflammation, making them an essential initiator of the inflammatory response. MCs recruit circulating eosinophils through direct secretion of eosinophil-attracting chemokines (i.e., eotaxins) and indirectly via secretion of histamine, inducing eotaxin secretion by endothelial cells [16].
MCs and eosinophils are the key effector cells in allergy and communicate with each other in a bidirectional manner in what is defined as the “Allergic Effector Unit”. This crosstalk is mediated by physical cell–cell contact through cell surface receptors/ligands and by released mediators, including specific granular factors, chemokines, cytokines, and their respective ligands. In the physical cell–cell crosstalk, CD48 on MCs and its high-affinity ligand, the 2B4 receptor on eosinophils, form a pivotal couple, initiating and maintaining this proinflammatory crosstalk [8][19].
Through complex cellular processes, MCs can influence the induction, amplitude, and function of the adaptive immune response. Via histamine secretion, MCs increase vessel permeability, aiding in the recruitment of adaptive cells to the site of inflammation [16].

References

  1. Hox, V.; Lourijsen, E.; Jordens, A.; Aasbjerg, K.; Agache, I.; Alobid, I.; Bachert, C.; Boussery, K.; Campo, P.; Fokkens, W.; et al. Benefits and harm of systemic steroids for short- and long-term use in rhinitis and rhinosinusitis: An EAACI position paper. Clin. Transl. Allergy 2020, 10, 1.
  2. Justiz Vaillant, A.A.; Vashisht, R.; Zito, P.M. Immediate Hypersensitivity Reactions. In StatPearls; StatPearls Publishing: Treasure Island, FL, USA, 2022. Available online: http://www.ncbi.nlm.nih.gov/books/NBK513315/ (accessed on 24 September 2022).
  3. Wise, S.K.; Lin, S.Y.; Toskala, E.; Orlandi, R.R.; Akdis, C.A.; Alt, J.A.; Azar, A.; Baroody, F.M.; Bachert, C.; Canonica, G.W.; et al. International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis: ICAR: Allergic Rhinitis. Int. Forum. Allergy Rhinol. 2018, 8, 108–352.
  4. Akhouri, S.; House, S.A. Allergic Rhinitis. In StatPearls; StatPearls Publishing: Treasure Island, FL, USA, 2021. Available online: http://www.ncbi.nlm.nih.gov/books/NBK538186/ (accessed on 7 November 2021).
  5. Di Lorenzo, G.; Mansueto, P.; Melluso, M.; Candore, G.; Colombo, A.; Pellitteri, M.E.; Drago, A.; Potestio, M.; Caruso, C. Allergic rhinitis to grass pollen: Measurement of inflammatory mediators of mast cell and eosinophils in native nasal fluid lavage and in serum out of and during pollen season. J. Allergy Clin. Immunol. 1997, 100, 832–837.
  6. Small, P.; Keith, P.K.; Kim, H. Allergic rhinitis. Allergy Asthma Clin. Immunol. 2018, 14, 51.
  7. Puzzovio, P.G.; Levi-Schaffer, F. Latest Progresses in Allergic Diseases Biomarkers: Asthma and Atopic Dermatitis. Front. Pharmacol. 2021, 12, 747364.
  8. Gangwar, R.S.; Pahima, H.; Puzzovio, P.G.; Levi-Schaffer, F. Update on Eosinophil Interaction with Mast Cells: The Allergic Effector Unit. In Eosinophils; Walsh, G.M., Ed.; Springer: New York, NY, USA, 2021; pp. 221–242.
  9. Pedersen, C.J.; Uddin, M.J.; Saha, S.K.; Darmstadt, G.L. Prevalence of atopic dermatitis, asthma and rhinitis from infancy through adulthood in rural Bangladesh: A population-based, cross-sectional survey. BMJ Open 2020, 10, e042380.
  10. Fokkens, W.J.; Lund, V.J.; Hopkins, C.; Hellings, P.W.; Kern, R.; Reitsma, S.; Toppila-Salmi, S.; Bernal-Sprekelsen, M.; Mullol, J.; Alobid, I.; et al. European Position Paper on Rhinosinusitis and Nasal Polyps 2020. Rhinol. Off. Organ Int. Rhinol. Soc. 2020, 58 (Suppl. S29), 1–464.
  11. Gelardi, M.; Giancaspro, R.; Cassano, M.; Ribatti, D. The Underestimated Role of Mast Cells in the Pathogenesis of Rhinopathies. Int. Arch. Allergy Immunol. 2022, 183, 153–159.
  12. Helman, S.N.; Barrow, E.; Edwards, T.; DelGaudio, J.M.; Levy, J.M.; Wise, S.K. The Role of Allergic Rhinitis in Chronic Rhinosinusitis. Immunol. Allergy Clin. North Am. 2020, 40, 201–214.
  13. Kuruvilla, M.E.; Vanijcharoenkarn, K.; Levy, J.M. The Role of Mast Cells in Aspirin-Exacerbated Respiratory Disease (AERD) Pathogenesis: Implications for Future Therapeutics. J. Asthma Allergy 2020, 13, 463–470.
  14. Krystel-Whittemore, M.; Dileepan, K.N.; Wood, J.G. Mast Cell: A Multi-Functional Master Cell. Front. Immunol. 2016, 6, 620.
  15. Kim, M.J.; Je, I.G.; Song, J.; Fei, X.; Lee, S.; Yang, H.; Kang, W.; Jang, Y.H.; Seo, S.Y.; Kim, S.H. SG-SP1 Suppresses Mast Cell-Mediated Allergic Inflammation via Inhibition of FcεRI Signaling. Front. Immunol. 2020, 11, 50.
  16. Katsoulis-Dimitriou, K.; Kotrba, J.; Voss, M.; Dudeck, J.; Dudeck, A. Mast Cell Functions Linking Innate Sensing to Adaptive Immunity. Cells 2020, 9, 2538.
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  19. Zoabi, Y.; Rahimli Alekberli, F.; Minai-Fleminger, Y.; Eliashar, R.; Levi-Schaffer, F. CD48 Expression on Eosinophils in Nasal Polyps of Chronic Rhinosinusitis Patients. Int. Arch. Allergy Immunol. 2021, 182, 962–970.
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Subjects: Allergy
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : Yara Zoabi ,
Francesca Levi-Schaffer
, Ron Eliashar
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Update Date: 27 Dec 2022
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