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The Road to Tolerance: Mechanism of Immune Homeostasis in Health and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 April 2025 | Viewed by 4167

Special Issue Editor

Dr. Toshiaki Nakano

E-Mail Website
Guest Editor
1. Graduate Institute of Clinical Medical Sciences, Chang Gung University College of Medicine, Taoyuan, Taiwan
2. Liver Transplantation Center, Kaohsiung Chang Gung Memotial Hospital, Kaohsiung, Taiwan
Interests: transplant immunology; liver biology; biomarker discovery; photobiomodulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Our immune system has a unique mechanism for immune homeostasis and its activation or suppression would be depending on pathophysiological conditions. For the protection from invading microorganisms, innate and adaptive immunity should be activated for the clearance of microorganisms. Alternatively, our immune system should be tolerance to nonharmful antigens/pathogens such as autoantigens, food antigens and commensal bacteria. For the inhibition of tumor cell growth and metastasis, our immune system surveys abnormal cell development (i.e., immune surveillance), while aggressive tumor cells would induce immunosuppressive tumor microenvironment for tumor immune escape. On the other hand, the induction of graft acceptance (tolerance) is an ultimate goal in transplant immunology. The scope of the Special Issue is to summarize the current understanding of immune regulatory mechanisms for immune homeostasis in various research models such as infection, autoimmunity, tumor immunity, transplant immunity and fetomaternal tolerance.

Topics include, but are not limited to:

  • Molecular mechanisms of self and non-self recognition;
  • Molecular mechanisms of immune activation and tolerance induction;
  • Molecular mechanisms of disease progression and its suppression;
  • Biomarker discovery for prediction of immune status in health and disease;
  • The development of therapeutic strategies for immune modulation.

Dr. Toshiaki Nakano
Guest Editor

Manuscript Submission Information

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Related Special Issue

Published Papers (4 papers)

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Research

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17 pages, 1722 KiB  
Article
Soluble Neuropilin-1 Is Elevated in Sepsis and Correlates with Organ Dysfunction and Long-Term Mortality in Critical Illness
by Philipp Hohlstein, Eileen Schumacher, Samira Abu Jhaisha, Jule K. Adams, Maike R. Pollmanns, Carolin V. Schneider, Karim Hamesch, Katarina Horvathova, Theresa H. Wirtz, Frank Tacke, Christian Trautwein, Ralf Weiskirchen and Alexander Koch
Int. J. Mol. Sci. 2024, 25(10), 5438; https://doi.org/10.3390/ijms25105438 - 16 May 2024
Viewed by 940
Abstract
Critical illness and sepsis may cause organ failure and are recognized as mortality drivers in hospitalized patients. Neuropilin-1 (NRP-1) is a multifaceted transmembrane protein involved in the primary immune response and is expressed in immune cells such as T and dendritic cells. The [...] Read more.
Critical illness and sepsis may cause organ failure and are recognized as mortality drivers in hospitalized patients. Neuropilin-1 (NRP-1) is a multifaceted transmembrane protein involved in the primary immune response and is expressed in immune cells such as T and dendritic cells. The soluble form of NRP-1 (sNRP-1) acts as an antagonist to NRP-1 by scavenging its ligands. The aim of this study was to determine the value of sNRP-1 as a biomarker in critical illness and sepsis. We enrolled 180 critically ill patients admitted to a medical intensive care unit and measured serum sNRP-1 concentrations at admission, comparing them to 48 healthy individuals. Critically ill and septic patients showed higher levels of sNRP-1 compared to healthy controls (median of 2.47 vs. 1.70 nmol/L, p < 0.001). Moreover, sNRP-1 was also elevated in patients with sepsis compared to other critical illness (2.60 vs. 2.13 nmol/L, p = 0.01), irrespective of disease severity or organ failure. In critically ill patients, sNRP-1 is positively correlated with markers of kidney and hepatic dysfunction. Most notably, critically ill patients not surviving in the long term (one year after admission) showed higher concentrations of sNRP-1 at the time of ICU admission (p = 0.036), with this association being dependent on the presence of organ failure. Critically ill and septic patients exhibit higher serum concentrations of circulating sNRP-1, which correlates to organ failure, particularly hepatic and kidney dysfunction. Full article
(This article belongs to the Special Issue The Road to Tolerance: Mechanism of Immune Homeostasis in Health and Disease)
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Review

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22 pages, 1781 KiB  
Review
Innate Immunity and Synovitis: Key Players in Osteoarthritis Progression
by Veronica Panichi, Silvia Costantini, Merimma Grasso, Carla Renata Arciola and Paolo Dolzani
Int. J. Mol. Sci. 2024, 25(22), 12082; https://doi.org/10.3390/ijms252212082 - 11 Nov 2024
Viewed by 403
Abstract
Osteoarthritis (OA) is a chronic progressive disease of the joint. Although representing the most frequent cause of disability in the elderly, OA remains partly obscure in its pathogenic mechanisms and is still the orphan of resolutive therapies. The concept of what was once [...] Read more.
Osteoarthritis (OA) is a chronic progressive disease of the joint. Although representing the most frequent cause of disability in the elderly, OA remains partly obscure in its pathogenic mechanisms and is still the orphan of resolutive therapies. The concept of what was once considered a “wear and tear” of articular cartilage is now that of an inflammation-related disease that affects over time the whole joint. The attention is increasingly focused on the synovium. Even from the earliest clinical stages, synovial inflammation (or synovitis) is a crucial factor involved in OA progression and a major player in pain onset. The release of inflammatory molecules in the synovium mediates disease progression and worsening of clinical features. The activation of synovial tissue-resident cells recalls innate immunity cells from the bloodstream, creating a proinflammatory milieu that fuels and maintains a damaging condition of low-grade inflammation in the joint. In such a context, cellular and molecular inflammatory behaviors in the synovium could be the primum movens of the structural and functional alterations of the whole joint. This paper focuses on and discusses the involvement of innate immunity cells in synovitis and their role in the progression of OA. Full article
(This article belongs to the Special Issue The Road to Tolerance: Mechanism of Immune Homeostasis in Health and Disease)
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16 pages, 1605 KiB  
Review
Lessons from IgA Nephropathy Models
by Toshiki Kano, Hitoshi Suzuki, Yuko Makita, Yoshihito Nihei, Yusuke Fukao, Maiko Nakayama, Mingfeng Lee, Ryosuke Aoki, Koshi Yamada, Masahiro Muto and Yusuke Suzuki
Int. J. Mol. Sci. 2024, 25(21), 11484; https://doi.org/10.3390/ijms252111484 - 25 Oct 2024
Viewed by 800
Abstract
IgA nephropathy (IgAN) is the most common type of primary glomerulonephritis worldwide; however, the underlying mechanisms of this disease are not fully understood. This review explores several animal models that provide insights into IgAN pathogenesis, emphasizing the roles of aberrant IgA1 glycosylation and [...] Read more.
IgA nephropathy (IgAN) is the most common type of primary glomerulonephritis worldwide; however, the underlying mechanisms of this disease are not fully understood. This review explores several animal models that provide insights into IgAN pathogenesis, emphasizing the roles of aberrant IgA1 glycosylation and immune complex formation. It discusses spontaneous, immunization, and transgenic models illustrating unique aspects of IgAN development and progression. The animal models, represented by the grouped ddY (gddY) mouse, have provided guidance concerning the multi-hit pathogenesis of IgAN. In this paradigm, genetic and environmental factors, including the dysregulation of the mucosal immune system, lead to increased levels of aberrantly glycosylated IgA, nephritogenic immune complex formation, and subsequent glomerular deposition, followed by mesangial cell activation and injury. Additionally, this review considers the implications of clinical trials targeting molecular pathways influenced by IgAN (e.g., a proliferation-inducing ligand [APRIL]). Collectively, these animal models have expanded the understanding of IgAN pathogenesis while facilitating the development of therapeutic strategies that are currently under clinical investigation. Animal-model-based studies have the potential to facilitate the development of targeted therapies with reduced side effects for IgAN patients. Full article
(This article belongs to the Special Issue The Road to Tolerance: Mechanism of Immune Homeostasis in Health and Disease)
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20 pages, 2136 KiB  
Review
Mechanisms of Tolerance Induction in Liver Transplantation: Lessons Learned from Fetomaternal Tolerance, Autoimmunity and Tumor Immunity
by Toshiaki Nakano, Shigeru Goto and Chao-Long Chen
Int. J. Mol. Sci. 2024, 25(17), 9331; https://doi.org/10.3390/ijms25179331 - 28 Aug 2024
Viewed by 894
Abstract
Since the first published report of experimental kidney transplantation in dogs in 1902, there were many experimental and clinical trials of organ transplantation, with many sacrifices. After the establishment of the surgical technique and the discovery of immunosuppressive drugs, transplantation became the definitive [...] Read more.
Since the first published report of experimental kidney transplantation in dogs in 1902, there were many experimental and clinical trials of organ transplantation, with many sacrifices. After the establishment of the surgical technique and the discovery of immunosuppressive drugs, transplantation became the definitive treatment strategy for patients with terminal organ failure. However, this is not a common therapy method due to the difficulty of solving the fundamental issues behind organ transplantation, including the shortage of donor graft, potential risks of transplant surgery and economic capability. The pre- and post-transplant management of recipients is another critical issue that may affect transplant outcome. Most liver transplant recipients experience post-transplant complications, including infection, acute/chronic rejection, metabolic syndrome and the recurrence of hepatocellular carcinoma. Therefore, the early prediction and diagnosis of these complications may improve overall and disease-free survival. Furthermore, how to induce operational tolerance is the key to achieving the ultimate goal of transplantation. In this review, we focus on liver transplantation, which is known to achieve operational tolerance in some circumstances, and the mechanical similarities and differences between liver transplant immunology and fetomaternal tolerance, autoimmunity or tumor immunity are discussed. Full article
(This article belongs to the Special Issue The Road to Tolerance: Mechanism of Immune Homeostasis in Health and Disease)
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