Unlabelled: COVID-19 infection not only profoundly impacts the detection of tuberculosis infection (Tbc) but also affects modality in tuberculosis patient immune response. It is important to determine immune response alterations in latent tuberculosis infection as well as in SARS-CoV-2-infected tuberculosis patients. Such changes may have underlying effects on the development and course of further tuberculosis. Here, we aimed to review the characteristics of immune response in TB patients or convalescent COVID-19 patients with latent TB infection (LTBI).
Materials And Methods: We analyzed the features of immune response in tuberculosis and COVID-19 patients. For this, we analyzed publications released from December 2019 to March 2023; those which were published in accessible international databases ("Medline", "PubMed", "Scopus") and with keywords such as "COVID-19", "SARS-CoV-2", "tuberculosis", "pulmonary tuberculosis", "latent tuberculosis infection", "Treg", "follicular Treg", and "Treg subsets", we considered.
Results: Through our analysis, we found that tuberculosis patients who had been infected with COVID-19 previously and elevated Th1 and Th2 cell levels. High levels of Th1 and Th2 cells may serve as a positive marker, characterizing activated immune response during TB infection. COVID-19 or post-COVID-19 subjects showed decreased Th17 levels, indicating a lack of tuberculosis development. Moreover, the typical course of tuberculosis is associated with an increase in Treg level, but COVID-19 contributes to a hyperinflammatory response.
Conclusion: According to the data obtained, the course of tuberculosis proceeds in a dissimilar way due to the distinct immune response, elicited by SARS-CoV-2. Importantly, the development of active tuberculosis with a severe course is associated with a decline in Treg levels. Both pathogens lead to disturbed immune responses, increasing the risk of developing severe TB. The insights and findings of this paper may be used to improve the future management of individuals with latent and active tuberculosis.
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http://dx.doi.org/10.3390/biomedicines11082123 | DOI Listing |
Noise Health
January 2025
Department of Geriatric Health Internal Medicine, Qingdao Municipal Hospital, Qingdao 266000, China.
Objective: Evaluate the effect of white noise intervention on sleep quality and immunological indicators of patients with breast cancer undergoing neoadjuvant chemotherapy (NAC).
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Br J Dermatol
January 2025
Division of Infection & Immunity, Cardiff University, Cardiff, UK.
Am J Physiol Endocrinol Metab
January 2025
National Agri-Food and Biomanufacturing Institute (BRIC-NABI), Food & Nutrition Biotechnology Division, S.A.S Nagar, Sector 81 (Knowledge City), Punjab, India.
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January 2025
NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, CA, USA.
The metabolic landscape of cancer greatly influences antitumor immunity, yet it remains unclear how organ-specific metabolites in the tumor microenvironment influence immunosurveillance. We found that accumulation of primary conjugated and secondary bile acids (BAs) are metabolic features of human hepatocellular carcinoma and experimental liver cancer models. Inhibiting conjugated BA synthesis in hepatocytes through deletion of the BA-conjugating enzyme bile acid-CoA:amino acid -acyltransferase (BAAT) enhanced tumor-specific T cell responses, reduced tumor growth, and sensitized tumors to anti-programmed cell death protein 1 (anti-PD-1) immunotherapy.
View Article and Find Full Text PDFCancer Immunol Res
January 2025
University of Padua, Padua, PD, Italy.
T cell-based therapies, including Tumor Infiltrating Lymphocyte Therapy (TIL), T cell receptor engineered T cells (TCR T), and Chimeric Antigen Receptor T cells (CAR T), are powerful therapeutic approaches for cancer treatment. While these therapies are primarily known for their direct cytotoxic effects on cancer cells, accumulating evidence indicates that they also influence the tumor microenvironment (TME), by altering the cytokine milieu and recruiting additional effector populations to help orchestrate the antitumor immune response. Conversely, the TME itself can modulate the behaviour of these therapies within the host by either supporting or inhibiting their activity.
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