Bonhagen K, Thoma S, Leithäuser F, Möller P, Reimann J
Department of Medical Microbiology and Immunology, University of Ulm, Germany.
Clin Exp Immunol. 1998 Jun;112(3):443-52.
CD4+ TCRalphabeta+ T cells from the colonic lamina propria of athymic (nude) mice were adoptively transferred into histocompatible (SCID) mice homozygous for the autosomal recessive mutation scid (severe combined immunodeficiency). Transfer of these extrathymic CD4+ T cells into SCID mice induced a pancolitis in the adoptive host. The histopathology of this inflammatory response was restricted to the colon and closely resembled human UC. CD4+ T cells infiltrating the colonic lamina propria of diseased SCID mice displayed the surface phenotype of mucosa-seeking memory/effector cells, expressed interferon-gamma (IFN-gamma), and lysed targets in a Fas (CD95)/FasL-dependent pathway. Massive accumulation of oligoclonal CD4+ T cells of athymic origin with the phenotype of Th1 memory/effector T cells in the colonic lamina propria of a histocompatible, immunodeficient host elicits a pancolitis that morphologically mimics human UC.
将无胸腺（裸）小鼠结肠固有层的CD4⁺TCRαβ⁺T细胞过继转移到同基因的、常染色体隐性突变scid（严重联合免疫缺陷）纯合的组织相容性（SCID）小鼠体内。将这些胸腺外CD4⁺T细胞转移到SCID小鼠体内可在过继宿主中诱发全结肠炎。这种炎症反应的组织病理学局限于结肠，且与人类溃疡性结肠炎极为相似。浸润患病SCID小鼠结肠固有层的CD4⁺T细胞表现出黏膜归巢记忆/效应细胞的表面表型，表达γ干扰素（IFN-γ），并通过Fas（CD95）/FasL依赖途径杀伤靶细胞。在组织相容性免疫缺陷宿主的结肠固有层中，大量具有Th1记忆/效应T细胞表型的无胸腺来源寡克隆CD4⁺T细胞积聚，引发了在形态学上模拟人类溃疡性结肠炎的全结肠炎。
