Pino Steve, Brehm Michael A, Covassin-Barberis Laurence, King Marie, Gott Bruce, Chase Thomas H, Wagner Jennifer, Burzenski Lisa, Foreman Oded, Greiner Dale L, Shultz Leonard D
Department of Medicine, The University of Massachusetts Medical School, Worcester, MA, USA.
Methods Mol Biol. 2010;602:105-17. doi: 10.1007/978-1-60761-058-8_7.
Immunodeficient mice have been used as recipients of human peripheral blood mononuclear cells (PBMC) for in vivo analyses of human xeno-graft-versus-host disease (GVHD). This xeno-GVHD model system in many ways mimics the human disease. The model system is established by intravenous or intraperitoneal injection of human PBMC or spleen cells into unconditioned or irradiated immunodeficient recipient mice. Recently, the development of several stocks of immunodeficient Prkdc ( scid ) (scid) and recombination activating 1 or 2 gene (Rag1 or Rag2) knockout mice bearing a targeted mutation in the gene encoding the IL2 receptor gamma chain (IL2rgamma) have been reported. The addition of the mutated IL2rgamma gene onto an immunodeficient mouse stock facilitates heightened engraftment with human PBMC. Stocks of mice with mutations in the IL2rgamma gene have been studied in several laboratories on NOD-scid, NOD-Rag1 ( null ), BALB/c-Rag1 ( null ), BALB/c-Rag2 ( null ), and Stock-H2(d)-Rag2 ( null ) strain backgrounds. Parameters to induce human xeno-GVHD in H2(d)-Rag2 ( null ) IL2rgamma ( null ) mice have been published, but variability in the frequency of disease and kinetics of GVHD were observed. The availability of the NOD-scid IL2rgamma ( null ) stock that engrafts more readily with human PBMC than does the Stock-H2(d)-Rag2 ( null ) IL2rgamma ( null ) stock should lead to a more reproducible humanized mouse model of GVHD and for the use in drug evaluation and validation. Furthermore, GVHD in human PBMC-engrafted scid mice has been postulated to result predominately from a human anti-mouse major histocompatibility complex (MHC) class II reactivity. Our recent development of NOD-scid IL2rgamma ( null ) beta2m ( null ) and NOD-scid IL2rgamma ( null ) Ab ( null ) stocks of mice now make it possible to investigate directly the role of host MHC class I and class II in the pathogenesis of GVHD in humanized mice using NOD-scid IL2rgamma ( null ) stocks that engraft at high levels with human PBMC and are deficient in murine MHC class I, class II, or both classes of MHC molecules.
免疫缺陷小鼠已被用作人类外周血单个核细胞(PBMC)的受体,用于对人类异种移植物抗宿主病(GVHD)进行体内分析。这种异种GVHD模型系统在许多方面模拟了人类疾病。该模型系统是通过将人类PBMC或脾细胞静脉内或腹腔内注射到未预处理或经辐照的免疫缺陷受体小鼠中建立的。最近,有报道称开发了几种免疫缺陷的Prkdc(scid)(scid)和重组激活基因1或2(Rag1或Rag2)敲除小鼠品系,这些小鼠在编码IL2受体γ链(IL2rgamma)的基因中存在靶向突变。将突变的IL2rgamma基因添加到免疫缺陷小鼠品系上有助于提高人类PBMC的植入率。几个实验室已经在NOD-scid、NOD-Rag1(无效)、BALB/c-Rag1(无效)、BALB/c-Rag2(无效)和Stock-H2(d)-Rag2(无效)品系背景下研究了IL2rgamma基因发生突变的小鼠品系。已发表了在H2(d)-Rag2(无效)IL2rgamma(无效)小鼠中诱导人类异种GVHD的参数,但观察到疾病发生率和GVHD动力学存在变异性。与Stock-H2(d)-Rag2(无效)IL2rgamma(无效)品系相比,NOD-scid IL2rgamma(无效)品系更容易植入人类PBMC,这应该会导致更可重复的GVHD人源化小鼠模型,并用于药物评估和验证。此外,据推测,人类PBMC植入的scid小鼠中的GVHD主要源于人类抗小鼠主要组织相容性复合体(MHC)II类反应性。我们最近开发的NOD-scid IL2rgamma(无效)beta2m(无效)和NOD-scid IL2rgamma(无效)Ab(无效)小鼠品系现在使得使用能够高效植入人类PBMC且缺乏小鼠MHC I类、II类或两类MHC分子的NOD-scid IL2rgamma(无效)品系,直接研究宿主MHC I类和II类在人源化小鼠GVHD发病机制中的作用成为可能。