At pharmacological levels, glucocorticosteroids inhibited two antigen-induced lymphocyte functions, in vitro proliferation and lymphokine synthesis. Lymphocyte production of both macrophage chemotactic factor (CTX) and macrophage inhibition factor (MIF) were decreased in the presence of hydrocortisone. The corticosteroid also blocked the action of MIF on macrophages but did not interfere with the action of CTX on macrophages. Thus, steroids can suppress the immune response at two different stages: by blocking lymphocyte activation and mediator synthesis and also by interfering with the interaction of certain effector molecules with their target cells. Furthermore, these findings suggested that MIF and CTX have distinct mechanisms of action on the effector macrophages, one being sensitive and one resistant to steroids.
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Front Immunol
January 2025
Aix-Marseille Université, INSERM, INRAE, C2VN, Marseille, France.
Rationale: COVID-19-associated acute-respiratory distress syndrome (C-ARDS) results from a direct viral injury associated with host excessive innate immune response mainly affecting the lungs. However, cytokine profile in the lung compartment of C-ARDS patients has not been widely studied, nor compared to non-COVID related ARDS (NC-ARDS).
Objectives: To evaluate caspase-1 activation, IL-1 signature, and other inflammatory cytokine pathways associated with tissue damage using post-mortem lung tissues, bronchoalveolar lavage fluids (BALF), and serum across the spectrum of COVID-19 severity.
Front Immunol
January 2025
Department of Otorhinolaryngology, Head and Neck surgery, University Hospital Leipzig, Leipzig, Germany.
Background: Adding pembrolizumab, an anti-PD-1 antibody approved for treatment of head and neck squamous cell carcinoma (HNSCC) to neoadjuvant (induction-) chemotherapy utilizing docetaxel and cisplatin (TP) followed by radiotherapy may improve outcome in larynx organ-preservation (LOP) that is investigated in the European Larynx-Organ preservation Study (ELOS). As biomarkers for response to TP and pembrolizumab +TP are missing but may include cytokines, this work aims on determining cytokines potentially linked to outcome as prognostic markers sufficient to predict and/or monitor response to successful LOP.
Methods: Collagenase IV digests were generated from 47 histopathological confirmed HNSCC tumor samples and seeded in 96-well plates containing pembrolizumab, docetaxel, cisplatin either solely or in binary or ternary combination.
J Biol Dyn
December 2025
School of Mathematics and Statistics, Donghua University, Shanghai, People's Republic of China.
We use mathematical modeling to study the proliferation dynamics of CD4+ T cells within an immune response. This proliferation is driven by the autocrine reaction of helper T cells and interleukin-2 (IL-2), and regulated by natural regulatory T cells (nTregs). Previous studies suggested that a fratricidal mechanism is necessary to eliminate helper T cells post-infection.
View Article and Find Full Text PDFFront Immunol
January 2025
The Catholic University of Korea and Ho-Youn Kim's Clinic for Arthritis Rheumatism, Seoul, Republic of Korea.
Introduction: Our aim was to investigate the insufficiently understood differences in the immune system between anti-citrullinated peptide antibody (ACPA)-positive (ACPA) and ACPA-negative (ACPA) early rheumatoid arthritis (eRA) patients.
Methods: We performed multiple cytokine assays using sera from drug-naïve ACPA and ACPA eRA patients. Additionally, we conducted single-cell RNA sequencing of CD45 cells from peripheral blood samples to analyze and compare the distribution and functional characteristics of the cell subsets based on the ACPA status.
Cancer Biol Ther
December 2025
Department of Pharmacology, Physiology, and Cancer Biology, Thomas Jefferson University, Philadelphia, PA, USA.
Adaptive immune resistance in cancer describes the various mechanisms by which tumors adapt to evade anti-tumor immune responses. IFN-γ induction of programmed death-ligand 1 (PD-L1) was the first defined and validated adaptive immune resistance mechanism. The endoplasmic reticulum (ER) is central to adaptive immune resistance as immune modulatory secreted and integral membrane proteins are dependent on ER.
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