Background: Identification of serum proteins that track with disease course in sarcoidosis may have clinical and pathologic importance. We previously identified up-regulated transcripts for interferon-inducible chemokines CXCL9, and CXCL10, in blood of sarcoidosis patients compared to controls. The objective of this study was to determine whether proteins encoded by these transcripts were elevated in serum and identified patients with remitting vs. chronic progressive sarcoidosis longitudinally.
Methods: Serum levels of CXCL9, CXCL10, and proteins associated with inflammation and/or disease activity (sIL2R, ACE, ESR and CRP) were measured in a prospective cohort of sarcoidosis subjects and controls. Comparisons were made between groups and clinical course using pulmonary function measures and a severity score developed by Wasfi et al.
Results: In a cross-sectional analysis of 36 non-immunosuppressed sarcoidosis subjects, serum CXCL9, CXCL10, and sIL2R were significantly elevated compared to 46 controls (p < 0.0001). CXCL9 and CXCL10 were strongly inter-correlated (p = 0.0009). CXCL10 and CXCL9 were inversely correlated with FVC% predicted and DLCO% predicted, respectively. CXCL10 and CXCL9 significantly correlated with sarcoidosis severity score. sIL2R, ESR, CRP, and ACE serum levels did not correlate with pulmonary function measures or severity score. In the longitudinal analysis of 26 subjects, changes in serum CXCL10 level over time corresponded with progression versus remission of disease.
Conclusions: Interferon-γ-inducible chemokines, CXCL9 and CXCL10, are elevated in sarcoidosis and inter-correlated with each other. Chemokine levels correlated with measures of disease severity. Serial measurements of CXCL10 corresponded to clinical course.
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http://dx.doi.org/10.1186/1465-9921-14-121 | DOI Listing |
Clin Epigenetics
January 2025
Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Background: The primary objective of this study was to examine whether ARID1A mutations confer a fitness advantage to gastric cancer from an immunological perspective, along with elucidating the underlying mechanism. Additionally, we aimed to identify the clinical potential of combining epigenetic inhibitors with immune checkpoint inhibitors to improve the efficacy of immunotherapy for gastric cancer.
Methods: The correlation between ARID1A gene expression and gastric cancer patient survival was analyzed using the GEO dataset GSE62254.
Cancer Immunol Immunother
January 2025
Geneis Beijing Co., Ltd, Beijing, 100102, China.
Limited research into the tumor immune microenvironment (TIME) for bladder urothelial carcinoma (BUC), particularly the neglect of the intratumoral microbiota, has hindered the development of immunotherapies targeting BUC. Here, we collect 401 patients with BUC with host transcriptome samples and matched tumor microbiome samples from The Cancer Genome Atlas database. Besides, two independent BUC cohorts receiving immunotherapy were obtained.
View Article and Find Full Text PDFJ Invest Dermatol
December 2024
Department of Dermatology and Allergy, Technical University of Munich, Munich, Germany; Department of Dermatology, Ludwig-Maximilians University Hospital, Munich, Germany. Electronic address:
Lichen planus (LP) is a chronic inflammatory disease (ISD) affecting skin, mucosa, nail, and hair. Previous studies demonstrated a pivotal role of type 1 immunity in LP, as infiltrating T cells trigger apoptosis and necroptosis in the epidermis. In this study, we investigated the role of DAPK1 in LP with special focus on its role in mediating cell death and inflammation.
View Article and Find Full Text PDFFEBS Lett
January 2025
Centre for Inflammation Research, Institute for Regeneration and Repair, University of Edinburgh, UK.
Cancer-associated fibroblasts (CAFs) are the dominant nonmalignant component of the tumour microenvironment (TME). CAFs demonstrate a high level of inter- and intra-tumour heterogeneity in solid tumours, though the drivers of CAF subpopulations are not fully understood. Here, we demonstrate that non-small cell lung cancer (NSCLC) patient-derived CAFs upregulate the secretion of inflammatory cytokines (IL6, LIF, IL33, GM-CSF, IL1ra) and chemokines (CCL2, CCL3, CCL4, CCL20, CXCL8, CXCL9, CXCL10, CXCL11) in response to in vitro co-culture with anti-CD3/anti-CD28-stimulated peripheral blood mononuclear cells (PBMCs) via IFNγ and TNFα.
View Article and Find Full Text PDFBr J Dermatol
December 2024
Department of Dermatology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Background: The tumour microenvironment significantly influences the clinical response of patients to therapeutic immune checkpoint inhibition (ICI), but a comprehensive understanding of the underlying immune-regulatory proteome is still lacking.
Objectives: To decipher targetable biologic processes that determine tumour-infiltrating lymphocytes (TiLs) as a cellular equivalent of clinical response to ICI.
Methods: We mapped the spatial distribution of proteins in TiL-enriched vs.
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