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Biology subjects

Ahn, S. H.

Publications and source records attributed to Ahn, S. H..

8 recordsLinked to original sources

Profiling of intestinal T cells reveals antigen-specific dependency on early-life programming for the generation of microbiota-reactive Tregs

The generation of appropriate responses to the intestinal microbiota is an essential aspect of immune homeostasis. Studies of microbes that elicit stereotyped, antigen-specific CD4 T cell responses support the view that immune recognition of the microbiota is specific, relatively limited, and largely skewed toward Tregs, but recent profiling efforts have suggested that recognition of the microbiota may be broader and less regulatory. Such studies have mostly tracked responses to single antigens or used mice that acquire their microbiota after weaning, which has made it difficult to generalize the rules that govern microbiota-mediated T cell responses. Here we comprehensively profile, for the first time, the T cell response to the microbiota at homeostasis, and develop a panel of tools to track multiple, endogenous microbiota-reactive CD4 T cell populations in vivo. Our profiling reveals a broad microbiota-reactive T cell response that is Treg-biased but that also contains non-Treg responses to specific microbes. We find that certain microbiota-reactive T cells require priming during early-life to efficiently establish their Treg identity, while others do not. Our findings illustrate an unappreciated antigen-specific complexity in programming of microbiota-reactive T cells and underscore the importance of studying responses to the microbiota under homeostatic conditions.

immunology↗

Intratumoral dose heterogeneity promotes adaptive anti-tumor immunity and predicts clinical response to radiopharmaceutical therapy

Radiopharmaceutical therapies (RPT) deliver non-uniform radiation dose in tumors and the impact of this on response is poorly understood. Dose heterogeneity could engender treatment resistance in low dose regions, yet we hypothesize that a broader array of dose-dependent immuno-radiobiological mechanisms in tumor microenvironments (TME) and preservation of immune function in low-dose regions could promote adaptive anti-tumor immunity and response. In murine models, non-uniform lutetium-177 delivering <2.5 Gy to >20 Gy in a TME induced broader immunomodulatory effects and T cell-dependent survival improvement compared to more uniform distributions. Preserving low-dose regions promoted dendritic cell activation and TME infiltration of clonally expanded CD8+ T cells. In three independent cohorts of patients with prostate cancer, heterogeneous tumor dose distribution strongly correlated with improved clinical outcomes. These findings defy expected radiobiological dose-response and define a novel mechanism of action for RPT, supporting clinical investigation of dose distribution for optimizing patient selection and personalized dosing.

cancer biology↗

Revealing Spatial Heterogeneity across the Gut Tissue-Lumen Interface through MALDI Mass Spectrometry Imaging

AbstractMetabolites play critical roles in modulating gut-microbe interactions and are closely related to health and disease consequences. One critical aspect of the gut-microbe interactions is spatial heterogeneity, particularly at the interface space between gut tissue and luminal contents, where a unique microhabitat of diverse microbial functions encounters the host tissues. Exploring the spatial heterogeneity of this interface enables insights into these gut-microbe interactions. Previous studies commonly investigated metabolome through tissue homogenization and bulk analysis, but these methods result in the loss of spatial information. In this project, we use high-resolution matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) approaches to reveal the chemical spatial heterogeneity of colon tissue, luminal contents, and the tissue-lumen interface across multiple colonic regions. We applied a swiping technique to aid the preservation of luminal content integrity and used two MALDI matrices to cover a wide range of metabolites. The MALDI-MSI analyses revealed distinct patterns of metabolite spatial localization across the gut tissue-lumen interfaces, amongst which the interface-enriched features are of particular interest due to their possibly connection to the gut-microbe interactions. Overall, the rich spatial heterogeneity of metabolomic profiles across the gut tissue-lumen interfaces highlight the molecular participants in host-microbe interactions, providing new opportunities for examining host-microbiome-metabolome dynamics.

biochemistry↗

An All-In-One Software Solution for Automated Processing of LA-ICP-TOF-MS datasets

LA-ICP-TOF-MS provides rapid, high resolution elemental analysis of biological and non-biological samples. However, accurate real-time data analysis frequently requires the user to account for several instrumental and experimental variables that can change during data acquisition. AutoSpect is a novel software tool designed to automate the processing and fitting of LA-ICP-TOF-MS data, addressing key challenges such as time-dependent spectral drift, instrument sensitivity drift calibration inaccuracies, and peak deconvolution, enabling researchers to rapidly and accurately process complex datasets. The tool is optimized to be robustly applicable across scientific fields (e.g., geochemistry, biology, and materials science), providing a streamlined solution for end users seeking to maximize the potential of LA-ICP-TOF-MS for high-resolution elemental mapping and isotopic analysis. Significance to JAASAnalysis of fast transient signals using laser ablation inductively coupled plasma time-of-flight mass spectrometry (LA-ICP-TOF-MS) has become mainstream for elemental mapping. Advancements in LA-ICP-TOF-MS technology continue to accelerate the collective understanding of the role inorganic chemistry plays in dynamic processes. To ensure accurate quantitative results, the vast amount of complex spectral data generated requires elegant solutions to perform a variety of functions including data partitioning, peak fitting, drift correction, mass-to-charge calibration, peak profiling, and spectral fitting. AutoSpect is an all-in-one software solution that provides high level automation with a user-friendly graphical interface to perform complex data analyses for ICP-TOF-MS datasets.

scientific communication and education↗

Autoimmune regulator deficiency causes sterile epididymitis and impacts male fertility through disruption of inorganic physiology

Autoimmune regulator (AIRE), a transcription factor expressed by medullary thymic epithelial cells, is required for shaping the self-antigen tolerant T cell receptor repertoire. Humans with mutations in AIRE suffer from Autoimmune Polyglandular Syndrome Type 1 (APS-1). Among many symptoms, men with APS-1 commonly experience testicular insufficiency and infertility, but the mechanisms causing infertility are unknown. Using an Aire-deficient mouse model, we demonstrate that male subfertility is caused by sterile epididymitis characterized by immune cell infiltration and extensive fibrosis. In addition, we reveal that the presence of autoreactive immune cells and inflammation in epididymides of Aire-deficient mice are required for iron (Fe) deposition in the interstitium, which is brought on by macrophages. We further demonstrate that male subfertility is associated with a decrease in metals zinc (Zn), copper (Cu), and selenium (Se) which serve as cofactors in several antioxidant enzymes. We also show increase in DNA damage of epididymal sperm of Aire-/- animals as a key contributing factor to subfertility. The absence of Aire results in autoimmune attack of the epididymis leading to fibrosis, Fe deposition, and Cu, Zn and Se imbalance, ultimately resulting in sperm DNA damage and subfertility. These results highlight the requirement of Aire to promote immune tolerance throughout the epididymis, disruption of which causes an imbalance of inorganic elements with resulting consequence on male fertility. Key pointsBreakdown of epididymal self-tolerance promotes disruption of inorganic elements. Autoimmunity causes interstitial fibrosis resulting in sperm DNA damage and subfertility. Elevated interstitial iron and macrophages contribute to fibrosis.

pathology↗

The dysregulated IL-23/TH17 axis in endometriosis pathophysiology

Endometriosis is a chronic inflammatory disease where endometrial-like tissue grows ectopically, resulting in pelvic pain and infertility. Interleukin (IL)-23 is established as a key contributor in the development and differentiation of a subset of T cells known as T-helper 17 (TH17) cells, driving TH17 cells towards a pathogenic profile. In a variety of inflammatory and autoimmune disorders, such as psoriasis and rheumatoid arthritis, TH17 cells secrete proinflammatory cytokines including IL-17, contributing to the disease pathophysiology. Our studies and others have implicated IL-17 and TH17 cell dysregulation in endometriosis, which is associated with disease severity. Here we address whether IL-23 driven TH17 cells contribute to the cardinal features of lesion proliferation, vascularization, and inflammation in endometriosis using patient samples, representative cell lines, and our established mouse model of endometriosis. Our results indicate significantly dysregulated expression of key genes in the IL-23/TH17 axis in patient ectopic and eutopic endometrial samples and increased IL-23 protein in patient plasma compared to healthy controls. In-vitro studies using primary human TH cells determined that IL-23 cocktail treatment significantly increased the frequency of pathogenic TH17 cells. Similarly, treatment with recombinant human (rh)IL-23 on cell lines (12Z, EECC, HUVEC, and hESC) representative of the endometriotic lesion microenvironment led to a significant increase in cytokines and growth factors known to play a role in lesion establishment and maintenance. In a syngeneic mouse model of endometriosis, treatment with recombinant mouse (rm)IL-23 led to significant alterations in numbers of myeloid and T cell subsets in peritoneal fluid and significantly increased numbers of giant cells within the lesion. Endometriotic lesions from rmIL-23 mice did not reveal significant alterations in proliferation and vascularization, although trends of increased proliferation and vascularization were observed. Collectively, these findings provide insights into the impact of the IL-23/TH17 axis on local immune dysfunction and broadly on the pathophysiology of endometriosis.

immunology↗

Sus1 maintains a normal lifespan through regulation of TREX-2 complex-mediated mRNA export

Eukaryotic gene expression requires multiple cellular events, including transcription and RNA processing and transport. Sus1, a common subunit in both the Spt-Ada-Gcn5 acetyltransferase (SAGA) and transcription and export complex-2 (TREX-2) complexes, is a key factor in coupling transcription activation to mRNA nuclear export. Here we present that the SAGA DUB module and TREX-2 regulates distinctly yeast replicative lifespan in a Sir2-dependent and - independent manner, respectively. The growth and lifespan impaired by SUS1 loss depend on TREX-2 but not on the SAGA DUB module. Notably, an increased dosage of the mRNA export factors Mex67 and Dbp5 rescues the growth defect, shortened lifespan, and nuclear accumulation of poly(A)+ RNA in sus1{Delta} cells, suggesting that boosting the mRNA export process restores the mRNA transport defect and damage in the growth and lifespan of sus1{Delta} cells. Moreover, Sus1 is required for the proper association of Mex67 and Dbp5 with the nuclear rim. Together, these data suggest that Sus1 links transcription and mRNA nuclear export to the lifespan control pathway, indicating that prevention of an abnormal accumulation of nuclear RNA is necessary for maintaining a normal lifespan.

cell biology↗

INTEGRINS MEDIATE PLACENTAL EXTRACELLULAR VESICLE TRAFFICKING TO LUNG AND LIVER IN VIVO

Membrane-bound extracellular vesicles (EVs) mediate intercellular communication in all organisms, and those produced by placental mammals have become increasingly recognized as significant mediators of fetal-maternal communication. Here, we aimed to identify maternal cells targeted by placental EVs and elucidate the mechanisms by which they traffic to these cells. Exogenously administered pregnancy-associated EVs traffic specifically to the lung; further, placental EVs associate with lung interstitial macrophages and liver Kupffer cells in an integrin-dependent manner. Localization of EV to maternal lungs was confirmed in unmanipulated pregnancy using a transgenic reporter mouse model, which also provided in situ and in vitro evidence that fetally-derived EVs, rarely, may cause genetic alteration of maternal cells. These results provide for the first time direct in vivo evidence for targeting of placental EVs to maternal immune cells, and further, evidence that EVs can alter cellular phenotype.

cell biology↗