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Murdaca, G.; Allegra, A.; Tonacci, A.; Musolino, C.; Ricciardi, L.; Gangemi, S. Mast Cells and Vitamin D Status. Encyclopedia. Available online: (accessed on 17 June 2024).
Murdaca G, Allegra A, Tonacci A, Musolino C, Ricciardi L, Gangemi S. Mast Cells and Vitamin D Status. Encyclopedia. Available at: Accessed June 17, 2024.
Murdaca, Giuseppe, Alessandro Allegra, Alessandro Tonacci, Caterina Musolino, Luisa Ricciardi, Sebastiano Gangemi. "Mast Cells and Vitamin D Status" Encyclopedia, (accessed June 17, 2024).
Murdaca, G., Allegra, A., Tonacci, A., Musolino, C., Ricciardi, L., & Gangemi, S. (2023, June 02). Mast Cells and Vitamin D Status. In Encyclopedia.
Murdaca, Giuseppe, et al. "Mast Cells and Vitamin D Status." Encyclopedia. Web. 02 June, 2023.
Mast Cells and Vitamin D Status

The immune system is made up by an extremely composite group of cells, whose regulated and harmonious activity is fundamental to maintain health. The mast cells are an essential effector of inflammatory response which is characterized by a massive release of mediators accumulated in cytoplasmic secretory granules. However, beyond the effects on immune response, mast cells can modify bone metabolism and are capable of intervening in the genesis of pathologies such as osteoporosis and osteopenia. Vitamin D is recognized to induce changes in bone metabolism, but it is also able to influence immune response, suppressing mast cell activation and IgE synthesis from B cells and increasing the number of dendritic cells and IL-10-generating regulatory T cells. 

mast cell vitamin D allergy osteoporosis mastocytosis

1. Introduction

Allergies and osteoporosis are disorders with a great incidence in the overall population and constitute a real danger for community health [1]. Furthermore, several experimental findings have shown a close correlation between the two conditions. Many allergic conditions such as asthma, eczema, chronic respiratory pathologies, and pollen allergy are correlated with fracture risk [2][3], while increased percentages of bone diseases are described in patients with allergic syndromes, in both adults and children [4].
For instance, the connection of asthma with osteoporosis is well established, although up until the recent past, most studies attributed the correlation to the unfavorable effect exerted by protracted steroid therapies on the bone. New findings have instead highlighted the responsibility of the systemic inflammation present in allergic diseases in the osteoporosis onset [5][6], and a correlation between allergies and osteoporosis has been also demonstrated in patients suffering from chronic rhinosinusitis [5].
As for the mechanisms capable of connecting bone diseases and allergic pathologies, a correlation between bone and immune effectors is now recognized, and several relevant communications are seen in the bone milieu, such as the enrolment and growth of T cells [7]. It is also known that bone cells and immune effectors originate from the same precursors in the bone marrow (BM) and that the same compounds can control bone cell’s proliferation and activity, immune response, and haematopoiesis [8]. Moreover, the destiny of hematopoietic stem cells is regulated by autocrine and paracrine systems, these phenomena being controlled by bone tissue, osteoclasts, osteoblasts, and immune effectors interacting with each other. Several blood cells, including basophils, mast cells, eosinophils, lymphocytes, and neutrophils contribute to this composite crosstalk, which causes the allergic inflammation. This condition can generate cytokines, reactive oxygen species, chemokines, and lipids leading to a plethora of effects which are able to elicit bone modifications [9].
For instance, the Cysteinyl leukotrienes (CysLTs) are a group of lipid mediators originating from arachidonic acid [10]. The CysLTs receptor (CysLTR1) has a relevant effect in the onset of asthma, and montelukast is a CysLTR1 antagonist employed for the therapy of asthma. An experimentation demonstrated that montelukast effectively inhibits RANKL-caused osteoclast generation and bone damage in vivo [11].
However, one of the main actors of this communication is represented by mast cells (MCs), which play an extremely important role both in the onset of allergic pathologies and in diseases of bone metabolism, and the effect exerted by vitamin D on these cells could constitute a unifying element for apparently heterogeneous alterations (Figure 1).
Figure 1. Possible effects of vitamin D on the onset of allergic diseases and on bone metabolism.

2. General Considerations on Vitamin D

Vitamin D3 (cholecalciferol) is mainly produced in the epidermis when pre-vitamin D3, the compound originating from 7-dehydrocholesterol after ultraviolet-B (UVB) irradiation of the skin, undertakes thermal isomerization. The transformation of vitamin D3 to its active form 1α,25(OH)2D3, is due to a sequence of hydroxylation procedures, initially caused by liver cytochrome P450 proteins, which can produce the transitional metabolite, 25OHD3 and, subsequently, 25-hydroxyvitamin 1αhydroxylase in the renal tubule to generate 1α,25(OH)2D3. This compound operates by joining to the vitamin D receptor (VDR), which provokes the enrolment of the retinoid X receptor, to generate a heterodimeric structure that affects vitamin D (VD) response factors in the promoter areas of genes. According to the concurrent joining of nuclear co-stimulators or coinhibitory factors, the complex can operate as a ligand-dependent stimulator or an inhibitor of gene transcription [12][13][14].
VD deficit has been recognized as a main health problem, which is constantly more prevalent [15]. Even though there is no agreement on the ideal concentrations of 25(OH)D, a VD deficit is identified when concentrations of VD less than 50 nmol/L occurs [16].
All organs and cells feature a VDR, including immune and bone cells, skin, brain, gonads, and heart cells. A reduction on VD levels may change the activity of these tissues. This factor explains the extensive effects of VD and justifies why a decrease in VD levels has been related with several different chronic pathologies. Regarding the subject of analysis, VD has a main action in calcium/phosphate equilibrium and provokes profound consequences on the bone metabolism, beyond having a pivotal effect as an anti-inflammatory mediator. VD deficit increases the possible occurrence of osteoporosis and several other pathologies that present alterations of bone metabolisms, such as hematological malignancies, bone marrow transplantation, inflammatory bowel diseases, and endocrinological diseases [17].
Furthermore, VD modifies relevant activities of the immune system and may change the development of immune-mediated diseases, including allergies and autoimmune diseases. VD operates by steering T lymphocytes to Th2 polarization and blocking Th1 and Th17 function and growth. The stimulation of T regulatory cells (Treg) might be its principal immunological function [18]. Numerous reports indicate a VD favorable action on diseases correlated to hyperstimulation of Th1 cells, such as psoriasis, multiple sclerosis, rheumatoid arthritis, and type 1 diabetes [19]. In allergic pathologies, where Th2 cells have a central effect, VD has a more complex effect. However, several experimentations displayed a positive action on the progression of allergic conditions, although the causal mechanisms have not always been fully explained [20].

3. Vitamin D and Allergies

Epidemiological data have also indicated the existence of a correlation of VD reduction with several conditions including allergies. The relationship of VD deficit and asthma is described, and several studies stated a connection with disease course worsening and a worse outcome. It is possible that VD, by improving the inflammation state, can decrease the rate of respiratory sepsis and exacerbations [21][22]. Although the correlation between VD concentrations and allergies has been questioned in a cross-sectional analysis including only allergic subjects [23], an effect of VD in the eosinophil activities is demonstrated. VD decreases the immunoglobulin E (IgE) synthesis and increases expression of interleukin-10 [24].
Other studies confirmed the correlation of VD with allergic diseases [25][26]. Some experimentations were conducted to evaluate the effect of VD in chronic urticaria (CU), allergic contact dermatitis (ACD), and atopic dermatitis (AD) [27][28], and a relationship between VD deficit with ACD and AD severity was reported [29][30], while a work proved a relevant difference between CSU subjects and controls in blood concentrations of VD [31].
An interesting analysis has reported that the period of birth and UBV exposure is correlated to the incidence of food allergy (FA). The concentrations of VD generated from skin after UBV might justify this correlation, while maternal or VD deficiency occurring in the first years of life also remarkably predisposed the FA onset in an experimental animal model [32][33].
Still in the framework of FA, employing results obtained from a nutritional investigation, it was stated that allergic sensitization to several different allergens, including foods, was more frequent in young subjects with a 25(OH)D deficit, while no relevant correlation was found between VD concentrations and FA in adults [34]. Although, a different study performed by Beak et al. reported that reduced concentrations of VD might be correlated to polysensitization of nutrition allergens [35]. Therefore, the correlation between VD and FA is still debatable.
However, other findings support the existence of a tight relationship between VD and allergies, and the beneficial action of VD supplementation in CSU subjects has been proved in several small clinical experimentations [36][37]. In a prospective research, patients suffering from CSU were treated with low or high vitamin D3 supplement for 12 weeks. All patients demonstrated a significantly decreased urticaria severity score, but the reduction was greater in patients treated with a higher VD dosage at week six. The medication score was also remarkably decreased, without distinguishing the two groups [38].
Some researches report in the table some of the works that confirm the existence of a relationship between VD levels and allergic diseases [27][34][37][38][39][40][41][42][43][44][45][46], (Table 1).
Table 1. Effects of Vitamin D on allergies.

4. Vitamin D and Immune Response

Several other relevant connections have been reported between blood cells, both lymphoid and myeloid cells, and VD concentrations. For instance, B cells can produce VD [47], while naïve T cells grown with VD-primed B cells demonstrated decreased proliferation, provoked by the presence of CD86 on B cells [48].
As reported above, VD has a main effect in IgE provoked responses, and it was displayed that IgE serum concentrations are enhanced in VDR-knockout animals [49]. Similarly, VD reduced IgE generation by B lymphocytes, and the IgE reaction in a type 1 allergy animal model can be altered by employing a VDR agonist [50].
Furthermore, VD can act on other effectors of the immune system, and Szeles et al. have stated that an increase of 25(OH)D provokes dendritic cells (DCs) to switch on VD related genes, and stimulation of VDRs by VD resets the DCs to turn out to be tolerogenic [51]. Remarkably, when VD was added to monocyte, DCs were less mature, presenting different amounts of MHC class II molecules and transforming CD4+ T cells to IL-10-producing Tregs [52]. Thus, VD not only produces a repressive consequence on DC development but also instructs the DCs to stimulate Tregs to generate IL-10 [53]. Almerighi et al. have confirmed that VD reduces inflammation caused by CD40L and increases IL-10 generation by CD4+ T cells [54], stimulating the expansion of Tregs presenting forkhead box P3 and cytotoxic T-lymphocyte-associated protein 4 [55] (Figure 2).
Figure 2. Effects of Vitamin D on immune effectors.

5. Vitamin D and Mast Cells: Effects on Allergies

VD also seems to have a role in allergic diseases and bone pathologies mediated by Th2 cells, via the IL-31/IL-33 axis [56], which is another new area to investigate the intricate overlapping mechanisms that connect allergies and osteoporosis. IL-31 is a cytokine that is able to provoke inflammation, which was proposed as a marker of tissue remodeling and different allergic and immunologic pathologies [56]. It is released by Th2 cells and, in smaller amounts, also by DCs and MCs. IL-31 stimulates eosinophils and fibroblasts, and its receptor is present in skin and endothelium. It is correlated with the onset of itch and chronic skin inflammation. An increased amount of IL-31 was reported in the skin and serum of patients suffering from AD, CSU, contact dermatitis, prurigo nodularis, cutaneous lymphoma, and mastocytosis, correlating with disease severity [57][58]. It is therefore interesting that increased concentrations of serum IL-31 are present in postmenopausal women with a reduction of bone mineral density (BMD), although there is no correlation with the degree of osteoporosis [59].
Mast cells are myeloid cells that transfer into practically all tissues, where they perform tissue–specialized evolution. They are a constituent of connective tissue and are numerous in areas such as the gut, mucous membranes, and skin [60][61], near to vessels and nerves [62]. This tactical settlement and the mediators generated from MCs explain their ability to quickly modify their milieu, and to control other forms of inflammatory cells [63][64].
MCs have a relevant effect in immediate hypersensitivity reactions, but also in late phase responses and innate immune response, by generating a large number of different mediators either from storage places in their granules or by delivering substances which are able to regulate different signaling pathways after adequate stimulation [65].
In allergic reactions, IgE joins to the IgE receptor to produce complexes on the cellular membrane of MCs to induce MC sensitization. After new contact with particular antigens, they combine with the IgE/FceRI complex to stimulate MCs [66]. Moreover, MCs also can be stimulated by temperature modifications and microbial factors [67][68].
However, beyond allergic diseases, MCs are involved in the genesis of a massive variety of pathological conditions including chronic inflammation, autoimmunity, and cancer [69].
As for the relationship between MCs and VD, the cells discharged several mediators in a VD-lacking milieu without the need of any activators. Presence of calcitriol in the culture medium increased the number of VDRs in the MCs, and VDRs provoked complexes with Lyn in MCs to block the connection of Lyn to MyD88 and to the β chain of FcεRI, which diminished the amounts of NF-kB and MAPK and reduced the phosphorylation of Syk. Moreover, VDRs connected to the promoter of TNF-α reduce the acetylation of RNA polymerase II and histone H3/H4, reducing the production of TNF-α in MCs. These findings make evident that VD is necessary to preserve the steadiness of MCs, whereas the deficit of VD provokes the stimulation of MCs [70][71].
This has been demonstrated under numerous experimental conditions. It is notorious that the release of granules and the discharge of histamine from MCs are involved in the genesis of urticaria [72][73]. VD has been suggested for this therapy and for the one concerning other allergic pathology [74][75], as MCs own the VDR capable of blocking degranulation of compounds provoked by IgE [76].
Finally, it may be important to consider how the strong correlations between MCs and VD can aid to clarify some contradictory actions provoked by MCs. Although MCs were once believed to operate essentially as cells which were able to induce inflammation that can provoke allergic responses and inflammation induced by exogenic factors such as UV irradiation [63][77], novel findings suggest that, in specific conditions, MCs can reduce cellular damage and decrease inflammation provoked by UVB irradiation [78]. Even though most UVB rays do not enter the dermis, the UVB–supported stimulation of dermal MCs is believed to be obtained through a nerve growth factor, that originated from the epidermis [79], or by nervous sensory C fibers that have been stimulated by cis-urocanic acid [80]. This secondary mechanism of MC stimulation seems to participate in the UVB-provoked systemic immunosuppression in animals exposed to an acute single dose of UVB irradiation [79]. The intimate mechanism of this condition could be constituted by the production of specific cytokines, including IL-10 (Figure 3).
Figure 3. Effects of Vitamin D on mast cells.


  1. De Martinis, M.; Sirufo, M.M.; Viscido, A.; Ginaldi, L. Food Allergy Insights: A Changing Landscape. Arch. Immunol. Ther. Exp. 2020, 68, 8.
  2. Garg, N.; Silverberg, J.I. Association between eczema and increased fracture and bone or joint injury in adults a us population-based study. JAMA Dermatol. 2015, 151, 33–41.
  3. Chen, Y.W.; Ramsook, A.H.; Coxson, H.O.; Bon, J.; Reid, W.D. Prevalence and Risk Factors for Osteoporosis in Individuals with COPD: A Systematic Review and Meta-analysis. Chest 2019, 156, 1092–1110.
  4. Barrick, B.J.; Jalan, S.; Tollefson, M.M.; Milbrandt, T.A.; Larson, A.N.; Rank, M.A.; Lohse, C.M.; Davis, D.M.R. Associations of self-reported allergic diseases and musculoskeletal problems in children: A US population-based study. Ann. Allergy Asthma Immunol. 2017, 119, 170–176.
  5. Aljubran, S.A.; Whelan, G.J.; Glaum, M.C.; Lockey, R.F. Osteoporosis in the at-risk asthmatic. Allergy 2014, 69, 1429–1439.
  6. Jung, J.-W.; Kang, H.-R.; Kim, J.-Y.; Lee, S.-H.; Kim, S.S.; Cho, S.H. Are asthmatic patients prone to bone loss? Ann. Allergy Asthm. Immunol. 2014, 112, 426–431.
  7. Choi, H.G.; Kong, I.G. Association between chronic rhinosinusitis and osteoporosis: A case-control study using a national sample color. Int. Forum Allergy Rhinol. 2019, 9, 1010–1016.
  8. Zupan, J.; Jeras, M.; Marc, J. Osteoimmunology and the influence of pro-inflammatory cytokines on osteoclasts. Biochem. Med. 2013, 23, 43–63.
  9. Ponzetti, M.; Rucci, N. Updates on Osteoimmunology: What’s New on the Cross-Talk between Bone and Immune System. Front. Endocrinol. 2019, 10, 236.
  10. Naik, S.R.; Wala, S.M. Inflammation, allergy and asthma, complex immune origin diseases: Mechanisms and therapeutic agents. Recent Patents Inflamm. Allergy Drug Discov. 2013, 7, 62–95.
  11. Kang, J.; Lim, H.; Lee, D.; Yim, M. Montelukast inhibits RANKL-induced osteoclast formation and bone loss via CysLTR1 and P2Y12. Mol. Med. Rep. 2018, 18, 2387–2398.
  12. Bouillon, R.; Carmeliet, G.; Verlinden, L.; van Etten, E.; Verstuyf, A.; Luderer, H.F.; Lieben, L.; Mathieu, C.; Demay, M. Vitamin D and human health: Lessons from vitamin D receptor null mice. Endocr Rev. 2008, 29, 726–776.
  13. Pike, J.W. Genome-wide principles of gene regulation by the vitamin D receptor and its activating ligand. Mol. Cell. Endocrinol. 2011, 347, 3–10.
  14. Haussler, M.R.; Jurutka, P.W.; Mizwicki, M.; Norman, A.W. Vitamin D receptor (VDR)-mediated actions of 1alpha,25(OH)(2)vitamin D(3): Genomic and non-genomic mechanisms. Best Pract. Res. Clin. Endocrinol. Metab. 2011, 25, 543–559.
  15. Elsori, D.H.; Hammoud, M.S. Vitamin D deficiency in mothers, neonates and children. J. Steroid Biochem. Mol. Biol. 2018, 175, 195–199.
  16. Holick, M. Vitamin D deficiency. N. Engl. J. Med. 2007, 357, 266–281.
  17. De Martinis, M.; Allegra, A.; Sirufo, M.M.; Tonacci, A.; Pioggia, G.; Raggiunti, M.; Ginaldi, L.; Gangemi, S. Vitamin D Deficiency, Osteoporosis and Effect on Autoimmune Diseases and Hematopoiesis: A Review. Int. J. Mol. Sci. 2021, 22, 8855.
  18. Bivona, G.; Agnello, L.; Ciaccio, M. The immunological implication of the new vitamin D metabolism. Cent. Eur. J. Immunol. 2018, 43, 331–334.
  19. Ciccarelli, F.; De Martinis, M.; Sirufo, M.M.; Ginaldi, L. Psoriasis Induced by Anti-Tumor Necrosis Factor Alpha Agents: A Comprehensive Review of the Literature. Acta Dermatovenerol. Croat. ADC 2016, 24, 169–174.
  20. Muehleisen, B.; Gallo, R.L. Vitamin D in allergic disease: Shedding light on a complex problem. J. Allergy Clin. Immunol. 2013, 131, 324–329.
  21. Bouillon, R.; Marcocci, C.; Carmeliet, G.; Bikle, D.; White, J.H.; Dawson-Hughes, B.; Lips, P.; Munns, C.F.; Lazaretti-Castro, M.; Giustina, A.; et al. Skeletal and Extraskeletal Actions of Vitamin D: Current Evidence and Outstanding Questions. Endocr. Rev. 2019, 40, 1109–1151.
  22. Marino, R.; Misra, M. Extra-Skeletal Effects of Vitamin D. Nutrients 2019, 11, 1460.
  23. Lombardi, C.; Passalacqua, G. Italian Vitamin D Allergy Group Vitamin D levels and allergic diseases. An Italian cross-sectional multicenter survey. Eur. Ann. Allergy Clin. Immunol. 2017, 49, 75–79.
  24. Souto Filho, J.T.D.; de Andrade, A.S.; Ribeiro, F.M.; Alves, P.A.S.; Simonini, V.R.F. Impact of vitamin D deficiency on increased blood eosinophil counts. Hematol. Oncol. Stem Cell Ther. 2018, 11, 25–29.
  25. Alyasin, S.; Momen, T.; Kashef, S.; Alipour, A.; Amin, R. The relationship between serum 25-hydroxyvitamin D levels and asthma in children. Allergy Asthma Immunol. Res. 2011, 3, 251–255.
  26. Arshi, S.; Fallahpour, M.; Nabavi, M.; Bemanian, M.H.; Javad-Mousavi, S.A.; Nojomi, M.; Esmaeilzadeh, H.; Molatefi, R.; Rekabi, M.; Jalali, F.; et al. The effects of vitamin D supplementation on airway functions in mild to moderate persistent asthmal. Ann. Allergy Asthma Immunol. 2014, 113, 404–409.
  27. Peroni, D.; Piacentini, G.; Cametti, E.; Chinellato, I.; Boner, A. Correlation between serum 25-hydroxyvitamin D levels and severity of atopic dermatitis in children. Br. J. Dermatol. 2011, 164, 1078–1082.
  28. Dogru, M. Is vitamin D level associated with the natural course of atopic dermatitis? Allergol. Immunopathol. 2018, 46, 546–551.
  29. Grzanka, A.; Machura, E.; Mazur, B.; Misiolek, M.; Jochem, J.; Kasperski, J.; Kasperska-Zajac, A. Relationship between vitamin D status and the inflammatory state in patients with chronic spontaneous urticarial. J. Inflamm. 2014, 11, 24484740.
  30. Quirk, S.K.; Rainwater, E.; Shure, A.K.; Agrawal, D.K. Vitamin D in atopic dermatitis, chronic urticaria and allergic contact dermatitis. Exp. Rev. Clin. Immunol. 2016, 12, 839–847.
  31. Kolkhir, P.; André, F.; Church, M.K.; Maurer, M.; Metz, M. Potential blood biomarkers in chronic spontaneous urticaria. Clin. Exp. Allergy 2017, 47, 19–36.
  32. Heine, G.; Tabeling, C.; Hartmann, B.; Gonzalez Calera, C.R.; Kuhl, A.A.; Lindner, J.; Radbruch, A.; Witzenrath, M.; Worm, M. 25-hydroxvitamin D3 promotes the long-term effect of specific immunotherapy in a murine allergy model. J. Immunol. 2014, 193, 1017–1023.
  33. Wu, J.; Zhong, Y.; Shen, X.; Yang, K.; Cai, W. Maternal and early-life vitamin D deficiency enhances allergic reaction in an ovalbumin-sensitized BALB/c mouse model. Food Nutr. Res. 2018, 62, 1401.
  34. Sharief, S.; Jariwala, S.; Kumar, J.; Muntner, P.; Melamed, M.L. Vitamin D levels and food and environmental allergies in the United States: Results from the national health and nutrition examination survey 2005–2006. J Allergy Clin. Immunol. 2011, 127, 1195–1202.
  35. Baek, J.H.; Shin, Y.H.; Chung, I.H.; Kim, H.J.; Yoo, E.G.; Yoon, J.W.; Jee, H.M.; Chang, Y.E.; Han, M.Y. The link between serum vitamin D level, sensitization to food allergens, and the severity of atopic dermatitis in infancy. J. Pediatr. 2014, 165, 849–854.e1.
  36. Yepes-Nuñez, J.J.; Brożek, J.L.; Fiocchi, A.; Pawankar, R.; Cuello-García, C.; Zhang, Y.; Morgano, G.P.; Agarwal, A.; Gandhi, S.; Terracciano, L.; et al. Vitamin D supplementation in primary allergy prevention: Systematic review of randomized and non-randomized studies. Allergy 2018, 73, 37–49.
  37. Rorie, A.; Goldner, W.S.; Lyden, E.; Poole, J.A. Beneficial role for supplemental vitamin D3 treatment in chronic urticaria: A randomized study. Ann. Allergy Asthma Immunol. 2014, 112, 376–382.
  38. Nabavizadeh, S.H.; Alyasin, S.; Esmaeilzadeh, H.; Mosavat, F.; Ebrahimi, N. The effect of vitamin D add-on therapy on the improvement of quality of life and clinical symptoms of patients with chronic spontaneous urticaria. Asian Pac. J. Allergy Immunol. 2020.
  39. Vahavihu, K.; Ala-Houhala, M.; Peric, M.; Karisola, P.; Kautiainen, H.; Hasan, T.; Snellman, E.; Alenius, H.; Schauber, J.; Reunala, T. Narrowband ultraviolet B treatment improves vitamin D balance and alters antimicrobial peptide expression in skin lesions of psoriasis and atopic dermatitis. Br. J. Dermatol. 2010, 163, 321–328.
  40. Sidbury, R.; Sullivan, A.F.; Thadhani, R.I.; Camargo, C.A., Jr. Randomized controlled trial of vitamin D supplementation for winter-related atopic dermatitis in Boston: A pilot study. Br. J. Dermatol. 2008, 159, 245–247.
  41. Brehm, J.M.; Celedon, J.C.; Soto-Quiros, M.E.; Avila, L.; Hunninghake, G.M.; Forno, E.; Laskey, D.; Sylvia, J.S.; Hollis, B.W.; Weiss, S.T.; et al. Serum vitamin D levels and markers of severity of childhood asthma in Costa Rica. Am. J. Respir. Crit. Care Med. 2009, 179, 765–771.
  42. Goleva, E.; Searing, D.A.; Jackson, L.P.; Richers, B.N.; Leung, D.Y. Steroid requirements and immune associations with vitamin D are stronger in children than adults with asthma. J. Allergy Clin. Immunol. 2012, 129, 1243–1251.
  43. Urashima, M.; Segawa, T.; Okazaki, M.; Kurihara, M.; Wada, Y.; Ida, H. Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren. Am. J. Clin. Nutr. 2010, 91, 1255–1260.
  44. Majak, P.; Olszowiec-Chlebna, M.; Smejda, K.; Stelmach, I. Vitamin D supplementation in children may prevent asthma exacerbation triggered by acute respiratory infection. J. Allergy Clin. Immunol. 2011, 127, 1294–1296.
  45. Camargo, C.A., Jr.; Clark, S.; Kaplan, M.S.; Lieberman, P.; Wood, R.A. Regional differences in EpiPen prescriptions in the United States: The potential role of vitamin D. J. Allergy Clin. Immunol. 2007, 120, 131–136.
  46. Camargo, C.A., Jr.; Ingham, T.; Wickens, K.; Thadhani, R.; Silvers, K.M.; Epton, M.J.; Town, G.I.; Pattemore, P.K.; Espinola, J.A.; Crane, J. Cord-blood 25-hydroxyvitamin D levels and risk of respiratory infection, wheezing, and asthma. Pediatrics 2011, 127, e180–e187.
  47. Heine, G.; Niesner, U.; Chang, H.D.; Steinmeyer, A.; Zugel, U.; Zuberbier, T.; Radbruch, A. Worm, M. 1,25-dihydroxyvitamin D(3) promotes IL-10 production in human B cells. Eur. J. Immunol. 2008, 38, 2210–2218.
  48. Drozdenko, G.; Scheel, T.; Heine, G.; Baumgrass, R.; Worm, M. Impaired T cell activation and cytokine production by calcitriol-primed human B cells. Clin. Exp. Immunol. 2014, 178, 364–372.
  49. Wittke, A.; Weaver, V.; Mahon, B.D.; August, A.; Cantorna, M.T. Vitamin D receptor deficient mice fail to develop experimental allergic asthma. J. Immunol. 2004, 173, 3432–3436.
  50. Hartmann, B.; Heine, G.; Babina, M.; Steinmeyer, A.; Zugel, U.; Radbruch, A.; Worm, M. Targeting the vitamin D receptor inhibits the B cell-dependent allergic immune response. Allergy 2011, 66, 540–548.
  51. Széles, L.; Keresztes, G.; Töröcsik, D.; Balajthy, Z.; Krenács, L.; Póliska, S.; Steinmeyer, A.; Zuegel, U.; Pruenster, M.; Rot, A.; et al. 1,25-dihydroxyvitamin D3 is an autonomous regulator of the transcriptional changes leading to a tolerogenic dendritic cell phenotype. J. Immunol. 2009, 182, 2074–2083.
  52. Unger, W.W.; Laban, S.; Kleijwegt, F.S.; van der Slik, A.R.; Roep, B.O. Induction of Treg by monocyte-derived DC modulated by vitamin D3 or dexamethasone: Differential role for PD-L1. Eur. J. Immunol. 2009, 39, 3147–3159.
  53. Bakdash, G.; van Capel, T.M.; Mason, L.M.; Kapsenberg, M.L.; de Jong, E.C. Vitamin D3 metabolite calcidiol primes human dendritic cells to promote the development of immunomodulatory IL-10-producing T cells. Vaccine 2014, 32, 6294–6302.
  54. Almerighi, C.; Sinistro, A.; Cavazza, A.; Ciaprini, C.; Rocchi, G.; Bergamini, A. 1α,25-dihydroxyvitamin D3 inhibits CD40L-induced pro-inflammatory and immunomodulatory activity in human monocytes. Cytokine 2009, 45, 190–197.
  55. Jeffery, L.E.; Burke, F.; Mura, M.; Zheng, Y.; Qureshi, O.S.; Hewison, M.; Walker, L.S.; Lammas, D.A.; Raza, K.; Sansom, D.M. 1,25-Dihydroxyvitamin D3 and IL-2 combine to inhibit T cell production of inflammatory cytokines and promote development of regulatory T cells expressing CTLA-4 and FoxP3. J. Immunol. 2009, 183, 5458–5467.
  56. Murdaca, G.; Greco, M.; Tonacci, A.; Negrini, S.; Borro, M.; Puppo, F.; Gangemi, S. IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases. Int. J. Mol. Sci. 2019, 20, 5856.
  57. Fischer, K.D.; Agrawal, D.K. Hematopoietic Stem and Progenitor Cells in Inflammation and Allergy. Front. Immunol. 2013, 4, 428.
  58. Uasuf, C.G.; Sano, C.D.; Gangemi, S.; Albeggiani, G.; Cigna, D.; Dino, P.; Brusca, I.; Gjomarkaj, M.; Pace, E. IL-33/s-ST2 ratio, systemic symptoms, and basophil activation in Pru p 3-sensitized allergic patients. Inflamm. Res. 2018, 67, 671–679.
  59. Ginaldi, L.; De Martinis, M.; Ciccarelli, F.; Saitta, S.; Imbesi, S.; Mannucci, C.; Gangemi, S. Increased levels of interleukin 31 (IL-31) in osteoporosis. BMC Immunol. 2015, 16, 60.
  60. Tsai, M.; Grimbaldeston, M.; Galli, S.J. Mast cells and immunoregulation/immunomodulation. Adv. Exp. Med. Biol. 2011, 716, 186–211.
  61. Voehringer, D. Protective and pathological roles of mast cells and basophils. Nat. Rev. Immunol. 2013, 13, 362–375.
  62. Ribatti, D.; Crivellato, E. The role of mast cell in tissue morphogenesis. Thymus, duodenum, and mammary gland as examples. Exp. Cell Res. 2016, 341, 105–109.
  63. Galli, S.J.; Kalesnikoff, J.; Grimbaldeston, M.A.; Piliponsky, A.M.; Williams, C.M.; Tsai, M. Mast cells as “tunable” effector and immunoregulatory cells: Recent advances. Ann. Rev. Immunol. 2005, 23, 749–786.
  64. Madjene, L.C.; Danelli, L.; Dahdah, A.; Vibhushan, S.; Bex-Coudrat, J.; Pacreau, E.; Vaugier, C.; Claver, J.; Rolas, L.; Pons, M.; et al. Mast cell chymase protects against acute ischemic kidney injury by limiting neutrophil hyperactivation and recruitment. Kidney Int. 2020, 97, 516–527.
  65. Katsanos, G.S.; Anogeianaki, A.; Orso, C.; Tete, S.; Salini, V.; Antinolfi, P.L.; Sabatino, G. Mast cells and chemokines. J. Biol. Regul. Homeost. Agents 2008, 22, 145–151.
  66. Lieberman, P.; Garvey, L.H. Mast cells and anaphylaxis. Curr. Allergy Asthma Rep. 2016, 16, 20.
  67. Finkelman, F.D.; Khodoun, M.V.; Strait, R. Human IgE-independent systemic anaphylaxis. J. Allergy Clin. Immunol. 2016, 137, 1674–1680.
  68. Afrin, L.B. Mast cell activation disease and the modern epidemic of chronic inflammatory disease. Transl. Res. 2016, 174, 33–59.
  69. Wernersson, S.; Pejler, G. Mast cell secretory granules: Armed for battle. Nat. Rev. Immunol. 2014, 14, 478–494.
  70. Liu, Z.Q.; Li, X.X.; Qiu, S.Q.; Yu, Y.; Li, M.G.; Yang, L.T.; Li, L.J.; Wang, S.; Zheng, P.Y.; Liu, Z.G.; et al. Vitamin D contributes to mast cell stabilization. Allergy 2017, 72, 1184–1192.
  71. Biggs, L.; Yu, C.; Fedoric, B.; Lopez, A.F.; Galli, S.J.; Grimbaldeston, M.A. Evidence that vitamin D(3) promotes mast cell-dependent reduction of chronic UVB-induced skin pathology in mice. J. Exp. Med. 2010, 207, 455–463.
  72. Asero, R.; Ferrucci, S.; Casazza, G.; Marzano, A.V.; Cugno, M. Total IgE and atopic status in patients with severe chronic spontaneous urticaria unresponsive to omalizumab treatment. Allergy 2019, 74, 1561–1563.
  73. Lakin, E.; Church, M.K.; Maurer, M.; Schmetzer, O. On the Lipophilic Nature of Autoreactive IgE in Chronic Spontaneous Urticaria. Theranostics 2019, 9, 829–836.
  74. Rivero-Yeverino, D.; López-García, A.I.; Caballero-López, C.G.; Ríos-López, J.J.; Papaqui-Tapia, J.S.; Ortega-Jordá Rodríguez, E.E.; Álvarez-Rivera, A.; Ruiz-Sánchez, D.M.; Flores-Gonzaga, E. Vitamin D and respiratory allergy: State of the art. Rev. Alergy Mex. 2022, 69 (Suppl. S1), s46–s54.
  75. He, L.; Yi, W.; Huang, X.; Long, H.; Lu, Q. Chronic Urticaria: Advances in Understanding of the Disease and Clinical Management. Clin. Rev. Allergy Immunol. 2021, 61, 424–448.
  76. Redegeld, F.A.; Yu, Y.; Kumari, S.; Charles, N.; Blank, U. Non-IgE mediated mast cell activation. Immunol. Rev. 2018, 282, 87–113.
  77. Metz, M.; Lammel, V.; Gibbs, B.F.; Maurer, M. Inflammatory murine skin responses to UV-B light are partially dependent on endothelin-1 and mast cells. Am. J. Pathol. 2006, 169, 815–822.
  78. Galli, S.J.; Grimbaldeston, M.; Tsai, T. Immunomodulatory mast cells: Negative, as well as positive, regulators of immunity. Nat. Rev. Immunol. 2008, 8, 478–486.
  79. Hart, P.H.; Townley, S.L.; Grimbaldeston, M.A.; Khalil, Z.; Finlay Jones, J.J. Mast cells, neuropeptides, histamine, and prostaglandins in UV-induced systemic immunosuppression. Methods 2002, 28, 79–89.
  80. Khalil, Z.; Townley, S.L.; Grimbaldeston, M.A.; Finlay-Jones, J.J.; Hart, P.H. cis-Urocanic acid stimulates neuropeptide release from peripheral sensory nerves. J. Investig. Dermatol. 2002, 117, 886–891.
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