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Allogeneic Hemopoietic Stem Cell Transplantation in Animal Models of Autoimmune Disease
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
In 1985, we demonstrated that allo (not syngeneic) BMT across MHC barriers can be used to treat established autoimmune diseases in autoimmune-prone mice.1 To our knowledge, this was the first report indicating that glomerular damage induced by lupus nephritis is reversible. Similar studies have been performed in many other experimental autoimmune disease models, such as NOD mice,27-29 NZB/KN mice,30 and BB rats.31
Immunopathogenesis of Type I Diabetes Mellitus
Published in George S. Eisenbarth, Immunotherapy of Diabetes and Selected Autoimmune Diseases, 2019
Richard J. Keller, George S. Eisenbarth
The fact that approximately 50% of initially discordant identical twins also get Type I diabetes has been advanced as evidence for environmental factors at work. Yet during the ontogeny of B and T lymphocytes, gene rearrangements occur creating a great diversity of immunoglobulin and T cell receptors30. Accordingly, identical twins may not have identical T cell receptors or immunoglobulin genes. In fact, there is no autoimmune disease with a 100% concordance in identical twins. Discordance may therefore reflect the stochiastic processes of the immune system or other somatic mutational events. Environmental factors may influence the rate of development of Type I diabetes. Inbred NOD mice develop diabetes at different rates in different laboratories. In this regard it is noteworthy that several recent epidemiologic studies report that the incidence of Type I diabetes is increasing, suggesting that long-term changes in the environment are altering the probability of eventual diabetes.31
Pancreas Microcirculation
Published in John H. Barker, Gary L. Anderson, Michael D. Menger, Clinically Applied Microcirculation Research, 2019
Michael D. Menger, Brigitte Vollmar
For the induction of acute experimental hyperglycemia, glucose may be administered intravenously. For induction of long-term hyperglycemia, pharmacological compounds, such as streptozotocin or alloxan, respectively, may be applied. However, these models only simulate hyperglycemic conditions, but do not manifest true diabetic disease. To approximate more appropriately the clinical disease of diabetes mellitus, the use of particular animal strains, such as ob/ob mice or non-obese diabetic (NOD) mice, provides a more distinct approach for the study of diabetes-induced pathomechanisms.
Exploring the mechanisms of action of Zengye decoction (ZYD) against Sjogren’s syndrome (SS) using network pharmacology and animal experiment
Published in Pharmaceutical Biology, 2023
Jiake Yu, Shuying Wang, Jie Yang, Wuxinrui Huang, Beikang Tang, Weijun Peng, Jing Tian
Network pharmacology, a comprehensive, systematic, and holistic approach, predicts the target profiles and pharmacological actions of TCM (Luo et al. 2020). As a novel research approach, TCM network pharmacology is anticipated to succeed in achieving the transformation from experience-based to evidence-based therapy (Li and Zhang 2013; Zhang et al. 2019). The NOD mice with polyautoimmunity are an excellent model for studying autoimmune diseases, such as autoimmune thyroiditis, neuropathies, and SS, except for diabetes (Aubin et al. 2022). We acquired the active compounds and possible targets of ZYD against SS, built a network of drug–target–disease relationship, and predicted the pharmacological mechanisms of ZYD against SS using the TCM network pharmacology method. Animal experiments on NOD mice further proved the efficacy of ZYD and the predicted results of network pharmacology. Our research offers a theoretical foundation for the pathogenesis and clinical management of SS.
Type 1 diabetes: key drug targets and how they could influence future therapeutics
Published in Expert Opinion on Therapeutic Targets, 2023
Yoon Kook Kim, Kashif M. Munir, Stephen N. Davis
Animal models with NOD mice have shown favorable results in the past, and a dose-finding study in latent autoimmune diabetes of adults (LADA) showed some evidence of preservation of endogenous insulin secretion. However, a 12-month follow-up comparison study of 145 participants in three experiment groups, three injections of vaccine vs two injections of vaccine vs aluminum only, failed to show a significant effect from GAD-Alum use in terms of preserving C-peptide, improving HbA1c, or decreasing insulin dose [40]. This multi-center randomized controlled study was terminated after phase 2. Interestingly, the GAD antibody titer in the treatment groups were higher than in the control group, indicating a non-protective immune response from GAD-Alum injections. A similar study of 334 patients with T1DM, fasting c-peptide > 0.3 ng/ml, and detectable serum GAD antibodies were randomly assigned to receive GAD-alum only, GAD-alum followed by placebo, or placebo only [41]. The primary outcome of stimulated c-peptide after a mixed-meal tolerance test did not differ significantly among the groups. Changes in insulin doses, HbA1c, or rates of hypoglycemia were also similar among the groups.
Particulate Matter, Asian Sand Dust Delays Cyclophosphamide-induced Type 1 Diabetes in NOD Mice
Published in Immunological Investigations, 2020
Kentaro Morita, Duo Wang, Ryoko Baba, Hiroyuki Morimoto, Yuan Song, Tamotsu Kanazawa, Yasuhiro Yoshida
For diabetes research based on animal models, NOD mice are widely used as they spontaneously develop T1D, and the disease presents a phenotype similar to that in humans (Leiter 2001). It is well known that the results obtained using the cyclophosphamide (CY)-induced model are equivalent to those obtained using the spontaneous models (Harada and Makino 1984; Rehni et al. 2017). In addition, the onset time of diabetes is more well defined in the CY-induced model than in the spontaneous onset model, and thus the blood glucose level can be monitored more efficiently. Therefore, we chose to adopt the CY induction model based on evidence provided in previous papers. Here, we evaluated the effect of ASD on T1D by inducing the onset of diabetes in NOD mice model via the administration of CY.