Vrije Universiteit Brussel (VUB), Skin Immunology & Immune Tolerance (SKIN) Research Group, Laarbeeklaan 103, 1090, Brussels, Belgium.
Vrije Universiteit Brussel (VUB), Skin Immunology & Immune Tolerance (SKIN) Research Group, Laarbeeklaan 103, 1090, Brussels, Belgium; Vrije Universiteit Brussel (VUB), Universitair Ziekenhuis Brussel (UZ Brussel), Department of Dermatology, Universitair Ziekenhuis Brussel, Laarbeeklaan 101, 1090, Brussels, Belgium.
J Autoimmun. 2021 Jun;120:102634. doi: 10.1016/j.jaut.2021.102634. Epub 2021 Apr 20.
Atopic dermatitis (AD) is an itchy, non-contagious relapsing and chronic inflammatory skin disease that usually develops in early childhood. This pathology is associated with food allergy, allergic asthma, allergic rhinitis and anaphylaxis which may persist in adulthood. The underlying mechanisms of AD (endotypes) are just beginning to be discovered and show a complex interaction of various pathways including skin barrier function and immune deviation. Immune reactions to self-proteins (autoantigens) of the skin have been identified in patients with inflammatory skin diseases, such as chronic spontaneous urticaria, connective tissue disease, pemphigus vulgaris and bullous pemphigoid. IgE antibodies and T cells directed against epitopes of the skin were observed in adult patients with severe and chronic AD as well. This was associated with disease severity and suggests a progression from allergic inflammation to severe autoimmune processes against the skin. IgE-mediated autoimmunity and self-reactive T cells might accelerate the ongoing skin inflammation or might contribute to the relapsing course of the disease. However, to date, the exact mechanisms of IgE-mediated autoimmunity and self-reactive T cells in the pathophysiology of AD are still unclear. The aim of this review is to evaluate the development of (autoreactive) T cells and their response to (auto)antigens, as well as the role of the peripheral tolerance in autoimmunity in the pathophysiology of AD, including the unmet needs and gaps.
特应性皮炎（AD）是一种瘙痒、非传染性、反复发作和慢性炎症性皮肤病，通常在儿童早期发病。这种病理学与食物过敏、过敏性哮喘、过敏性鼻炎和过敏反应有关，这些疾病可能会持续到成年期。AD 的潜在机制（表型）才刚刚开始被发现，并显示出各种途径的复杂相互作用，包括皮肤屏障功能和免疫偏差。在炎症性皮肤病患者中，如慢性自发性荨麻疹、结缔组织疾病、寻常型天疱疮和大疱性类天疱疮，已经发现了针对皮肤自身蛋白（自身抗原）的免疫反应。在患有严重和慢性 AD 的成年患者中也观察到针对皮肤表位的 IgE 抗体和 T 细胞。这与疾病严重程度相关，并提示从过敏炎症进展为针对皮肤的严重自身免疫过程。IgE 介导的自身免疫和自身反应性 T 细胞可能会加速正在进行的皮肤炎症，或者可能导致疾病的反复发作过程。然而，迄今为止，AD 病理生理学中 IgE 介导的自身免疫和自身反应性 T 细胞的确切机制仍不清楚。本综述的目的是评估（自身反应性）T 细胞的发展及其对（自身）抗原的反应，以及外周耐受在 AD 自身免疫中的作用，包括未满足的需求和差距。
