Tertiary lymphoid structures (TLSs) are organized aggregates of immune cells associated with favourable prognosis and response to immunotherapy in cancer, but the immune architecture of TLSs remains poorly elucidated. Here, we hypothesize that the spatial architecture of leukocytes in TLSs can be reconstructed de novo, at least partially, by cell-inherent chemokine receptors profiles. Single-cell RNA-sequencing (scRNA-seq) revealed 47 subpopulations of leukocytes in head and neck squamous cell carcinoma (HNSC). Combined with bulk RNA-seq, we observed that CXCR3, CCR7, CCR6, CXCR5, and CCR1 are TLS-associated chemokine receptors. According to the spatial reference, the cellular atlas with TLS-associated chemokine receptors in HNSC TLSs was elaborately portrayed by multiplex immunohistochemistry (mIHC). Subsequently, we explored the functions and evolutionary trajectory of cells distributed in TLSs. Our investigation presents an approach to reconstructing the immune architecture of TLSs, which would help boost the antitumor immune response by inducing neogenesis TLSs in HNSC.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.canlet.2023.216105 | DOI Listing |
Nat Commun
December 2024
Department of Vascular Surgery, Zhongshan Hospital, Fudan University, 200032, Shanghai, China.
Adverse aortic remodeling increases the risk of aorta-related adverse events (AAEs) after thoracic endovascular aortic repair (TEVAR) and affects the overall prognosis of aortic dissection (AD). It is imperative to delve into the exploration of prognostic indicators to streamline the identification of individuals at elevated risk for postoperative AAEs, and therapeutic targets to optimize the efficacy of TEVAR for patients with AD. Here, we perform proteomic and single-cell transcriptomic analyses of peripheral blood and aortic lesions, respectively, from patients with AD and healthy subjects.
View Article and Find Full Text PDFNat Commun
December 2024
Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou Branch, Taoyuan, Taiwan.
Immune checkpoint inhibitors (ICI) represent new anticancer agents and have been used worldwide. However, ICI can potentially induce life-threatening severe cutaneous adverse reaction (SCAR), such as Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN), hindering continuous ICI therapy. We examine 6 cohorts including 25 ICI-induced SJS/TEN patients and conduct single-cell RNA sequencing (scRNA-seq) analysis, which shows overexpression of macrophage-derived CXCL10 that recruits CXCR3 cytotoxic T lymphocytes (CTL) in blister cells from ICI-SJS/TEN skin lesions.
View Article and Find Full Text PDFFront Immunol
December 2024
Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche (UMR), Université Paris Cité, Paris, France.
Introduction: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by an overactive immune response, particularly involving excessive production of type I interferons. This overproduction is driven by the phosphorylation of IRF7, a crucial factor in interferon gene activation. Current treatments for SLE are often not very effective and can have serious side effects.
View Article and Find Full Text PDFJ Transl Med
December 2024
Department of Urology, Xinjiang Medical University Affiliated Cancer Hospital, Urumqi, China.
Background: Immune checkpoint inhibitors (ICIs) are a cornerstone therapy for advanced renal cell carcinoma (RCC). However, significant rates of primary resistance hinder their efficacy, and the underlying mechanisms remain poorly understood. This study aims to unravel the tumor-immune interactions and signaling pathways driving primary resistance to ICIs in RCC.
View Article and Find Full Text PDFBrain Behav Immun
December 2024
Wolfson Sensory, Pain and Regeneration Centre, King's College London, Guy's Campus, London Bridge, London SE1 1UL, UK. Electronic address:
Angiotensin II is well known to have an important influence on blood pressure, mediated via the angiotensin II type 1 receptor (AT1R), and more recent studies have shown that angiotensin II may play an important additional role in eliciting pain via a distinct action at the angiotensin II type 2 receptor (AT2R). Signalling pathways that link activation of AT2R to a sensation of pain are, however, incompletely understood. Here we use rodent inflammatory pain models to confirm that selective activation of AT2R triggers aversive responses, and that these are abolished by either antagonism or genetic deletion of AT2R.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!