Meister Michael, Tounsi Amel, Gaffal Evelyn, Bald Tobias, Papatriantafyllou Maria, Ludwig Julia, Pougialis Georg, Bestvater Felix, Klotz Luisa, Moldenhauer Gerhard, Tüting Thomas, Hämmerling Günter J, Arnold Bernd, Oelert Thilo
Department of Molecular Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Department of Dermatology and Allergy, Laboratory of Experimental Dermatology, University of Bonn, Bonn, Germany.
J Invest Dermatol. 2015 Aug;135(8):1996-2004. doi: 10.1038/jid.2015.130. Epub 2015 Apr 2.
Keratinocytes have a pivotal role in the regulation of immune responses, but the impact of antigen presentation by these cells is still poorly understood, particularly in a situation where the antigen will be presented only in adult life. Here, we generated a transgenic mouse model in which keratinocytes exclusively present a myelin basic protein (MBP) peptide covalently linked to the major histocompatibility complex class II β-chain, solely under inflammatory conditions. In these mice, inflammation caused by epicutaneous contact sensitizer treatment resulted in keratinocyte-mediated expansion of MBP-specific CD4(+) T cells in the skin. Moreover, repeated contact sensitizer application preceding a systemic MBP immunization reduced the reactivity of the respective CD4(+) T cells and lowered the symptoms of the resulting experimental autoimmune encephalomyelitis. This downregulation was CD4(+) T-cell-mediated and dependent on the presence of the immune modulator Dickkopf-3. Thus, presentation of a neo self-antigen by keratinocytes in the inflamed, adult skin can modulate CD4(+) T-cell auto-aggression at a distal organ.
角质形成细胞在免疫反应调节中起关键作用,但这些细胞的抗原呈递影响仍知之甚少,特别是在抗原仅在成年期才会呈递的情况下。在此,我们构建了一种转基因小鼠模型,在该模型中,仅在炎症条件下,角质形成细胞专门呈递与主要组织相容性复合体II类β链共价连接的髓鞘碱性蛋白(MBP)肽。在这些小鼠中,经皮接触致敏剂处理引起的炎症导致皮肤中角质形成细胞介导的MBP特异性CD4(+) T细胞扩增。此外,在全身MBP免疫之前重复应用接触致敏剂可降低相应CD4(+) T细胞的反应性,并减轻由此产生的实验性自身免疫性脑脊髓炎的症状。这种下调是由CD4(+) T细胞介导的,并依赖于免疫调节剂Dickkopf-3的存在。因此,炎症成年皮肤中的角质形成细胞呈递新的自身抗原可调节远端器官处CD4(+) T细胞的自身攻击。