Vičić Marijana, Peternel Sandra, Simonić Edita, Sotošek-Tokmadžić Vlatka, Massari Dražen, Brajac Ines, Kaštelan Marija, Prpić-Massari Larisa
Department of Dermatovenerology, Clinical Hospital Center Rijeka, Medical Faculty, University of Rijeka, Krešimirova 42, 51000 Rijeka, Croatia.
Department of Physiology and Immunology, Medical Faculty, University of Rijeka, B. Branchetta 20, 51000 Rijeka, Croatia.
Med Hypotheses. 2016 Feb;87:66-8. doi: 10.1016/j.mehy.2015.12.004. Epub 2015 Dec 12.
Psoriasis is a chronic papulosquamous skin disease, histologically characterized by epidermal hyperproliferation and dermal infiltration of inflammatory cells. The majority of T lymphocytes infiltrating dermis are CD4+ T lymphocytes secreting type 1 and type 17 cytokines. These cytokines are responsible for triggering keratinocyte proliferation as well as chemokine secretion and subsequent migration of other inflammatory cells in the skin. Contrarily, lymphocytes that accumulate in epidermis are mainly CD8+ T lymphocytes. According to the recent findings, these cells can also secrete type 1 and type 17 cytokines. However, it is demonstrated so far that epidermal CD8+ T lymphocytes contain higher amounts of cytolytic molecules, such as perforin, granzyme B and granulysin whose role in psoriasis pathogenesis is still unknown. Therefore, in this article we hypothesize the active involvement of cell mediated cytotoxicity in killing the proliferating keratinocytes as a mechanism of potential self-defense and possible brake in psoriatic plaque formation, maintaining skin homeostasis.
银屑病是一种慢性丘疹鳞屑性皮肤病，组织学特征为表皮过度增殖和真皮炎症细胞浸润。浸润真皮的大多数T淋巴细胞是分泌1型和17型细胞因子的CD4+ T淋巴细胞。这些细胞因子负责触发角质形成细胞增殖以及趋化因子分泌，并随后促使其他炎症细胞在皮肤中迁移。相反，积聚在表皮的淋巴细胞主要是CD8+ T淋巴细胞。根据最近的研究结果，这些细胞也能分泌1型和17型细胞因子。然而，迄今为止已证实，表皮CD8+ T淋巴细胞含有较高量的细胞溶解分子，如穿孔素、颗粒酶B和颗粒溶素，它们在银屑病发病机制中的作用仍不清楚。因此，在本文中，我们推测细胞介导的细胞毒性在杀死增殖的角质形成细胞中发挥积极作用，这是一种潜在的自我防御机制，也是银屑病斑块形成的可能制动因素，有助于维持皮肤的稳态。
