Benyon R C
Immunopharmacology Group, University of Southampton, U.K.
Clin Exp Allergy. 1989 Jul;19(4):375-87. doi: 10.1111/j.1365-2222.1989.tb02402.x.
The abundance of mast cells in human dermis, together with their ability to release a variety of vasoactive and pro-inflammatory mediators following cross-linkage of their cell-surface receptors for IgE, enables these cells to provide an effective defence mechanism within this organ. A similar defensive function is attributed to mast cells of other human organs such as intestine and lung which are in contact with the external environment and therefore susceptible to infiltration by foreign allergens and micro-organisms. However, mast cells of the skin apparently differ from those present in lung and intestine in being activated for histamine release by a variety of endogenous neuropeptides which stimulate the rapid release of histamine in the virtual absence of eicosanoids. This would provide a mechanism of neurogenic control of a variety of homeostatic functions such as blood flow, angiogenesis and fibroblast proliferation. Such processes would aid in the remodelling of tissue during wound healing, and increased numbers of mast cells have been noted around healing wounds of rat skin and areas of developing fibrosis. Neuropeptides modulate the activity of a variety of immuno-competent leucocytes including macrophages, monocytes and lymphocytes. The findings that skin mast cells are activated by neuropeptides suggest that these cells may also be included amongst those involved in neuro-immune interactions. Activation of skin mast cells by non-immunological stimuli may contribute to the aetiology of some forms of skin disease. Patients with chronic idiopathic urticaria appear to have enhanced vascular responsiveness to intradermal injections of the histamine liberator codeine suggesting that this disease may involve hyper-responsiveness of their mast cells to endogenous non-immunological stimuli. The findings of large increases in histamine accompanied by small increases in PGD2 in venous effluent of thermally challenged limbs of patients with cold- or heat-induced urticaria may suggest that their mast cells had been activated by a non-immunological stimulus. However, the interpretation of results gained using such relatively complex in-vivo systems are difficult, as the cellular origin of the detected mediators is by no means clear. However, it is hoped that in the future the alliance of newly developed in-vitro techniques to investigate mast cell function together with in-vivo methods to investigate their interaction with elements in their tissue environment will greatly increase our understanding of the role of the human skin mast cell in health and disease.
人类真皮中肥大细胞数量丰富，且在其细胞表面IgE受体交联后能够释放多种血管活性和促炎介质，这使得这些细胞能够在该器官内提供有效的防御机制。类似的防御功能也归因于人体其他器官（如肠道和肺）中的肥大细胞，这些器官与外部环境接触，因此容易受到外来过敏原和微生物的侵入。然而，皮肤中的肥大细胞显然与肺和肠道中的肥大细胞不同，它们可被多种内源性神经肽激活而释放组胺，这些神经肽在几乎没有类花生酸的情况下刺激组胺快速释放。这将提供一种对多种稳态功能（如血流、血管生成和成纤维细胞增殖）进行神经源性控制的机制。这些过程将有助于伤口愈合过程中的组织重塑，并且在大鼠皮肤愈合伤口周围和正在形成纤维化的区域已观察到肥大细胞数量增加。神经肽可调节多种免疫活性白细胞（包括巨噬细胞、单核细胞和淋巴细胞）的活性。皮肤肥大细胞被神经肽激活的发现表明，这些细胞也可能参与神经免疫相互作用。非免疫刺激激活皮肤肥大细胞可能导致某些形式皮肤病的病因。慢性特发性荨麻疹患者似乎对皮内注射组胺释放剂可待因的血管反应性增强，这表明该疾病可能涉及肥大细胞对内源性非免疫刺激的高反应性。冷诱导或热诱导性荨麻疹患者热刺激肢体静脉流出物中组胺大幅增加而PGD2小幅增加的发现可能表明，他们的肥大细胞已被非免疫刺激激活。然而，使用这种相对复杂的体内系统获得的结果难以解释，因为所检测到的介质的细胞来源并不明确。然而，希望未来新开发的用于研究肥大细胞功能的体外技术与用于研究其与组织环境中元素相互作用的体内方法相结合，将大大增加我们对人类皮肤肥大细胞在健康和疾病中作用的理解。
