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Immune Modulation of Mucosal Inflammation
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Immune Modulation of Mucosal Inflammation

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 (24 September 2021) | Viewed by 29313

Special Issue Editor

Dr. José Luis Subiza

E-Mail Website
Guest Editor
Inmunotek, SL, Madrid, Spain
Interests: allergy; immunology; vaccines; dendritic cells; regulatory T cells; allergens
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mucous membranes are lined by an epithelial layer that covers the respiratory, gastrointestinal and genitourinary tracts from the external environment.  Although it is an effective barrier against external insults, the mucosal tissues are continuously challenged by a plethora of microorganisms, allergens and other substances that can access to the mucosal surface. As a consequence, the mucosal immune system has evolved to discriminate when to respond, when to tolerate, and to what extent. To this end, there is interplay among microbiota, epithelial cells, innate immune cells and resident and circulating lymphocytes.

In situations derived from infections, epithelia disruption, disbiosis, allergy, autoimmune phenomena and others, an inflammatory response may occur altering the mucosal homeostasis. This gives rises to a number of acute or chronic conditions, from rhinosinusitis or allergic asthma in airways to different inflammatory disorders in intestinal and other mucosal tissues.

Down-regulating mucosal inflammation and restoring mucosal homeostasis by inducing tolerance is a topic of great interest.  Different approaches are being considered, from targeting tolerogenic dendritic cells to modulating regulatory T cells.

Therefore, authors are invited to submit original research and review articles which address the progress and current standing of immunomodulation of mucosal inflammation.

Topics include, but are not limited to:

  • Epithelial cells and triggers of mucosal inflammation
  • Induction of tolerogenic dendritic cells
  • Induction of regulatory T cells
  • Immunomodulation by mucosal microbiota

Dr. José Luis Subiza
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. 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

  • mucosal
  • inflammation
  • dendritic cells
  • regulatory T cells
  • mucosal epithelial cells
  • gut microbiota
  • bronchial microbiota
  • tolerance
  • allergens
  • infections

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Related Special Issue

Published Papers (5 papers)

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Research

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18 pages, 2087 KiB  
Article
Absent in Melanoma 2 (AIM2) Regulates the Stability of Regulatory T Cells
by Beatriz Lozano-Ruiz, Amalia Tzoumpa, Claudia Martínez-Cardona, David Moreno, Ana M. Aransay, Ana R. Cortazar, Joanna Picó, Gloria Peiró, Juanjo Lozano, Pedro Zapater, Rubén Francés and José M. González-Navajas
Int. J. Mol. Sci. 2022, 23(4), 2230; https://doi.org/10.3390/ijms23042230 - 17 Feb 2022
Cited by 10 | Viewed by 3216
Abstract
Absent in melanoma 2 (AIM2) is a cytosolic dsDNA sensor that has been broadly studied for its role in inflammasome assembly. However, little is known about the function of AIM2 in adaptive immune cells. The purpose of this study was to investigate whether [...] Read more.
Absent in melanoma 2 (AIM2) is a cytosolic dsDNA sensor that has been broadly studied for its role in inflammasome assembly. However, little is known about the function of AIM2 in adaptive immune cells. The purpose of this study was to investigate whether AIM2 has a cell-intrinsic role in CD4+ T cell differentiation or function. We found that AIM2 is expressed in both human and mouse CD4+ T cells and that its expression is affected by T cell receptor (TCR) activation. Naïve CD4+ T cells from AIM2-deficient (Aim2−/−) mice showed higher ability to maintain forkhead box P3 (FOXP3) expression in vitro, while their capacity to differentiate into T helper (Th)1, Th2 or Th17 cells remained unaltered. Transcriptional profiling by RNA sequencing showed that AIM2 might affect regulatory T cell (Treg) stability not by controlling the expression of Treg signature genes, but through the regulation of the cell’s metabolism. In addition, in a T cell transfer model of colitis, Aim2−/−-naïve T cells induced less severe body weight loss and displayed a higher ability to differentiate into FOXP3+ cells in vivo. In conclusion, we show that AIM2 function is not confined to innate immune cells but is also important in CD4+ T cells. Our data identify AIM2 as a regulator of FOXP3+ Treg cell differentiation and as a potential intervention target for restoring T cell homeostasis. Full article
(This article belongs to the Special Issue Immune Modulation of Mucosal Inflammation)
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Review

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14 pages, 2029 KiB  
Review
Immune Tolerance in the Oral Mucosa
by Hector F. Pelaez-Prestel, Jose L. Sanchez-Trincado, Esther M. Lafuente and Pedro A. Reche
Int. J. Mol. Sci. 2021, 22(22), 12149; https://doi.org/10.3390/ijms222212149 - 10 Nov 2021
Cited by 25 | Viewed by 4073
Abstract
The oral mucosa is a site of intense immune activity, where a large variety of immune cells meet to provide a first line of defense against pathogenic organisms. Interestingly, the oral mucosa is exposed to a plethora of antigens from food and commensal [...] Read more.
The oral mucosa is a site of intense immune activity, where a large variety of immune cells meet to provide a first line of defense against pathogenic organisms. Interestingly, the oral mucosa is exposed to a plethora of antigens from food and commensal bacteria that must be tolerated. The mechanisms that enable this tolerance are not yet fully defined. Many works have focused on active immune mechanisms involving dendritic and regulatory T cells. However, epithelial cells also make a major contribution to tolerance by influencing both innate and adaptive immunity. Therefore, the tolerogenic mechanisms concurring in the oral mucosa are intertwined. Here, we review them systematically, paying special attention to the role of oral epithelial cells. Full article
(This article belongs to the Special Issue Immune Modulation of Mucosal Inflammation)
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17 pages, 1058 KiB  
Review
Probiotic-Induced Tolerogenic Dendritic Cells: A Novel Therapy for Inflammatory Bowel Disease?
by Shaghayegh Baradaran Ghavami, Hamid Asadzadeh Aghdaei, Dario Sorrentino, Shabnam Shahrokh, Maryam Farmani, Fatemeh Ashrafian, Maria Pina Dore, Shahrbanoo Keshavarz Azizi Raftar, Seyed Mobin Khoramjoo and Mohammad Reza Zali
Int. J. Mol. Sci. 2021, 22(15), 8274; https://doi.org/10.3390/ijms22158274 - 31 Jul 2021
Cited by 19 | Viewed by 4908
Abstract
Inflammatory bowel diseases (IBDs) are immune-mediated, chronic relapsing diseases with a rising prevalence worldwide in both adult and pediatric populations. Treatment options for immune-mediated diseases, including IBDs, are traditional steroids, immunomodulators, and biologics, none of which are capable of inducing long-lasting remission in [...] Read more.
Inflammatory bowel diseases (IBDs) are immune-mediated, chronic relapsing diseases with a rising prevalence worldwide in both adult and pediatric populations. Treatment options for immune-mediated diseases, including IBDs, are traditional steroids, immunomodulators, and biologics, none of which are capable of inducing long-lasting remission in all patients. Dendritic cells (DCs) play a fundamental role in inducing tolerance and regulating T cells and their tolerogenic functions. Hence, modulation of intestinal mucosal immunity by DCs could provide a novel, additional tool for the treatment of IBD. Recent evidence indicates that probiotic bacteria might impact immunomodulation both in vitro and in vivo by regulating DCs’ maturation and producing tolerogenic DCs (tolDCs) which, in turn, might dampen inflammation. In this review, we will discuss this evidence and the mechanisms of action of probiotics and their metabolites in inducing tolDCs in IBDs and some conditions associated with them. Full article
(This article belongs to the Special Issue Immune Modulation of Mucosal Inflammation)
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24 pages, 5598 KiB  
Review
Innate Lymphoid Cells in Intestinal Homeostasis and Inflammatory Bowel Disease
by Angela Saez, Raquel Gomez-Bris, Beatriz Herrero-Fernandez, Claudia Mingorance, Cristina Rius and Jose M. Gonzalez-Granado
Int. J. Mol. Sci. 2021, 22(14), 7618; https://doi.org/10.3390/ijms22147618 - 16 Jul 2021
Cited by 103 | Viewed by 9976
Abstract
Inflammatory bowel disease (IBD) is a heterogeneous state of chronic intestinal inflammation of unknown cause encompassing Crohn’s disease (CD) and ulcerative colitis (UC). IBD has been linked to genetic and environmental factors, microbiota dysbiosis, exacerbated innate and adaptive immunity and epithelial intestinal barrier [...] Read more.
Inflammatory bowel disease (IBD) is a heterogeneous state of chronic intestinal inflammation of unknown cause encompassing Crohn’s disease (CD) and ulcerative colitis (UC). IBD has been linked to genetic and environmental factors, microbiota dysbiosis, exacerbated innate and adaptive immunity and epithelial intestinal barrier dysfunction. IBD is classically associated with gut accumulation of proinflammatory Th1 and Th17 cells accompanied by insufficient Treg numbers and Tr1 immune suppression. Inflammatory T cells guide innate cells to perpetuate a constant hypersensitivity to microbial antigens, tissue injury and chronic intestinal inflammation. Recent studies of intestinal mucosal homeostasis and IBD suggest involvement of innate lymphoid cells (ILCs). These lymphoid-origin cells are innate counterparts of T cells but lack the antigen receptors expressed on B and T cells. ILCs play important roles in the first line of antimicrobial defense and contribute to organ development, tissue protection and regeneration, and mucosal homeostasis by maintaining the balance between antipathogen immunity and commensal tolerance. Intestinal homeostasis requires strict regulation of the quantity and activity of local ILC subpopulations. Recent studies demonstrated that changes to ILCs during IBD contribute to disease development. A better understanding of ILC behavior in gastrointestinal homeostasis and inflammation will provide valuable insights into new approaches to IBD treatment. This review summarizes recent research into ILCs in intestinal homeostasis and the latest advances in the understanding of the role of ILCs in IBD, with particular emphasis on the interaction between microbiota and ILC populations and functions. Full article
(This article belongs to the Special Issue Immune Modulation of Mucosal Inflammation)
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15 pages, 990 KiB  
Review
Intestinal Homeostasis under Stress Siege
by Fabiola Guzmán-Mejía, Marycarmen Godínez-Victoria, Alan Vega-Bautista, Judith Pacheco-Yépez and Maria Elisa Drago-Serrano
Int. J. Mol. Sci. 2021, 22(10), 5095; https://doi.org/10.3390/ijms22105095 - 12 May 2021
Cited by 21 | Viewed by 4971
Abstract
Intestinal homeostasis encompasses a complex and balanced interplay among a wide array of components that collaborate to maintain gut barrier integrity. The appropriate function of the gut barrier requires the mucus layer, a sticky cushion of mucopolysaccharides that overlays the epithelial cell surface. [...] Read more.
Intestinal homeostasis encompasses a complex and balanced interplay among a wide array of components that collaborate to maintain gut barrier integrity. The appropriate function of the gut barrier requires the mucus layer, a sticky cushion of mucopolysaccharides that overlays the epithelial cell surface. Mucus plays a critical anti-inflammatory role by preventing direct contact between luminal microbiota and the surface of the epithelial cell monolayer. Moreover, mucus is enriched with pivotal effectors of intestinal immunity, such as immunoglobulin A (IgA). A fragile and delicate equilibrium that supports proper barrier function can be disturbed by stress. The impact of stress upon intestinal homeostasis results from neuroendocrine mediators of the brain-gut axis (BGA), which comprises a nervous branch that includes the enteric nervous system (ENS) and the sympathetic and parasympathetic nervous systems, as well as an endocrine branch of the hypothalamic-pituitary-adrenal axis. This review is the first to discuss the experimental animal models that address the impact of stress on components of intestinal homeostasis, with special emphasis on intestinal mucus and IgA. Basic knowledge from animal models provides the foundations of pharmacologic and immunological interventions to control disturbances associated with conditions that are exacerbated by emotional stress, such as irritable bowel syndrome. Full article
(This article belongs to the Special Issue Immune Modulation of Mucosal Inflammation)
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