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Molecular Immunology in Hematological Disorders 2.0
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Molecular Immunology in Hematological Disorders 2.0

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: closed (31 October 2023) | Viewed by 5464

Special Issue Editors

Prof. Dr. Akiyoshi Takami

E-Mail Website
Guest Editor
Department of Medicine, Division of Hematology, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan
Interests: immunotherapy for hematological cancers; hematopoietic stem cell transplantation; laboratory hematology; the immunological effects of phytochemicals; transfusion medicine; bone marrow failure
Special Issues, Collections and Topics in MDPI journals
Dr. Jorge Luis Espinoza

E-Mail Website
Guest Editor
Faculty of Health Sciences, Kanazawa University, 5-11-80 Kodatsuno, Kanazawa, Ishikawa 920-0942, Japan
Interests: hematology and oncology; microbe-induced carcinogenesis; cancer drug discovery; parasitic infections; opportunistic microorganisms; immunology; microbiota; infectious diseases; artificial intelligence and medical sciences
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The mechanism by which hematological malignancies such as leukemia, lymphoma, and myeloma develop and proliferate in vivo is not yet fully understood. However, the possibility of eradicating cancer cells not only through allogeneic hematopoietic stem cell transplantation but also single-molecule targeted therapy, such as with CAR-T cells, suggests that the immune system, including innate and adaptive immunity, plays an important role in the development and pathophysiology of hematological malignancies. The involvement of immunological mechanisms has also been suggested in benign hematological disorders such as acquired aplastic anemia, paroxysmal nocturnal hemochromatosis, immune thrombocytopenia, thrombotic microangiopathy, and hemolytic anemia. In addition, hematological abnormalities associated with immunological dysregulation have also been noted in infectious diseases such as COVID-19 and autoimmune diseases. Therefore, there is a close pathophysiological relationship between hematological disorders and the immune system, and elucidation of these molecular mechanisms will advance the diagnosis and treatment of benign and malignant hematologic diseases, infectious diseases, and autoimmune diseases. This Special Issue focuses on molecular immunology in hematology and specifically welcomes studies that elucidate molecular immunological mechanisms in the diagnosis and treatment of hematological disorders, in addition to other topics that are relevant to the Special Issue theme.

Prof. Dr. Akiyoshi Takami
Dr. Jorge Luis Espinoza
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • anemia
  • bioinformatics
  • COVID-19
  • functional genetics
  • genetically-engineered therapy
  • hematopoietic stem cell transplantation
  • leukemia
  • lymphoma
  • myeloma
  • thrombocytopenia

Published Papers (4 papers)

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Research

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9 pages, 1736 KiB  
Communication
Immunosuppressive Activity of Exosomes from Granulocytic Myeloid-Derived Suppressor Cells in a Murine Model of Immune Bone Marrow Failure
by Ash Lee Manley, Jichun Chen, Wendy Fitzgerald, Xingmin Feng and Neal S. Young
Int. J. Mol. Sci. 2023, 24(19), 14661; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms241914661 - 28 Sep 2023
Cited by 1 | Viewed by 985
Abstract
We previously reported that granulocytic myeloid-derived suppressor cells (G-MDSCs) suppressed T-cell activation and attenuated bone marrow failure (BMF) in a minor histocompatibility (minor-H) antigen mismatched murine aplastic anemia (AA) model. In the current study, we tested the hypothesis that exosomes, a subset of [...] Read more.
We previously reported that granulocytic myeloid-derived suppressor cells (G-MDSCs) suppressed T-cell activation and attenuated bone marrow failure (BMF) in a minor histocompatibility (minor-H) antigen mismatched murine aplastic anemia (AA) model. In the current study, we tested the hypothesis that exosomes, a subset of extracellular vesicles, are responsible at least partially for G-MDSCs’ therapeutic efficacy. Indeed, exosomes isolated from GMDSCs (G-MDSC-exos) suppressed CD4+ and CD8+ T-cell proliferation in vitro and mildly attenuated immune BMF in the minor-H mismatched AA model. G-MDSC-exos treatment significantly increased red blood cells, hemoglobin, and total bone marrow (BM) cells, and moderately reduced BM CD8+ T cells. G-MDSC-exos’ effects were associated with upregulations in an array of lymphocyte-suppression-related miRNAs such as hsa-miR-142-5p, miR-19a-3p, and miR-19b-3p in both BM CD4+ and CD8+ T cells. We concluded that G-MDSC-exos attenuate immune BMF via modulating the delivery of immunosuppressive miRNAs into activated T lymphocytes. Full article
(This article belongs to the Special Issue Molecular Immunology in Hematological Disorders 2.0)
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20 pages, 4901 KiB  
Article
JAK3 Y841 Autophosphorylation Is Critical for STAT5B Activation, Kinase Domain Stability and Dimer Formation
by Georgialina Rodriguez, George Steven Martinez, Omar Daniel Negrete, Shengjie Sun, Wenhan Guo, Yixin Xie, Lin Li, Chuan Xiao, Jeremy Aaron Ross and Robert Arthur Kirken
Int. J. Mol. Sci. 2023, 24(15), 11928; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms241511928 - 25 Jul 2023
Viewed by 1394
Abstract
Janus tyrosine kinase 3 (JAK3) is primarily expressed in immune cells and is needed for signaling by the common gamma chain (γc) family of cytokines. Abnormal JAK3 signal transduction can manifest as hematological disorders, e.g., leukemia, severe combined immunodeficiency (SCID) and autoimmune disease [...] Read more.
Janus tyrosine kinase 3 (JAK3) is primarily expressed in immune cells and is needed for signaling by the common gamma chain (γc) family of cytokines. Abnormal JAK3 signal transduction can manifest as hematological disorders, e.g., leukemia, severe combined immunodeficiency (SCID) and autoimmune disease states. While regulatory JAK3 phosphosites have been well studied, here a functional proteomics approach coupling a JAK3 autokinase assay to mass spectrometry revealed ten previously unreported autophosphorylation sites (Y105, Y190, Y238, Y399, Y633, Y637, Y738, Y762, Y824, and Y841). Of interest, Y841 was determined to be evolutionarily conserved across multiple species and JAK family members, suggesting a broader role for this residue. Phospho-substitution mutants confirmed that Y841 is also required for STAT5 tyrosine phosphorylation. The homologous JAK1 residue Y894 elicited a similar response to mutagenesis, indicating the shared importance for this site in JAK family members. Phospho-specific Y841-JAK3 antibodies recognized activated kinase from various T-cell lines and transforming JAK3 mutants. Computational biophysics analysis linked Y841 phosphorylation to enhanced JAK3 JH1 domain stability across pH environments, as well as to facilitated complementary electrostatic JH1 dimer formation. Interestingly, Y841 is not limited to tyrosine kinases, suggesting it represents a conserved ubiquitous enzymatic function that may hold therapeutic potential across multiple kinase families. Full article
(This article belongs to the Special Issue Molecular Immunology in Hematological Disorders 2.0)
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17 pages, 6166 KiB  
Article
JAK1 Pseudokinase V666G Mutant Dominantly Impairs JAK3 Phosphorylation and IL-2 Signaling
by Alice H. Grant, Alejandro C. Rodriguez, Omar J. Rodriguez Moncivais, Shengjie Sun, Lin Li, Jonathon E. Mohl, Ming-Ying Leung, Robert A. Kirken and Georgialina Rodriguez
Int. J. Mol. Sci. 2023, 24(7), 6805; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24076805 - 06 Apr 2023
Cited by 5 | Viewed by 2017
Abstract
Overactive Janus kinases (JAKs) are known to drive leukemia, making them well-suited targets for treatment. We sought to identify new JAK-activating mutations and instead found a JAK1-inactivating pseudokinase mutation, V666G. In contrast to other pseudokinase mutations that canonically lead to an active kinase, [...] Read more.
Overactive Janus kinases (JAKs) are known to drive leukemia, making them well-suited targets for treatment. We sought to identify new JAK-activating mutations and instead found a JAK1-inactivating pseudokinase mutation, V666G. In contrast to other pseudokinase mutations that canonically lead to an active kinase, the JAK1 V666G mutation led to under-activation seen by reduced phosphorylation. To understand the functional role of JAK1 V666G in modifying kinase activity we investigated its influence on other JAK kinases and within the Interleukin-2 pathway. JAK1 V666G not only inhibited its own activity, but its presence could inhibit other JAK kinases. These findings provide new insights into the potential of JAK1 pseudokinase to modulate its own activity, as well as of other JAK kinases. Thus, the features of the JAK1 V666 region in modifying JAK kinases can be exploited to allosterically inhibit overactive JAKs. Full article
(This article belongs to the Special Issue Molecular Immunology in Hematological Disorders 2.0)
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Review

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25 pages, 704 KiB  
Review
How We Interpret Thrombosis with Thrombocytopenia Syndrome?
by Shinya Yamada and Hidesaku Asakura
Int. J. Mol. Sci. 2024, 25(9), 4956; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25094956 - 01 May 2024
Viewed by 251
Abstract
Platelets play an important role in hemostasis, and a low platelet count usually increases the risk of bleeding. Conditions in which thrombosis occurs despite low platelet counts are referred to as thrombosis with thrombocytopenia syndrome, including heparin-induced thrombocytopenia, vaccine-induced immune thrombotic thrombocytopenia, paroxysmal [...] Read more.
Platelets play an important role in hemostasis, and a low platelet count usually increases the risk of bleeding. Conditions in which thrombosis occurs despite low platelet counts are referred to as thrombosis with thrombocytopenia syndrome, including heparin-induced thrombocytopenia, vaccine-induced immune thrombotic thrombocytopenia, paroxysmal nocturnal hemoglobinuria, antiphospholipid syndrome, thrombotic microangiopathy (TMA), and disseminated intravascular coagulation. TMA includes thrombotic thrombocytopenic purpura, Shiga toxin-producing Escherichia coli-associated hemolytic uremic syndrome (HUS), and atypical HUS. Patients with these pathologies present with thrombosis and consumptive thrombocytopenia associated with the activation of platelets and the coagulation system. Treatment varies from disease to disease, and many diseases have direct impacts on mortality and organ prognosis if therapeutic interventions are not promptly implemented. Underlying diseases and the results of physical examinations and general laboratory tests as part of a thorough workup for patients should promptly lead to therapeutic intervention before definitive diagnosis. For some diseases, the diagnosis and initial treatment must proceed in parallel. Utilization of not only laboratory tests but also various scoring systems is important for validating therapeutic interventions based on clinical information. Full article
(This article belongs to the Special Issue Molecular Immunology in Hematological Disorders 2.0)
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