bioRxiv ScienceSearch

bioRxiv · 10.1101/2021.04.05.438347

Single-cell sequencing unveils distinct immune microenvironment with CCR6-CCL20 crosstalk in human chronic pancreatitis

Abstract

ObjectiveChronic pancreatitis (CP) is a potentially fatal disease of the exocrine pancreas, with no specific or effective approved therapies. Due to difficulty in accessing pancreas tissues, little is known about local immune responses or pathogenesis in human CP. We sought to characterize pancreas immune responses using tissues derived from patients with different etiologies of CP and non-CP organ donors in order to identify key signaling molecules associated with human CP. DesignWe performed single-cell level cellular indexing of transcriptomes and epitopes by sequencing (CITE-Seq) and T cell receptor sequencing of pancreatic immune cells isolated from organ donors, hereditary, and idiopathic CP patients who underwent total pancreatectomy. We validated gene expression data by performing flow cytometry and functional assay in the second CP patient cohort. ResultsDeep single-cell sequencing revealed distinct immune characteristics and significantly enriched CCR6+ CD4+ T cells in hereditary compared with idiopathic CP. In hereditary CP, a reduction in T cell clonality was observed due to the increased CD4+ T (Th) cells that replaced tissue-resident CD8+ T cells. Shared TCR clonotype analysis among T cell lineages also unveiled unique interactions between CCR6+ Th and Th1 subsets, and TCR clustering analysis showed unique common antigen binding motifs in hereditary CP. In addition, we observed a significant upregulation of the CCR6 ligand (CCL20) among monocytes in hereditary CP as compared with those in idiopathic CP. The functional significance of CCR6 expression in CD4+ T cells was confirmed by flow cytometry and chemotaxis assay. ConclusionSingle-cell sequencing with pancreatic immune cells in human CP highlights pancreas-specific immune crosstalk through the CCR6-CCL20 axis that might be leveraged as a potential future target in human hereditary CP. Significance of this studyO_ST_ABSWhat is already known about this subject?C_ST_ABSO_LIChronic pancreatitis (CP) is considered an irreversible fibroinflammatory pancreatic disease and remains a major source of morbidity among gastrointestinal diseases with no active approved therapy. C_LIO_LIInflammation is a known hallmark and contributor to CP pathogenesis. However, little is known about local immune responses in human CP especially with different etiologies. C_LI What are the new findings?O_LISingle-cell RNA sequencing of pancreatic immune cells from CP patients and organ donors revealed distinct immune transcriptomic features in CP versus non-diseased controls and hereditary versus idiopathic CP. C_LIO_LISingle-cell T cell receptor sequencing unveiled pancreas-specific clonal expansion in CD8+ T cells and CD4+ T cells-driven unique TCR repertoire changes in hereditary CP. C_LIO_LIWe identified that the CCR6-CCL20 axis was significantly upregulated in hereditary CP compared with controls or idiopathic CP suggesting a potential future target for human hereditary CP. C_LI How might it impact on clinical practice in the foreseeable future?O_LIThe results of this study will improve our understanding of CP heterogeneity and identify distinct immune responses in different types of human CP that could provide novel conceptual directions for therapeutic strategies in treating hereditary and idiopathic CP. C_LIO_LIThe CCR6-CCL20 axis found in hereditary CP could be a potential novel targetable signaling pathways in the treatment of hereditary CP. C_LI

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Lee, B., Namkoong, H., Yang, Y., Huang, H., Heller, D., Szot, G. L., Davis, M. M., Pandol, S. J., Bellin, M. D., Habtezion, A.. 2021-04-06. Single-cell sequencing unveils distinct immune microenvironment with CCR6-CCL20 crosstalk in human chronic pancreatitis. https://doi.org/10.1101/2021.04.05.438347

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

De novo design of CR2 binder as vaccine scaffold

Efficient B cell activation during vaccine-induced humoral immunity relies on both B cell receptor (BCR) antigen recognition and synergistic signaling from co-receptors. Complement receptor 2 (CR2), the primary BCR co-receptor on B cells, lowers the activation threshold and amplifies downstream kinase signaling by orders of magnitude when engaged by complement fragment C3d decorated antigens. Targeting CR2 therefore represents a rational vaccine enhancement strategy, yet native C3d suffers from low affinity, poor stability, and manufacturing challenges. Here, we report the de novo design of a highly stable, high-affinity CR2 binder using deep learning driving protein design methods. Biophysical characterization, high-resolution cryoEM structural determination, and functional assays in vitro and in vivo confirm that the designed binder matches computational design models and specifically engages CR2 to boost B cell activation. When fused to antigen as a vaccine scaffold, the trimeric CR2 binder elicits robust humoral immune responses comparable to nanoparticle vaccines, while retaining the simplicity of single-chain protein production. Our work establishes a modular CR2 targeting vaccine scaffold platform with broad translational potential for next-generation protein vaccines.

immunology

Chronic opioid-associated immune dysregulation among people living with HIV

Objectives: Persistent immune dysregulation contributes to chronic disease among people living with HIV (PWH), even after viral suppression with antiretroviral therapy (ART). Although chronic opioid exposure is associated with adverse clinical outcomes, its impact on immune homeostasis during ART remains incompletely understood. We investigated whether opioid use disorder (OUD) is associated with persistent systemic and cellular immune dysregulation despite ART-mediated reductions in HIV viral load (VL). Methods: Peripheral blood was collected longitudinally from PWH with OUD (PWH/OUD+) and detectable HIV VL during 6 months of optimized ART (months 0, 3, and 6). A reference cohort of PWH without OUD (PWH/OUD-) and suppressed HIV VL provided a single blood sample. Immune profiling included plasma inflammatory biomarkers, multiplex cytokine analyses, spectral flow cytometry, and assessment of monocyte cytokine responses following lipopolysaccharide (LPS) stimulation. Mixed-effects models adjusted for HIV VL and VL-stratified analyses were performed. Results: PWH/OUD+ exhibited persistent immune dysregulation despite reductions in HIV VL. Plasma sCD163, sCD14, fractalkine, and I-TAC remained elevated, whereas TGF-{beta}1 was reduced. OUD was associated with expansion of CD16 monocytes and altered expression of CCR2, CD38, and CD11b. CD4 and CD8 T cells, NK cells, and B cells also exhibited persistent alterations in markers of activation, metabolism, and trafficking. Monocytes from PWH/OUD+ displayed attenuated cytokine responses following LPS stimulation. Conclusions: OUD is associated with persistent systemic and cellular immune dysfunction in PWH despite ART-mediated viral suppression, supporting opioid exposure as an independent contributor to chronic immune dysregulation that may promote inflammation, immune dysfunction, and long-term HIV-associated comorbidities. Keywords: HIV, Opioid-use disorder, innate immunity, cytokine

immunology

The mitochondrial RNA extrusion-induced innate immunity is regulated by N6-methyladenosine machinery

Mitochondrial RNA (mtRNA) released into the cytosol functions as a damage associated molecular pattern that activates pattern-recognition receptor (PRR)-mediated inflammation, yet its release mechanisms and cytoplasmic fate remain poorly understood. Here we report that chemical Abt-373-treatment and Vesicular stomatitis virus (VSV) infection induce mtRNA extrusion through Bax/Bak and VDAC1 channels, accompanied by mtDNA release. Extruded mtRNA in A549 cells activates multiple cytosolic PRRs, including RIG-I, MDA5, TLR3/7/8, and PKR, each contributing differentially to the innate immune signaling. Analysis of GEO datasets and methylated RNA immunoprecipitation (MeRIP) assays further reveals that mtRNA carries methyladenosine (m6A) modification. m6A machinery proteins are involved in the cytoplasmic retention time of mtRNA and its interaction with RIG-I, thereby modulating mtRNA-induced innate immunity. Thus, our work establishes in vitro models of mtRNA extrusion, and highlights m6A-dependent modulation as a potential therapeutic target for mtRNA-driven inflammation.

immunology