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CD38 and Disease: A Bi-Directional Cross-Talk between Pathology and Physiology...
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CD38 and Disease: A Bi-Directional Cross-Talk between Pathology and Physiology II

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (10 March 2022) | Viewed by 37361

Special Issue Editors

Prof. Dr. Fabio Malavasi

E-Mail Website
Guest Editor
Department of Medical Science, University of Turin and Fondazione Ricerca Molinette, 10123 Turin, Italy
Interests: antibody therapy; human myeloma; leukemia; IgG receptors; immune modulation
Special Issues, Collections and Topics in MDPI journals
Dr. Aneel Paulus

E-Mail Website
Guest Editor
1. Department of Cancer Biology, Mayo Clinic, Jacksonville, FL 32224, USA
2. Division of Hematology & Oncology, Mayo Clinic, Jacksonville, FL 32224, USA
Interests: multiple myeloma; MGUS; chronic lymphocytic leukemia; waldenstrom macroglobulinemia; immunotherapy; cancer vaccines; antibody therapy
Special Issues, Collections and Topics in MDPI journals
Dr. Claudio Cerchione

E-Mail Website
Guest Editor
Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori, 47014 Meldola, Italy
Interests: acute lymphoblastic leukemia; acute myeloid leukemia; myelodysplastic syndromes; multiple myeloma and MGUS; non-Hodgkin and Hodgkin lymphoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The products of the CD38/CD157 gene family are attracting attention from the scientific and medical communities. More than three decades of research on CD38 and CD157 and their role in human diseases has recently culminated in the development of agents that target CD38 for therapeutic exploit. The use of anti-CD38 therapeutic antibodies has emerged as an important treatment modality for the clinical management of patients with multiple myeloma. On the heels of this success, the efficacy of CD38-targeting agents is also being actively investigated for patients with other hematologic or solid-tumor cancers.

Although CD38 and CD157 are expressed on the cell surface, both molecules are endowed with pleiotropic functions and, therefore it is reasonable to expect that they may exert functions beyond that of a mere marker. An experimental approach based on analysis of the distribution of the molecules in the context of different diseases (from autoimmunity to more complex clinical entities such as aging, metabolism, or social behavior) may enrich our knowledge on the functions of these ancient cell-surface receptors beyond their current recognition as activation markers, adhesion molecules, and ectoenzymes.

The results may be expected to provide a comprehensive (and perhaps unified) view of the real in vivo function of these molecules, whose high conservation in phylogeny bears testament to their significant role in life.

This Special Issue of Cells “CD38 and Disease: A Bi-Directional Cross-Talk between Pathology and Physiology" welcomes contributions from basic and clinical scientists working in the field. The scientific contributions may be in the form of original research papers or reviews. We encourage papers starting from experimental observations and ending with a perspective related to the focus. The basic idea of the Issue is to dissect the roles of CD38/CD157 in the pathogenesis or progression of diseases and their potential application in therapy. Concurrently, these observations may contribute to the improvement of the therapeutic model in use today.

Relevant topics include:

  • CD38/CD157 and NAD+ metabolism;
  • CD38/CD157 and aging;
  • CD38/CD157 and multiple myeloma;
  • CD38/CD157 and leukemias;
  • CD38/CD157 and mesotheliomas;
  • CD38/CD157 and systemic sclerosis;
  • CD38/CD157 and T-cell lymphomas;
  • CD38/CD157 and behaviors;
  • CD38/CD157 and immune response;
  • CD38/CD157 and check-point inhibitors;
  • CD38/CD157 and solid tumors;
  • CD38/CD157 and cells with suppressive functions;
  • CD38/CD157 and alternative therapeutic approaches;
  • CD38/CD157 and central nervous system function.
Prof. Dr. Fabio Malavasi
Dr. Aneel Paulus
Dr. Claudio Cerchione
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • ectoenzymes and NAD and ATP metabolisms
  • immune activation and immune suppression
  • multiple myeloma therapy
  • CLL therapy
  • cancer therapy
  • aging
  • behavior
  • central nervous system

Related Special Issue

Published Papers (6 papers)

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Research

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15 pages, 1936 KiB  
Article
Expression of CD38 in Mast Cells: Cytological and Histotopographic Features
by Dmitri Atiakshin, Vera Samoilova, Igor Buchwalow and Markus Tiemann
Cells 2021, 10(10), 2511; https://doi.org/10.3390/cells10102511 - 22 Sep 2021
Cited by 4 | Viewed by 2565
Abstract
The biological significance of the CD38 molecule goes beyond metabolic, enzymatic, and proliferative functions. CD38 possesses the functions of an exoenzyme and receptor, and is actively involved in the mechanisms of adhesion, migration, intercellular signaling, formation of immune synapses, and modulation of the [...] Read more.
The biological significance of the CD38 molecule goes beyond metabolic, enzymatic, and proliferative functions. CD38 possesses the functions of an exoenzyme and receptor, and is actively involved in the mechanisms of adhesion, migration, intercellular signaling, formation of immune synapses, and modulation of the activity of a wide range of immune and non-immune cells. The aim of this study was the immunohistochemical assessment of the cytological and histotopographic characteristics of CD38 expression in mast cells. CD38 expression was found in a minority of the mast cell population. It is characterized by wide variability from low to high levels. The intensity of CD38 expression in mast cells has organ-specific features and depends on the development of pathological processes in a specific tissue microenvironment. The mechanisms of intercellular interaction between mast cells and CD38+ cells foster new understanding of the protumorigenic or antitumor potential of tryptase. Full article
(This article belongs to the Special Issue CD38 and Disease: A Bi-Directional Cross-Talk between Pathology and Physiology II)
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13 pages, 4410 KiB  
Article
Novel Insights in Anti-CD38 Therapy Based on CD38-Receptor Expression and Function: The Multiple Myeloma Model
by Beatrice Anna Zannetti, Angelo Corso Faini, Evita Massari, Massimo Geuna, Enrico Maffini, Giovanni Poletti, Claudio Cerchione, Giovanni Martinelli, Fabio Malavasi and Francesco Lanza
Cells 2020, 9(12), 2666; https://doi.org/10.3390/cells9122666 - 11 Dec 2020
Cited by 10 | Viewed by 4879
Abstract
Multiple myeloma (MM) is a hematological disease characterized by the proliferation and accumulation of malignant plasmacells (PCs) in the bone marrow (BM). Despite widespread use of high-dose chemotherapy in combination with autologous stem cell transplantation (ASCT) and the introduction of novel agents (immunomodulatory [...] Read more.
Multiple myeloma (MM) is a hematological disease characterized by the proliferation and accumulation of malignant plasmacells (PCs) in the bone marrow (BM). Despite widespread use of high-dose chemotherapy in combination with autologous stem cell transplantation (ASCT) and the introduction of novel agents (immunomodulatory drugs, IMiDs, and proteasome inhibitors, PIs), the prognosis of MM patients is still poor. CD38 is a multifunctional cell-surface glycoprotein with receptor and ectoenzymatic activities. The very high and homogeneous expression of CD38 on myeloma PCs makes it an attractive target for novel therapeutic strategies. Several anti-CD38 monoclonal antibodies have been, or are being, developed for the treatment of MM, including daratumumab and isatuximab. Here we provide an in-depth look atCD38 biology, the role of CD38 in MM progression and its complex interactions with the BM microenvironment, the importance of anti-CD38 monoclonal antibodies, and the main mechanisms of antibody resistance. We then review a number of multiparametric flow cytometry techniques exploiting CD38 antigen expression on PCs to diagnose and monitor the response to treatment in MM patients. Full article
(This article belongs to the Special Issue CD38 and Disease: A Bi-Directional Cross-Talk between Pathology and Physiology II)
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Review

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11 pages, 1051 KiB  
Review
Daratumumab in the Treatment of Light-Chain (AL) Amyloidosis
by Giovanni Palladini, Paolo Milani, Fabio Malavasi and Giampaolo Merlini
Cells 2021, 10(3), 545; https://doi.org/10.3390/cells10030545 - 4 Mar 2021
Cited by 25 | Viewed by 4968
Abstract
Systemic light-chain (AL) amyloidosis is caused by a small B cell, most commonly a plasma cell (PC), clone that produces toxic light chains (LC) that cause organ dysfunction and deposits in tissues. Due to the production of amyloidogenic, misfolded LC, AL PCs display [...] Read more.
Systemic light-chain (AL) amyloidosis is caused by a small B cell, most commonly a plasma cell (PC), clone that produces toxic light chains (LC) that cause organ dysfunction and deposits in tissues. Due to the production of amyloidogenic, misfolded LC, AL PCs display peculiar biologic features. The small, indolent plasma cell clone is an ideal target for anti-CD38 immunotherapy. A recent phase III randomized study showed that in newly diagnosed patients, the addition of daratumumab to the standard of care increased the rate and depth of the hematologic response and granted more frequent organ responses. In the relapsed/refractory setting, daratumumab alone or as part of combination regimens gave very promising results. It is likely that daratumumab-based regimens will become new standards of care in AL amyloidosis. Another anti-CD38 monoclonal antibody, isatuximab, is at an earlier stage of development as a treatment for AL amyloidosis. The ability to target CD38 on the amyloid PC offers new powerful tools to treat AL amyloidosis. Future studies should define the preferable agents to combine with daratumumab upfront and in the rescue setting and assess the role of maintenance. In this review, we summarize the rationale for using anti-CD38 antibodies in the treatment of AL amyloidosis. Full article
(This article belongs to the Special Issue CD38 and Disease: A Bi-Directional Cross-Talk between Pathology and Physiology II)
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21 pages, 623 KiB  
Review
CD38: T Cell Immuno-Metabolic Modulator
by Anwesha Kar, Shikhar Mehrotra and Shilpak Chatterjee
Cells 2020, 9(7), 1716; https://doi.org/10.3390/cells9071716 - 17 Jul 2020
Cited by 46 | Viewed by 10750
Abstract
Activation and subsequent differentiation of T cells following antigenic stimulation are triggered by highly coordinated signaling events that lead to instilling cells with a discrete metabolic and transcriptional feature. Compelling studies indicate that intracellular nicotinamide adenine dinucleotide (NAD+) levels have profound [...] Read more.
Activation and subsequent differentiation of T cells following antigenic stimulation are triggered by highly coordinated signaling events that lead to instilling cells with a discrete metabolic and transcriptional feature. Compelling studies indicate that intracellular nicotinamide adenine dinucleotide (NAD+) levels have profound influence on diverse signaling and metabolic pathways of T cells, and hence dictate their functional fate. CD38, a major mammalian NAD+ glycohydrolase (NADase), expresses on T cells following activation and appears to be an essential modulator of intracellular NAD+ levels. The enzymatic activity of CD38 in the process of generating the second messenger cADPR utilizes intracellular NAD+, and thus limits its availability to different NAD+ consuming enzymes (PARP, ART, and sirtuins) inside the cells. The present review discusses how the CD38-NAD+ axis affects T cell activation and differentiation through interfering with their signaling and metabolic processes. We also describe the pivotal role of the CD38-NAD+ axis in influencing the chromatin remodeling and rewiring T cell response. Overall, this review emphasizes the crucial contribution of the CD38−NAD+ axis in altering T cell response in various pathophysiological conditions. Full article
(This article belongs to the Special Issue CD38 and Disease: A Bi-Directional Cross-Talk between Pathology and Physiology II)
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10 pages, 961 KiB  
Review
CD38 in Neurodegeneration and Neuroinflammation
by Serge Guerreiro, Anne-Laure Privat, Laurence Bressac and Damien Toulorge
Cells 2020, 9(2), 471; https://doi.org/10.3390/cells9020471 - 18 Feb 2020
Cited by 77 | Viewed by 10009
Abstract
Neurodegenerative diseases are characterized by neuronal degeneration as well as neuroinflammation. While CD38 is strongly expressed in brain cells including neurons, astrocytes as well as microglial cells, the role played by CD38 in neurodegeneration and neuroinflammation remains elusive. Yet, CD38 expression increases as [...] Read more.
Neurodegenerative diseases are characterized by neuronal degeneration as well as neuroinflammation. While CD38 is strongly expressed in brain cells including neurons, astrocytes as well as microglial cells, the role played by CD38 in neurodegeneration and neuroinflammation remains elusive. Yet, CD38 expression increases as a consequence of aging which is otherwise the primary risk associated with neurodegenerative diseases, and several experimental data demonstrated that CD38 knockout mice are protected from neurodegenerative and neuroinflammatory insults. Moreover, nicotinamide adenine dinucleotide, whose levels are tightly controlled by CD38, is a recognized and potent neuroprotective agent, and NAD supplementation was found to be beneficial against neurodegenerative diseases. The aims of this review are to summarize the physiological role played by CD38 in the brain, present the arguments indicating the involvement of CD38 in neurodegeneration and neuroinflammation, and to discuss these observations in light of CD38 complex biology. Full article
(This article belongs to the Special Issue CD38 and Disease: A Bi-Directional Cross-Talk between Pathology and Physiology II)
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Other

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10 pages, 1534 KiB  
Brief Report
Detection of Human CD38 Using Variable Lymphocyte Receptor (VLR) Tetramers
by Srijit Khan, Yanling Liu, Laura M. Ernst, Leslie Y. T. Leung, Patrick Budylowski, Shilan Dong, Paolo Campisi, Evan J. Propst, Nikolaus E. Wolter, Eyal Grunebaum, Mario Ostrowski and Götz R. A. Ehrhardt
Cells 2020, 9(4), 950; https://doi.org/10.3390/cells9040950 - 12 Apr 2020
Cited by 2 | Viewed by 3109
Abstract
CD38 is a multifunctional cell surface receptor expressed on multiple cell lineages of hematopoietic origin with high levels of expression on human plasma cells. Previously, we isolated the monoclonal variable lymphocyte receptor B (VLRB) MM3 antibody from the evolutionarily distant sea lamprey, which [...] Read more.
CD38 is a multifunctional cell surface receptor expressed on multiple cell lineages of hematopoietic origin with high levels of expression on human plasma cells. Previously, we isolated the monoclonal variable lymphocyte receptor B (VLRB) MM3 antibody from the evolutionarily distant sea lamprey, which recognized the CD38 ectoenzyme exclusively on human plasma cells in a manner that correlated with CD38 enzymatic activity. The plasma cell-specific binding of VLRB MM3 contrasts with the broad pattern of expression of CD38-determined conventional antibodies specific for this antigen. In an effort to facilitate the application of this unique reagent in combination with conventional antibody panels, we explored a strategy to generate VLRB MM3 tetramers. The resulting reagent maintained the threshold-based recognition of CD38. Increased sensitivity achieved with VLRB MM3 tetramers also showed preferential recognition of germinal center centroblasts over centrocytes. VLRB MM3 tetramers thus provided a unique and versatile single-step staining reagent for the detection of human CD38 that is readily incorporated into multi-color flow cytometry panels. Full article
(This article belongs to the Special Issue CD38 and Disease: A Bi-Directional Cross-Talk between Pathology and Physiology II)
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