Background: Regulatory T-(Treg) and pro-inflammatory T-helper 17 (Th17) cells have been reported to be involved in the pathogenesis of pleural effusions caused by lung cancer. However, the presence of these subsets might not be a consequence of tumor pathogenesis, but rather a result of the pleural effusion itself, irrespective of its origin. In the present study, we analyzed the balance between these CD4+ T-cell subsets and compared them with those in non-malignant pleural effusions.

Patients And Methods: We detected the frequencies of Treg and Th17 cells, identified as cluster of differentiation (CD)3+CD4+CD25+CD127low/- and CD3+CD4+ retinoid-related orphan receptor γt (RORγt)+ cells respectively, and proportions of interleukin (IL)17A-producing CD4+ cells in pleural effusions of patients with lung cancer, tuberculous and non-chronic pathologies by flow cytometry. The cytokine profile of stimulated CD4+ T-cells from tuberculosis and cancer groups was compared.

Results: The proportion of Th17 cells were increased whereas Tregs were decreased in both tuberculosis and cancer, but not in non-chronic pathologies. Nevertheless, CD4+ T-cells from lung cancer effusions secreted interferon (IFN)γ, IL6 and IL17A, whereas CD4+ T-cells from tuberculous effusions secreted IL10 and low levels of IFNγ.

Conclusion: Although effusions from patients with chronic pathologies presented higher proportions of Th17 cells in comparison to those with non-chronic pathologies, only Th17 cells from malignant effusions maintained their proinflammatory profile after stimulation. Thus, in the pleural compartment of patients with lung cancer, a proinflammatory environment might be favored and possibly maintained by Th17 response.

Download full-text PDF

Source

Publication Analysis

Top Keywords

lung cancer
20
th17 cells
20
pleural effusions
12
effusions patients
12
patients lung
12
non-chronic pathologies
12
cd4+ t-cells
12
proinflammatory profile
8
tuberculosis cancer
8
effusions secreted
8

Similar Publications

Tumor cell-intrinsic signaling pathways can drastically affect the tumor immune microenvironment, promoting tumor progression and resistance to immunotherapy by excluding immune-cell populations from the tumor. Several tumor cell-intrinsic pathways have been reported to modulate myeloid-cell and T-cell infiltration creating "cold" tumors. However, clinical evidence suggests that excluding cytotoxic T cells from the tumor core also mediates immune evasion.

View Article and Find Full Text PDF

Antibodies targeting immune checkpoints, such as PD-1, PD-L1, or CTLA-4, have transformed the treatment of patients with lung cancers. Unprecedented rates of durable responses are achieved in an imperfectly characterized population of patients with metastatic disease. More recently, immune checkpoint inhibitors have been explored in patients with resectable non-small-cell lung cancers.

View Article and Find Full Text PDF

Lung cancers associated with cystic airspaces (LCCAs) are a rare and relatively novel concept analyzed in various case reports and retrospective studies. In this review, it was our aim to investigate the morphologic, imaging, and clinicopathologic characteristics of this entity, as well as its natural course in light of the current literature. Literature search including the years 2000-2022 was conducted in PubMed.

View Article and Find Full Text PDF

Background: Telecytology-assisted rapid on-site evaluation (ROSE) offers a cost-effective method to enhance minimally invasive biopsies like fine needle aspiration and core biopsies with touch preparation. By reducing nondiagnostic sampling and the need for repeat procedures, ROSE via telecytology facilitates prompt triage for ancillary tests, improving patient management. This study examines cases initially deemed adequate for diagnosis during telecytology-assisted ROSE but later categorized as nondiagnostic at final evaluation (NDIS).

View Article and Find Full Text PDF

Image-Based Phenotypic Profiling Enables Rapid and Accurate Assessment of EGFR-Activating Mutations in Tissues from Lung Cancer Patients.

J Am Chem Soc

January 2025

Department of Pulmonary and Critical Care Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, West China Hospital, Sichuan University, Chengdu 610065, China.

Determining mutations in the kinase domain of the epidermal growth factor receptor (EGFR) is critical for the effectiveness of EGFR tyrosine kinase inhibitors (TKIs) in lung cancer. Yet, DNA-based sequencing analysis of tumor samples is time-consuming and only provides gene mutation information on EGFR, making it challenging to design effective EGFR-TKI therapeutic strategies. Here, we present a new image-based method involving the rational design of a quenched probe based on EGFR-TKI to identify mutant proteins, which permits specific and "no-wash" real-time imaging of EGFR in living cells only upon covalent targeting of the EGFR kinase.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!