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The role of mast cells in skin diseases


As the largest organ of the human body, the skin is the boundary and important physical barrier of the human body and the external environment. It is also an important immune organ. It interacts with other immune systems in the body to form a complex network system to maintain the skin microenvironment and the stability of the internal environment. Mast cells are one of the main immune cells in the skin. They are widely distributed in the connective tissue of the whole body. distribution of capillaries, lymphatic vessels and peripheral nerves in the connective tissues of the submucosa such as skin, respiratory tract, digestive tract and genitourinary tract are mostly distributed. It is suggested that mast cells are an important force in protecting the first line of defense against pathogen invasion. After being activated by various physical, chemical and biological factors, mast cells release a variety of biologically active substances in a degranulation manner to cause corresponding physiological and pathological changes. The biological factors, lipid mediators, protease-like proteins released in different skin diseases are different, and the mechanism of action is also different. The role of mast cells in different skin diseases is reviewed.

1 mast cell hyperplasia

Mast cell hyperplasia is a major pathological manifestation of malignant growth and proliferation of mast cells in one or more organs, including cutaneous mastocytosis and systemic mastocytosis, its pathogenesis and cellular c-kit The point mutation of the gene is associated with C-KII protein autophosphorylation. Skin mastocytosis is the most common type of mast cell hyperplasia. It is more common in children. The clinical manifestations are local pigmentation in the epidermis of the trunk and extremities. It can also be expressed as rubella urticaria (Darier sign). When the Darier sign is aggravated, blistering or bullous lesions may occur in the skin lesions. Systemic mastocytosis is more common in adults. Clinical manifestations include systemic symptoms such as nausea, vomiting, abdominal pain, diarrhea, systemic allergic reactions and osteoporosis in addition to typical skin lesions. Whether it is skin symptoms or systemic manifestations, it is mostly caused by the medium secreted and released by abnormally proliferating mast cells.

2 The role of mast cells in urticaria

Urticaria is a localized edema reaction caused by reactive expansion of the skin and mucosal small blood vessels and increased permeability. Mast cells are the main effector cells of urticaria reaction and also the initiating effector cells of type I hypersensitivity. The pathogenesis can be divided into hypersensitivity reactions and non-hypersensitive reactions. Non-hypersensitive reactions usually cause urticaria due to the release of histamine from mast cells by certain foods, drugs and physical and mechanical stimuli. Most hypersensitivity reactions are type I. The type I hypersensitivity reaction mechanism is when the allergen enters the body to contact macrophages, presents antigen information, and induces B lymphocytes to produce specific antibody Ig E, which binds to the high affinity receptor FcεRI on the surface of mast cells to keep the body in the body. In a sensitized state, when the same or similar allergens re-enter the body, two adjacent high-affinity IgE receptors on the surface of the sensitized mast cells cross-link through the antigen, activating the signal transduction system leading to rapid degranulation of the mast cells, releasing A series of biologically active mediators such as histamine, leukotrienes, tryptase, prostaglandins and interleukins activate downstream secondary effector cells, causing a series of pathological changes such as telangiectasia, increased permeability, and increased glandular secretion. Causes local or systemic allergic reactions such as skin, mucous membranes, respiratory tract and digestive tract.

3 The role of mast cells in atopic dermatitis

Atopic dermatitis is a chronic inflammatory skin disease associated with genetic allergies. It is characterized by itching, pleomorphic skin lesions and exudation, often accompanied by asthma and allergic rhinitis. Mast cells play a central role in the pathogenesis of allergic inflammatory diseases. In the inflammatory state, mast cells express FcεRI more to bind antibody Ig E, which is beneficial to the activation and secretion of cytokines when mast cells are in contact with antigen. , inflammatory mediators, etc. In the early stage of the allergen challenge test, the primary effector cells represented by mast cells were the result of the effect; and the delayed response after 4 hours was the secondary effect represented by eosinophils and neutrophils. The result of cellular action. A variety of inflammatory mediators and cytokines secreted by mast cells participate in the immune regulation response by affecting the specific response of lymphocytes. IL-4 secreted by mast cells promotes Th0 differentiation into Th2 cells, and IL-4 and IL-5 secreted by Th2 cells induce Ig E production and eosinophil activation. Therefore, about 80% of patients with atopic dermatitis have elevated serum Ig E levels, and Th2 cells are significantly increased in the lesions of patients with atopic dermatitis. Mast cells can recruit Th1, Th2, CD8+ T cells expressing LTB4 receptor to reach the inflammatory region by producing leukotriene B4 (LTB4), and can also up-regulate endothelial cell vascular cell adhesion molecule-1 (VCAM) by TNF-a production. -1), E-selectin and other adhesion molecules express, promote circulating lymphocytes into the inflammatory area, tryptase and histamine can participate in the body’s immune response by activating neutrophils, lipid mediators can recruit T lymphocytes It also induces the activation and proliferation of antigen-specific CD8+ T cells, which secrete IL-2, INF-γ and macrophage inflammatory proteins. Mast cells can also accelerate the maturation of dendritic cells and enhance their function. Release of tumor necrosis factor recruits dendritic cells to migrate to the site of inflammation.

4 The role of mast cells in psoriasis

Psoriasis is a common chronic inflammatory skin disease caused by a combination of genetic factors, environmental factors and immune factors. The clinical manifestations are erythema plaques of varying sizes. Its histopathological features are hyperproliferation and maturation of epidermal cells, and inflammatory cell infiltration. Psoriasis is closely related to the complex cascades triggered by inflammatory mediators. Cytokines play a key role in the pathophysiology of psoriasis. IL-33 is the newest member of the IL-1 family of inflammatory factors that induces the release of IL-8 from mature mast cells derived from human bone marrow stem cells, which can cause neutrophil aggregation. IL-33 secreted by mast cells can cause lymphocyte infiltration, proliferation of stratum corneum cells, and proliferation of vascular endothelium. It has been found that sphingolipid metabolite sphingosine phospholipid SP is the main substance causing mast cell activation in allergic reactions. IL-33 can enhance SP action and stimulate mast cells to release vascular endothelial growth factor (VEGF). VEGF is a inflammatory disease. The angiogenic factor promotes vascular endothelial cell proliferation and increases vascular permeability, and plays an important role in the pathological process of psoriasis. With the development of psoriasis, mast cells gradually activated, and the level of corticotropin releasing hormone receptor (CRHR-1) was significantly increased. Activated mast cells increased vascular permeability by activation of CRHR-1. Studies have shown that the levels of IL-17 and IL-22 derived from mast cells in psoriatic lesions are significantly increased. IL-17 and IL-22 can inhibit the differentiation of keratinocytes and promote the proliferation and epidermal growth of keratinocytes. The upper layer migration leads to parakeratosis with hyperkeratosis and epidermal extension in psoriatic lesions.

5 The role of mast cells in keloids

Keloid is a fibrous sputum that occurs after skin damage such as cuts, lacerations, etc. It is a chronic inflammatory disease, which is histologically characterized by abnormally increased extracellular matrix, including local mast cells. Infiltration of inflammatory cells and accumulation of large amounts of cytokines. At present, the role of mast cells in the pathogenesis of keloids is not clear, but many studies have found that mast cells play an important role in the growth and proliferation of effector cells in keloids, namely fibroblasts. Active mediators and cytokines for the synthesis and secretion of mast cells, such as trypsin, chymotrypsin, inflammatory mediators and cytokines such as tumor necrosis factor-α (TNF-α, leukotrienes, prostaglandin E2 (PGE2), etc. Fibroblastosis and excessive accumulation of extracellular matrix promote tissue fibrosis. The number of mast cells in keloids and mast cell chymotrypsin and tryptase activity are significantly higher than normal skin tissue, chymotrypsin and tryptase on collagen fiber synthesis and The tissue remodeling process has a dual role. Tryptase can promote fibroblast proliferation, activate collagenase, promote metaplasia of collagen to fibrillar collagen, and also degrade fibrinogen and number by activating metalloproteinase and collagenase in matrix. Matrix proteins; chymotrypsins can promote the breakdown of collagen and other extracellular matrix proteins by activating metalloproteinases, or promote fibroblast proliferation by stimulating the release of transforming growth factor-β. In addition, chymotrypsin can also promote vascular tone Is converted to angiotensin II, through the latter Fiber into tissue reconstruction.

6 The role of mast cells in autoimmune bullous disease

Bullous skin disease is a group of skin diseases that occur in the skin mucosa and are mainly damaged by blisters and bullae. According to the pathogenesis, it can be divided into “autoimmune bullous disease” and “non-autoimmune bullous disease”. Bullous pemphigoid is the most common autoimmune bullous skin disease, clinically manifested as a nervous, unbreakable bullae, erosion, scarring, rash and delayed pruritus. The main pathological features were subepidermal vesicles, deposition of Ig G and C3 in the basement membrane, and antibodies to the basal membrane band components, ie, hemi-bridged antigens BP230 and BP180, in the serum. As a kind of autoimmune disease, the pathogenesis of pemphigus, including cellular immunity and humoral immunity, requires the mediated by T helper cells. Mast cells are increased in the lesions of bullous pemphigoid, and the mediators and proteases released by mast cells in patients with bullous pemphigoid are increased. Mast cells can present antigens to T cells or secrete cytokines to affect the function and activation of T cells. IL-4 secreted by mast cells can induce Th0 cells to differentiate into Th2 cells, and cytokines secreted by Th2 cells (IL-4, IL) -5, IL-6, IL-10 and IL-13) promote B cell proliferation, differentiation and antibody production involved in humoral immune responses.

7 The role of mast cells in cutaneous candidiasis

Candida is the most common conditional pathogen in human body, the destruction of skin mucosal barrier caused by various reasons, endocrine disorders, abuse of antibiotics lead to dysbacteriosis in the body, especially immunosuppressed patients are easily infected by conditional pathogenic pathogens. Mycosis, Candida albicans is the main pathogen, colonized on the skin and mucosal surface in a parasitic state. Mast cells in the skin are one of the first immune cells to directly contact Candida albicans, but the interaction between them and fungal cells is not clear. Mast cells degranulate at different stages before, during and after the reaction to produce different cytokines involved in the fungal immunity. At the initial stage of the reaction, Candida albicans can induce rapid degranulation of mast cells, and the formation of extracellular grids by special cytokines released by mast cells can temporarily inhibit the activity of Candida albicans and weaken its ability to colonize the skin. At the same time, internalized Candida albicans can also cause mast cell death in mast cells, and mast cells infected by fungi can secrete cytokine-collecting granulocytes, and mast cells can be secreted later in the reaction. A cytokine that releases anti-inflammatory effects modulates the immune response. The interaction between mast cells and fungi suggests that mast cells can regulate the body’s antifungal immune response by producing specific cytokines.

8 Conclusion

Mast cells release various biologically active substances by degranulation when stimulated, in view of the diversity of bioactive substances produced by mast cells in various skin diseases and the interaction mechanism between mast cells and pathogens and other immune cells. Diversity, the specific mechanism of action of mast cells in skin pathophysiology is still unclear. In-depth study of the role of mast cells in skin diseases can help clarify the pathogenesis of some skin diseases and provide new directions and choices for their treatment.

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