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Biomedicines
Special Issues
Innate Immune Memory in Health and Disease
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Innate Immune Memory in Health and Disease

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 10854

Special Issue Editor

Dr. Dhifaf Sarhan

E-Mail Website
Guest Editor
Karolinska Institutet, Department for Laboratory Medicine, Division of Pathology, Alfred Nobels allé 8, 8th Floor, 141 52 Huddinge, Stockholm, Sweden
Interests: tumor immunology; tumor microenvironment; immunotherapies; innate memory; Natural Killer cells; myeloid cells; sex immune dimorphism

Special Issue Information

Dear Colleagues,

The ability of the innate immune system to develop adaptive features and provide long-term protection against pathogenic reinfection is termed trained immunity or innate memory. Epigenetic modification of various transcriptional pathways, as well as metabolic reprogramming of innate immune cells by both endogenous and exogenous stimuli, is the main driving force for innate memory. Similar to adaptive immune response, innate memory is associated with an augmented immune reaction in response to secondary stimulations. In general, innate memory is known to provide relatively short-term protection ranging from about 3 months to 1 year. Nevertheless, recent findings have challenged our understanding of innate memory, with several laboratories showing that innate memory can be long-lived and transmitted across generations. On the other hand, there is a knowledge gap in how innate memory works during and against tumor development and progression. The immune cells primarily associated with innate immune memory response include monocytes, tissue macrophages, natural killer cells, as well as hematopoietic stem cells in the bone marrow. This Special Issue on innate immune memory provides a venue for publishing research that increases our understanding of cellular and molecular mechanisms that mediate those responses. Submissions should have a focus on the mechanisms that impact innate immune memory in health and disease.

Dr. Dhifaf Sarhan
Guest Editor

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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • innate
  • memory
  • molecular pathways
  • tumors
  • genetic
  • epigenetic

Published Papers (5 papers)

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Research

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13 pages, 2671 KiB  
Article
Inflammation Regulation by Bacterial Molecular Patterns
by Svetlana V. Guryanova and Anastasiya Kataeva
Biomedicines 2023, 11(1), 183; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11010183 - 11 Jan 2023
Cited by 2 | Viewed by 1351
Abstract
Stimulation of innate immunity by bacterial molecular patterns can induce an enhanced cellular immune response to pathogens that are associated with innate immune memory shaped by epigenetic changes. Immunological memory can be expressed in the acceleration/intensification of inflammation, as well as in the [...] Read more.
Stimulation of innate immunity by bacterial molecular patterns can induce an enhanced cellular immune response to pathogens that are associated with innate immune memory shaped by epigenetic changes. Immunological memory can be expressed in the acceleration/intensification of inflammation, as well as in the exact opposite—to maintain tolerance and non-response to a repeated stimulus. Tolerance is one of the central concepts of immunity and is ensured by the consistency of all parts of the immune response. The severe consequences of inflammation force researchers to study in detail all stages of the downstream pathways that are activated after exposure to a stimulus, while the formation of non-response to a pro-inflammatory stimulus has not yet received a detailed description. Elucidation of the mechanism of tolerance is an urgent task for the prevention and treatment of inflammatory diseases. The aim of this investigation was to study the dynamic changes in the gene expression of A20 and ATF3, the inflammation suppressors, against the background of the expression of the genes of the innate immunity receptors TLR4 and NOD2 and the pro-inflammatory cytokine TNF-α under the influence of TLR4 and NOD2 agonists, lipopolysaccharide (LPS) and glucosaminylmuramyl dipeptide (GMDP). The mechanism of inflammation regulation by bioregulators of bacterial origin—LPS and GMDP—was evaluated in vitro in human peripheral blood mononuclear cells and in vivo after i.p. administration of LPS and GMDP to mice. Gene expression was assessed by RT-PCR. Innate immune receptors and the pro-inflammatory cytokine TNF-α were found to develop early in response to LPS and GMDP, both in vitro and in vivo. Genes of cytosolic proteins controlling inflammation (A20 and ATF3) were expressed later. Prior exposure of the innate immune system to LPS and muramyl peptides may modulate host defense against acute inflammation. As a result of the study, new data were obtained on dynamic changes in deubiquitinase A20 and the transcription factor ATF3, which are involved in the limitation and suppression of inflammatory reactions caused by fragments of bacterial cell walls—LPS and GMDP. Thus, bioregulators of bacterial origin LPS and GMDP, along with pro-inflammatory factors, activate the expression of genes that suppress inflammation, which should be considered when analyzing data from studies of the pro-inflammatory properties of LPS and GMDP and when developing drugs based on them. Full article
(This article belongs to the Special Issue Innate Immune Memory in Health and Disease)
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17 pages, 2855 KiB  
Article
Engineering a Therapeutic Protein to Enhance the Study of Anti-Drug Immunity
by Patricia E. Zerra, Ernest T. Parker, Wallace Hunter Baldwin, John F. Healey, Seema R. Patel, James W. McCoy, Courtney Cox, Sean R. Stowell and Shannon L. Meeks
Biomedicines 2022, 10(7), 1724; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10071724 - 18 Jul 2022
Cited by 2 | Viewed by 1753
Abstract
The development of anti-drug antibodies represents a significant barrier to the utilization of protein-based therapies for a wide variety of diseases. While the rate of antibody formation can vary depending on the therapeutic employed and the target patient population receiving the drug, the [...] Read more.
The development of anti-drug antibodies represents a significant barrier to the utilization of protein-based therapies for a wide variety of diseases. While the rate of antibody formation can vary depending on the therapeutic employed and the target patient population receiving the drug, the antigen-specific immune response underlying the development of anti-drug antibodies often remains difficult to define. This is especially true for patients with hemophilia A who, following exposure, develop antibodies against the coagulation factor, factor VIII (FVIII). Models capable of studying this response in an antigen-specific manner have been lacking. To overcome this challenge, we engineered FVIII to contain a peptide (323–339) from the model antigen ovalbumin (OVA), a very common tool used to study antigen-specific immunity. FVIII with an OVA peptide (FVIII-OVA) retained clotting activity and possessed the ability to activate CD4 T cells specific to OVA323–339 in vitro. When compared to FVIII alone, FVIII-OVA also exhibited a similar level of immunogenicity, suggesting that the presence of OVA323–339 does not substantially alter the anti-FVIII immune response. Intriguingly, while little CD4 T cell response could be observed following exposure to FVIII-OVA alone, inclusion of anti-FVIII antibodies, recently shown to favorably modulate anti-FVIII immune responses, significantly enhanced CD4 T cell activation following FVIII-OVA exposure. These results demonstrate that model antigens can be incorporated into a therapeutic protein to study antigen-specific responses and more specifically that the CD4 T cell response to FVIII-OVA can be augmented by pre-existing anti-FVIII antibodies. Full article
(This article belongs to the Special Issue Innate Immune Memory in Health and Disease)
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15 pages, 2731 KiB  
Article
(Auto)Antibody Responses Shape Memory NK Cell Pool Size and Composition
by Cristina Capuano, Chiara Pighi, Simone Battella, Fabio Pulcinelli, Cristina Santoro, Antonietta Ferretti, Ombretta Turriziani, Davide De Federicis, Cinzia Fionda, Giuseppe Sciumè, Ricciarda Galandrini and Gabriella Palmieri
Biomedicines 2022, 10(3), 625; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10030625 - 08 Mar 2022
Viewed by 2061
Abstract
In vivo establishment and long-term persistence of a heterogeneous memory or an adaptive NK cell pool represents a functional adaptation to human cytomegalovirus (HCMV) infection in humans. Memory NK cells are commonly identified by lack of the FcεRIγ signalling chain, variably associated to [...] Read more.
In vivo establishment and long-term persistence of a heterogeneous memory or an adaptive NK cell pool represents a functional adaptation to human cytomegalovirus (HCMV) infection in humans. Memory NK cells are commonly identified by lack of the FcεRIγ signalling chain, variably associated to the preferential but not completely overlapping expression of the HLA-E receptor NKG2C and CD57 maturation marker. Although characterized by selective hyperresponsiveness to IgG stimulation, the impact of the CD16/antibody interaction in regulating the establishment/maintenance and size, and in determining the relative abundance of this population, is still under investigation. Memory NK cell subset ex vivo profile and in vitro responsiveness to CD16 stimulation was evaluated in HCMV+ healthy donors and in patients affected by immune thrombocytopenia (ITP), an antibody-mediated autoimmune disease. We identified the FcεRIγ− NKG2C+CD57+ memory NK cell subset, whose abundance is uniquely associated with anti-HCMV antibody levels in healthy seropositive donors, and which is significantly expanded in ITP patients. This fully mature memory subset robustly and selectively expands in vitro in response to mAb-opsonized targets or ITP-derived platelets and displays superior CD16-dependent IFNγ production. Our work identifies opsonizing antibodies as a host-dependent factor that shapes HCMV-driven memory NK cell compartment. We first demonstrate that chronic exposure to auto-antibodies contributes to the establishment/expansion of a highly specialized and unique memory NK cell subset with distinct CD16-dependent functional capabilities. We also identify the specific contribution of the lack of FcεRIγ chain in conferring to NKG2C+CD57+ memory cells a higher responsivity to CD16 engagement. Full article
(This article belongs to the Special Issue Innate Immune Memory in Health and Disease)
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Review

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10 pages, 621 KiB  
Review
Immunologic Role of Innate Lymphoid Cells against Mycobacterial tuberculosis Infection
by William Narinyan, Nicole Poladian, Davit Orujyan, Areg Gargaloyan and Vishwanath Venketaraman
Biomedicines 2022, 10(11), 2828; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10112828 - 06 Nov 2022
Cited by 2 | Viewed by 1835
Abstract
Tuberculosis (TB), caused by Mycobacterium tuberculosis (M. tb), is one of the leading causes of mortality due to respiratory tract infections worldwide. Infection by M. tb involves activation of a type I immune response characteristic of T helper type 1 (Th1) [...] Read more.
Tuberculosis (TB), caused by Mycobacterium tuberculosis (M. tb), is one of the leading causes of mortality due to respiratory tract infections worldwide. Infection by M. tb involves activation of a type I immune response characteristic of T helper type 1 (Th1) lymphocytes, natural killer (NK) cells, Interleukin-12 (IL-12), and interferon (IFN)-γ, all of which stimulate the activation of macrophages and robust phagocytosis in order to prevent further infectious manifestations and systemic dissemination. Recent discoveries about innate lymphoid cells (ILCs) have provided further insight about how these cells participate within the protective immune response against M. tb infection and help boost the type I immune response. In order to clearly understand the mechanisms of M. tb infection and advance the efficacy of future treatment and prevention, we must first look at the individual functions each type of immune cell plays within this process, specifically ILCs. By review of the recent literature and current evidence, our group aims to summarize the characterization of the three major groups of ILCs, including NK cells, and analyze the role that each group of ILCs play in the infectious process against M. tb in order to provide a more comprehensive understanding of the host immune response. Equally, previous studies have also highlighted the effects of how administration of the Bacille Calmette–Guérin (BCG) vaccine influences the cells and cytokines of the immune response against M. tb. Our group also aims to highlight the effects that BCG vaccine has on ILCs and how these effects provide added protection against M. tb. Full article
(This article belongs to the Special Issue Innate Immune Memory in Health and Disease)
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16 pages, 2394 KiB  
Review
Virus-Based Immuno-Oncology Models
by Juliana Sitta, Pier Paolo Claudio and Candace M. Howard
Biomedicines 2022, 10(6), 1441; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10061441 - 18 Jun 2022
Cited by 5 | Viewed by 2967
Abstract
Immunotherapy has been extensively explored in recent years with encouraging results in selected types of cancer. Such success aroused interest in the expansion of such indications, requiring a deep understanding of the complex role of the immune system in carcinogenesis. The definition of [...] Read more.
Immunotherapy has been extensively explored in recent years with encouraging results in selected types of cancer. Such success aroused interest in the expansion of such indications, requiring a deep understanding of the complex role of the immune system in carcinogenesis. The definition of hot vs. cold tumors and the role of the tumor microenvironment enlightened the once obscure understanding of low response rates of solid tumors to immune check point inhibitors. Although the major scope found in the literature focuses on the T cell modulation, the innate immune system is also a promising oncolytic tool. The unveiling of the tumor immunosuppressive pathways, lead to the development of combined targeted therapies in an attempt to increase immune infiltration capability. Oncolytic viruses have been explored in different scenarios, in combination with various chemotherapeutic drugs and, more recently, with immune check point inhibitors. Moreover, oncolytic viruses may be engineered to express tumor specific pro-inflammatory cytokines, antibodies, and antigens to enhance immunologic response or block immunosuppressive mechanisms. Development of preclinical models capable to replicate the human immunologic response is one of the major challenges faced by these studies. A thorough understanding of immunotherapy and oncolytic viruses’ mechanics is paramount to develop reliable preclinical models with higher chances of successful clinical therapy application. Thus, in this article, we review current concepts in cancer immunotherapy including the inherent and synthetic mechanisms of immunologic enhancement utilizing oncolytic viruses, immune targeting, and available preclinical animal models, their advantages, and limitations. Full article
(This article belongs to the Special Issue Innate Immune Memory in Health and Disease)
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