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Immune Reconstitution after Hematopoietic Stem Cell Transplantation
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Andreas Thiel, Tobias Alexander, Christian A. Schmidt, Falk Hiepe, Renate Arnold, Andreas Radbruch, Larissa Verda, Richard K. Burt
CD4+CD25+ T cells contain the high affinity interleukin-2 receptor alpha (IL-2Rα) also known as CD25, a T cell activation marker.54-55 From experiments with thymectomized mice, CD4+CD25+ T cells are thymic-derived.56 Once activated via their TCR, CD4+CD25+ cells exert an antigen independent inhibition of IL-2 production and promote cell cycle arrest.57 CD4+CD25+ T cells have been reported to inhibit by means of IL-10 and/or TGF-β.58-59 However, this remains controversial and while the mechanism CD4+CD25+ T cell suppression is unclear, the effect requires cell-cell contact.60-61 CD4+CD25+ T cells have been shown to be important in preventing several animal autoimmune disorders.62-64
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
CD4+ CD25+ T cells are a population for active suppression of autoimmunity. Specifically, CD4+ CD25+ T cells have been shown to prevent insulin-dependent diabetes mellitus, inflammatory bowel disease, and pancreatitis. Here, we present evidence that CD4+ CD25+ T cells also play a major role in controlling the severity of arthritis detected in B. burgdorferi–vaccinated gamma interferon–deficient (IFN-γo) C57BL/6 mice challenged with the Lyme spirochete. When B. burgdorferi–vaccinated and –challenged IFN-γo mice were treated with anti-IL-17 antibody, the number of CD4+ CD25+T cells increased in the local lymph nodes. Furthermore, this histopathologic examination showed the mice to be free of destructive arthritis. When these anti-IL-17-treated B. burgdorferi–vaccinated and –challenged mice were also administered anti-4 25 antibody, the number of CD4+ CD25+ T cells in the local lymph nodes decreased. More importantly, severe destructive arthopathy was induced. In addition, delayed administration of anti-CD25 antibody decreased the severity of the arthritis. These results suggest that CD4+ CD25+ T cells are involved in regulation of a severe destructive arthritis induced with an experimental model of vaccination and challenged with B. burgdorferi. Collectively, these results suggest that other immune mediators, but not IFN-γ, are responsible for the induction of arthritis. There is evidence, however, that IFN-γ can potentiate the proinflammatory effects of IL-17.
Effects of life-stage and passive tobacco smoke exposure on pulmonary innate immunity and influenza infection in mice
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Lei Wang, Maya Rajavel, Ching-Wen Wu, Chuanzhen Zhang, Morgan Poindexter, Ciara Fulgar, Tiffany Mar, Jasmine Singh, Jaspreet K. Dhillon, Jingjing Zhang, Yinyu Yuan, Radek Abarca, Wei Li, Kent E. Pinkerton
Infiltration of immune cells in bronchoalveolar lavage fluid (BALF), inflammation of lung tissue (histopathology), distribution of CD4-, CD8-, and CD25-positive T cell markers in lung tissue, and expression of interferon mRNA (IFN) in spleen tissue were determined following IAV inoculation. T cells are the most important lymphocyte trafficking to the lungs during the first week of viral infection. The CD4, CD8, and CD25 T cell markers were selected to visualize populations of helper, cytotoxic, and regulatory T cells, respectively. CD4-positive, helper, T cells interact with antigen-presenting cells (e.g., macrophages) to shape pathogen-specific, adaptive immune responses, such as antibody production and cytotoxic T cell activation (Figure 1; Sant et al. 2018a; Sant, Richards, and Nayak 2018b; Lee and Lawrence 2018). CD8-positive, cytotoxic, T cells induce death of pathogen-infected, damaged, or dysfunctional cells (Pizzolla et al. 2017; Smed-Sörensen et al. 2012). CD25-positive, regulatory T cells are a subset of CD4-positive cells which suppress the activities of other T cells, B cells, and antigen-presenting cells (Corthay 2009). These three cell types are important factors in the immune response to viral infections (Rosendahl Huber et al. 2014).
Tumor growth suppression by implantation of an anti-CD25 antibody-immobilized material near the tumor via regulatory T cell capture
Published in Science and Technology of Advanced Materials, 2021
Tsuyoshi Kimura, Rino Tokunaga, Yoshihide Hashimoto, Naoko Nakamura, Akio Kishida
Cancer immunotherapy can involve enhancement of immune attack or release of immune tolerance [17]. Importantly, FoxP3+ CD25+ CD4+ Tregs have been shown to strongly affect tumor immune tolerance [4]. In the tumor microenvironment, Tregs infiltrate and accumulate through the secretion of chemokines, such as CCL22, from cancer cells and inhibit the attack of immune cells, such as NK cells and effector T cells, to cancer cells [4,5]. In this study, in order to remove Tregs from the tumor and release immune tolerance, we designed and prepared an antibody-immobilized mesh and subsequently investigated the effects of the mesh on tumor growth suppression following implantation in mice. The transcription factor FoxP3 is a specific marker of Tregs and is FoxP3 expressed inside the cells; thus, this specific marker could not be used in our system. CD25 is a surface marker of Tregs; therefore, we chose anti-CD25 antibodies in this study. A recent study showed that three types of Tregs, including naïve Tregs, effector Tregs, and non-Tregs, were present and exhibited variations in immunosuppression. Among these types of Tregs, effector Tregs, which show high immunosuppressive ability, are present as the CD25++FoxP3++ cell population. Moreover, effector Tregs have been identified in proliferative tumors [18]. Therefore, in this study, we designed an anti-CD25 antibody-immobilized material to remove the effector Tregs from tumors.