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Immuno

Immuno is an international, peer-reviewed, open access journal on immunological research and clinical applications published quarterly online by MDPI.

Quartile Ranking JCR - Q3 (Immunology)

All Articles (194)

PD-1 Expression in Endometriosis

  • José Lourenço Reis,
  • Catarina Martins and
  • Miguel Ângelo-Dias
  • + 3 authors

Background: Endometriosis, believed by many to be rooted in immunology, is a chronic disease. Upregulation of programmed cell death protein 1 (PD-1) in immune cells may compromise their defensive function, a mechanism demonstrated in the context of cancer spread. This study aims to explore the potential involvement of PD-1 in the pathophysiology and progression of endometriosis. A total of 62 patients who underwent laparoscopic surgery were analyzed, with 47 diagnosed with endometriosis and 15 serving as controls. We collected peritoneal fluid and peripheral blood samples during surgery and examined them using flow cytometry. Using a panel of monoclonal antibodies, the samples were stained and the expression of PD-1 in immune cells was evaluated. Results: We observed a statistically significant rise in the percentage of the CD56+ CD16+ NK cell subset expressing PD-1 within the peritoneal fluid of endometriosis patients compared to the control group (p = 0.021). Similarly, we found that PD-1 expression on immune cells significantly differed based on factors such as body mass index and smoking habits. Moreover, peritoneal subsets of PD-1+ T and NK cells showed an increase in patients presenting symptomatic endometriosis and those with more widespread disease. Conclusions: Our evaluation of the inhibitory PD-1 receptor has strengthened the potential connection between immune escape mechanisms often seen in cancer cells and those in endometriotic cells. This concept could pave the way for future research in the field of immunomodulation and endometriosis.

17 October 2025

Gating strategy used to characterize PD-1 in lymphocyte subsets of peripheral blood and peritoneal fluid samples. (i) Gating Strategy used for the identification of major lymphocyte subsets in Peritoneal Fluid (PF) and Peripheral blood (PB) samples, i.e., T cells (CD45Hi SSCLo CD3+) and NK cells (CD45Hi SSCLo CD3− CD56+), within the single cell region; (ii) Gating strategy used for the identification of distinct NK cell subsets in PF (CD56Hi; CD16+ CD56+; CD16HiCD56Dim) and PB CD56Hi; CD16HiCD56Dim) samples, along with the subsequent analysis of PD-1 and CD57 in these populations (FMO tubes presented in the upper row); (iii) Gating strategy used for the identification of CD8+ and CD8− (CD4+ and DN) T cells, along with CD56+ T cells. The percentage of cells expressing PD-1 and CD57 was further analyzed in each one of these subsets. (FMO tubes presented in the upper row). DN, Double negative; FMO, Fluorescence Minus One.

From Incision to Immunity: Integrating Surgery and Immunotherapy in Non-Small Cell Lung Cancer

  • Michael J. Janes,
  • Aidan A. Schmidt and
  • Garret A. Krieg
  • + 3 authors

Lung cancer is the most common cause of death due to cancer in the world, and non-small cell lung cancer (NSCLC) is the most common form of lung cancer, representing approximately 84% of all cases. Due to its frequency and mortality, the amount of research on this subject has been greatly increased and new techniques to improve health outcomes have been established. While surgery remains the gold standard of treatment, immunotherapy used alone or in conjunction with surgery shows promising results. This review aims to give an overview of current and new surgical and immunotherapy methods used for the treatment of NSCLC, as well as ways in which they can be combined and the clinical outcomes for patients with each treatment modality. Additionally, it will seek to highlight any gaps in current knowledge of treatment and propose further studies to improve the efficacy of NSCLC treatments.

14 October 2025

Shows the mechanism of action of immune checkpoint inhibitors. Created in BioRender, version 1.0.0.5; Science Suite Inc.: Toronto, ON, Canada, 2025. https://BioRender.com/edjus7i (accessed on 13 October 2025).

Hydrogen Peroxide and Neutrophil Chemotaxis in a Mouse Model of Bacterial Infection

  • Hassan O. J. Morad,
  • Larissa Garcia-Pinto and
  • Georgia Clayton
  • + 3 authors

Neutrophils are an essential protective component of the innate immune system. However, in severe bacterial infections, neutrophils are known to mis-localise from the primary site of infection to other organs, where excessive release of cytokines, chemokines, and neutrophil extracellular traps (NETs) can induce organ damage and death. In this study, we use an animal model of bacterial infection originating in the peritoneum to show that hydrogen peroxide (H2O2, a potent neutrophil chemoattractant) is initially released in high concentrations both in the peritoneum and in multiple ‘off-target’ organs (lungs, liver and kidneys). The initial high H2O2 release inhibits neutrophil chemotaxis, but after 24 h concentrations of H2O2 reduce and can promote neutrophil migration to organs, where they release pro-inflammatory cytokines and chemokines along with NETs. The antimalarial compound artesunate potently inhibits neutrophil migration to off-target organs. It also abolishes cytokine, chemokine, and NET production, suggesting that artesunate may be a valuable novel therapy for preventing off-target organ inflammation associated with severe bacterial infections. Finally, the potency of H2O2 as a chemoattractant is shown by in vitro experiments in which, faced with competing gradients of H2O2 and other chemoattractants, neutrophils preferentially migrate towards H2O2.

8 October 2025

H2O2 released in response to i.p. injection of LPS promotes neutrophil chemotaxis at low concentrations but inhibits chemotaxis at high concentrations. (A) Invasion of neutrophils into the peritoneum was high 5 h after i.p. injection of 30 ng LPS but was suppressed with 3 μg LPS; (B) H2O2 i.p. concentration was 43.7 ± 3.04 μM 5 h following i.p. injection of 30 ng LPS but 197.5 ± 17.12 μM following 3 μg LPS. (C) Invasion of neutrophils into the lung was suppressed 5 h following i.p. injection of 3 μg LPS; (D) lung H2O2 concentration following i.p. injection of 3 μg LPS was 129.5 ± 17.73 μM. Bars show mean ± SEM, N = 6 mice per bar, with 6 independent experiments per result. Results with no visible bars were below the assay detection limits (see Section 2) and, for statistical purposes, were assumed to be equal to the detection limit. * p < 0.05; *** p < 0.001, **** p < 0.0001, ns = no significant difference (for (A,B): one-way ANOVA and Tukey–Kramer post hoc test, for (C,D): unpaired t-test).

Immune cells like neutrophils, monocytes/macrophages, and lymphocytes play key roles in the development, progression, and resolution of deep vein thrombosis (DVT) by contributing to inflammation, coagulation, and fibrinolysis. IFN-γ, a cytokine mainly secreted by natural killer (NK) and T cells, is a critical factor in DVT pathogenesis. It links immune responses to coagulation activation by promoting endothelial activation, leukocyte recruitment, cytokine release, and coagulation imbalance. Its strong pro-inflammatory and prothrombotic effects make IFN-γ a promising target for DVT treatment beyond standard anticoagulants. Exploring ways to block IFN-γ signaling or its downstream effects could open doors to novel therapies for DVT, aiding in resolution and preventing post-thrombotic complications. This review delves into DVT pathophysiology, diagnostics, and management, emphasizing the importance of targeting immune cells and IFN-γ to advance treatment options.

4 October 2025

An illustration showcasing the role of IFN-γ in driving inflammation and contributing to blood clot formation, progression, and spread in DVT. IFN-γ signaling activates immune cells and, once released, stimulates macrophages to enhance antigen presentation, produce inflammatory mediators, impact hematopoiesis, and prompt other immune cells to release more IFN-γ. This signaling works through the heterodimeric receptor complex (IFNGR1/IFNGR2), activating the JAK-STAT1 pathway to drive the transcription of interferon-stimulated genes (ISGs). IFN-γ disrupts endothelial cell barrier function, increasing permeability, and inducing adhesion molecules like ICAM-1 and VCAM-1. It promotes inflammation by boosting pro-inflammatory cytokines (TNF-α, IL-1β) and chemokines, while also enhancing coagulation. Furthermore, it affects anticoagulants and fibrinolytic factors, creating a pro-thrombotic state by reducing thrombomodulin levels and stimulating reactive oxygen species (ROS) and reactive nitrogen species (RNS) in vascular cells, potentially causing oxidative endothelial damage and encouraging clot formation.

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Immuno - ISSN 2673-5601Creative Common CC BY license