T Cells in Inflammation and Cancer

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

Deadline for manuscript submissions: 20 June 2025 | Viewed by 1007

Special Issue Editor

Department of Microbiology and Immunology, Center for Vaccine Biology and Immunology, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA
Interests: immunity to infectious diseases and cancer; crosstalk of innate and T cell immunity; immune cell migration; immunobiology of signal transduction; lung mucosal immunity; immunometabolism; immune memory
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are in a remarkable time of change and innovation in biomedical science and medicine, with T cells standing formidably at the center. Recent groundbreaking discoveries and innovations driven by T cells are highlighted by a few key examples. First, the COVID-19 mRNA vaccines have protected potentially hundreds of millions of people by generating robust anti-viral T cell memory. While initially expected to work primarily through the production of neutralizing antibodies, their effectiveness has been largely governed by T cell memory formation, especially as mutant strains of SARS-CoV-2 became dominant. Next is the advent of immune checkpoint inhibitor (ICI) therapy. Many patients have been diagnosed with advanced cancer that was unresponsive to traditional cancer therapies but have been able to achieve remission with ICI treatment. ICIs unleash anti-tumor T cell responses that may be otherwise subdued by the immunosuppressive conditions of advanced cancer patients. Although this treatment modality is effective for only a subset of patients, it is still revolutionary because it offers a lifeline to individuals who would otherwise have no viable treatment options. Finally, the biomedical advancement in our time has achieved more than 70% remission of certain types of advanced hematopoietic cancer by using adoptive cell therapy of engineered T cells, known as CAR T cell therapy. Importantly, all these achievements were made possible by decade-long collective efforts of numerous research teams over time and across regions. These successes are especially owed to the in-depth knowledge accumulated in classical T cell immunology, such as T cell immunity to pathogens. As such, this Special Issue hopes to be a forum for broadly discussing the immunology of T lymphocytes.

Topics include the following:

  • The protective and pathological roles of T cells in diseases, particularly inflammatory, infectious, and cancerous conditions;
  • The molecular, (epi)genetic, cellular, metabolic, and environmental mechanisms underlying T cell (dys)functions;
  • The crosstalk between T cell immunity and other components of the immune system or non-immune parts of the body;
  • Cutting-edge technologies and new methods for studying and understanding T cell immunobiology;
  • Immunotherapies designed to activate, control, or harness T cells.

Dr. Kihong Lim
Guest Editor

Manuscript Submission Information

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Keywords

  • T cell
  • immunity
  • disease
  • infection
  • cancer
  • inflammation
  • pathology
  • immunotherapy

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Published Papers (1 paper)

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Research

16 pages, 1998 KiB  
Article
Nicotinamide Inhibits CD4+ T-Cell Activation and Function
by Lotte Nijhuis, Alejandra Bodelόn, Rianne C. Scholman, Isabelle Houtzager, Lyanne J. P. M. Sijbers, Enric Mocholi, Lucas W. Picavet, Jorg J. A. Calis, Michal Mokry, Sebastiaan J. Vastert and Jorg van Loosdregt
Cells 2025, 14(8), 560; https://doi.org/10.3390/cells14080560 - 8 Apr 2025
Viewed by 539
Abstract
Chronic inflammation and autoimmune diseases are driven, in part, by the activation of (auto)reactive CD4+ T-cells, highlighting their potential as therapeutic targets for these diseases. Nicotinamide (NAM) has demonstrated anti-inflammatory properties in various disease models and has already demonstrated safety in several large [...] Read more.
Chronic inflammation and autoimmune diseases are driven, in part, by the activation of (auto)reactive CD4+ T-cells, highlighting their potential as therapeutic targets for these diseases. Nicotinamide (NAM) has demonstrated anti-inflammatory properties in various disease models and has already demonstrated safety in several large clinical trials in humans. The mechanisms behind these observations, and especially their direct effects on CD4+ T-cells, remain poorly understood. Here, we address this gap by investigating how NAM influences CD4+ T-cell activation and function. We also describe that NAM treatment significantly suppresses CD4+ T-cell activation in vitro, as evidenced by impaired proliferation and reduced expression of surface activation markers. Additionally, NAM treatment resulted in reduced production of pro-inflammatory cytokines, IL-2, IFNy, and IL-17, further highlighting its anti-inflammatory potential. We found that NAM modulates key metabolic processes, including glycolysis and reactive oxygen species (ROS) production—both essential to T-cell activation. Taken together, our findings provide novel mechanistic insight into the regulation of T-cell activation by NAM, suggesting NAM as an attractive candidate for novel therapies targeting immune-related diseases. Full article
(This article belongs to the Special Issue T Cells in Inflammation and Cancer)
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