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Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
It has been proposed that the pathophysiology of autoimmune diseases, including vitiligo, may be linked to immunodeficiency. The existence of mechanisms of central immune tolerance prevents the persistence of autoreactive immune cells in later life. Even if a few autoreactive cells escape deletion within the thymus, these cells lose reactivity peripherally by various mechanisms. A loss of this tolerance could lead to onset of autoimmunity in patients with preexisting immunodeficiency. Other than this, dysfunction or aberration of mechanisms of apoptosis, proliferation signaling pathways, immune-mediated clearance, or innate cellular immunity could also contribute to autoimmunity in patients with immunodeficiency [3].
Human T lymphotropic virus type 1 (HTLV-1)
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
HTLV-1 specific cytotoxic T lymphocytes (CTLs) are abundant in the peripheral blood and predominantly recognize HTLV-1 tax protein antigen. CTLs are important in virus elimination but may also contribute to detrimental neuroinflammatory effects. The frequency of HTLV-1 specific CTLs is increased in the CSF compared to the periphery suggesting that these cells are expanded in the CSF or specifically recruited to the CNS where they may contribute to the neuropathology of HAM/TSP [13]. Regulatory T cells (Tregs) normally maintain peripheral immune tolerance and suppress autoimmune responses. CD4+ CD25+ Treg cells are increased in HAM/TSP but have decreased suppressive activity [24]. The immune dysregulation in HAM/TSP is characterized by activated inflammatory response and diminished suppressive activity.
Preparing and administering sublingual allergen vaccines
Published in Richard F. Lockey, Dennis K. Ledford, Allergens and Allergen Immunotherapy, 2020
Miguel Casanovas, Jonathan Kilimajer, Enrique Fernández-Caldas
Immune tolerance predominates in the oral/sublingual mucosa, and the antigen-presenting cells, such as dendritic cells and various T-cell subtypes, serve as key players in oral mucosal tolerance induction [16]. In mice, immunohistologic analyses of the sublingual mucosa show that there is a dense network of dendritic-like (DC) cells, located both in lamina propria and in the epithelial compartment. These DCs share phenotypical characteristics with epidermal Langerhans cells and appear mainly composed of transitional DCs [17]. In humans, Allam et al. [18] showed that mucosal regions, such as the vestibule of the mouth, or cheek mucosa (vestibulum or bucca), have a high density of oral Langerhans cells and high FcεRI expression on these cells. These findings suggest these sites could be an appropriate application site, with potent allergen uptake, for SLIT.
Differential expression of CCR8 in tumors versus normal tissue allows specific depletion of tumor-infiltrating T regulatory cells by GS-1811, a novel Fc-optimized anti-CCR8 antibody
Published in OncoImmunology, 2022
Jessica D. Weaver, Edward C. Stack, Joshua A. Buggé, Changyun Hu, Lara McGrath, Amy Mueller, Masie Wong, Boris Klebanov, Tanzila Rahman, Rosemary Kaufman, Christine Fregeau, Vikki Spaulding, Michelle Priess, Kristen Legendre, Sarah Jaffe, Dhruvkumar Upadhyay, Anirudh Singh, Chang-Ai Xu, Kristin Krukenberg, Yan Zhang, Yassine Ezzyat, Dorothée Saddier Axe, Michelle R. Kuhne, Michael A. Meehl, Donald R. Shaffer, Brian M. Weist, Dmitri Wiederschain, Fabien Depis, Monica Gostissa
The immune system has evolved complex cellular and molecular mechanisms to prevent deleterious immune-mediated disorders. A subset of CD4 + T cells, known as T regulatory (Treg) cells, that express the X chromosome-linked transcription factor forkhead box P3 (FOXP3), are central to the prevention of autoimmunity.1 They act by suppressing aberrant immune responses against self-antigens, resulting in immune tolerance.2 This tolerance mechanism can be co-opted by tumors when FOXP3+ Tregs, localized to the tumor microenvironment (TME), suppress anti-tumor immunity. Tumor-infiltrating Tregs can disrupt the function of tumor-specific T effector cells through direct cell-cell interactions by engaging inhibitory co-signaling molecules expressed on their cell surface or by secreting anti-inflammatory soluble factors such as transforming growth factor β (TGFβ); both mechanisms are known to contribute to the immunosuppressive TME.3
Oral delivery of the intracellular domain of the insulinoma-associated protein 2 (IA-2ic) by bacterium-like particles (BLPs) prevents type 1 diabetes mellitus in NOD mice
Published in Drug Delivery, 2022
Ruifeng Mao, Menglan Yang, Rui Yang, Yingying Chen, Enjie Diao, Tong Zhang, Dengchao Li, Xin Chang, Zhenjing Chi, Yefu Wang
Apart from preventing invasion of pathogens, the immune response plays an important role in preventing reactivity to self-antigens, thereby preventing the development of autoimmunity by complicated suppression tolerance mechanisms. Immune tolerance, including central and peripheral tolerance, relies on complicated clonal deletion/anergy of T and B cells as well as suppression by regulatory immune cells (Issa & Wood, 2012; Wambre & Jeong, 2018). Tolerance induction can be achieved by introducing proteins or peptides through various methods, such as intravenous injection, intranasal administration, skin administration as well as oral administration (Wang & Tisch, 2008; Xu et al., 2013; Mao et al., 2020a, 2020b). As a result of its ability to induce systemic unresponsiveness to orally administered antigens and its non-invasiveness, oral tolerance has been intensively investigated (Sricharunrat et al., 2018). Most of these oral tolerance studies performed in animals and human clinical trials aim to prevent and treat allergies, transplantation rejection as well as autoimmune disorders, including type 1 diabetes mellitus (T1DM).
Locked and loaded: engineering and arming oncolytic adenoviruses to enhance anti-tumor immune responses
Published in Expert Opinion on Biological Therapy, 2022
Immune tolerance can be imposed during B and T cell ontogeny by central tolerance. However, the balance between immune activation and immune tolerance is also modulated later by innate immune cells, antigen-presenting cells (APCs), and other types of immune cells in the peripheral [94]. Innate immune cells can be activated by receptors of PAMPs and DAMPs to recognize pathogens [3]. These pattern recognition systems are good at detecting strange external invaders but less useful in detecting neoplastic cells as they lack these patterns. In the absence of innate immune triggers, long-term exposure of tumor antigens to T cells can gradually convert T cells into an anergic or dysfunctional state (Figure 4) [90]. Thus, slow growth in the absence of innate cell danger signals can allow tumor cells to evade T cell recognition. In other cases, inflammation itself can assist in the tumorigenesis [95], but this is a different discussion.