tbuckley/cabot-search huggingface dataset:
Current state and potential applications of neonatal Fc receptor (FcRn) inhibitors in hematologic conditions
Authors: Jeremy W. Jacobs, Garrett S. Booth, Sheharyar Raza, Landon M. Clark, Ross M. Fasano, Eleni Gavriilaki, Elizabeth A. Abels, Thomas C. Binns, Miriam Andrea Duque, Zoe K. McQuilten, María Eva Mingot‐Castellano, Bipin N. Savani, Deva Sharma, Minh‐Ha Tran, Christopher A. Tormey, Kenneth J. Moise, Evan M. Bloch, Brian D. Adkins
Journal: American Journal of Hematology (2024)

Abstract The neonatal fragment crystallizable (Fc) receptor (FcRn) transports IgG across mucosal surfaces and the placenta and protects IgG from degradation. Numerous clinical trials are investigating therapeutic FcRn inhibition for various immune‐mediated neuromuscular and rheumatologic conditions; however, FcRn inhibition also represents a potential therapy for IgG‐mediated hematologic conditions (e.g., immune thrombocytopenia, autoimmune hemolytic anemia, immune thrombotic thrombocytopenic purpura, acquired hemophilia, red blood cell/platelet alloimmunization). Current evidence derived from both in vitro and in vivo studies suggests that FcRn inhibitors effectively reduce total IgG levels without impacting its production or altering the levels of other immunoglobulin isotypes. Moreover, the risk of serious adverse events, including serious infections, appears to be lower than that seen with other commonly used immunomodulatory/immunosuppressive therapies, albeit in the setting of limited clinical trial data. Ultimately, additional clinical trials that include varied patient populations are required prior to incorporating these agents into standard treatment algorithms for most hematologic conditions. However, based on the pathophysiology of IgG‐mediated hematologic disorders and the mechanism of action of FcRn inhibitors, these agents may represent a future novel therapeutic strategy for patients with hematologic conditions caused by IgG antibodies.
Injectable Glucose‐Releasing Microgels Enhance the Survival and Therapeutic Potential of Transplanted MSCs Under Ischemic Conditions
Authors: Chieh‐Cheng Huang, Chun‐Kai Chang, Pei‐Ching Yang, Han Chiu, Shih‐Heng Chen, Li‐Wen Hsu
Journal: Advanced Healthcare Materials (2024)

Abstract Mesenchymal stem cell (MSC)‐based therapies show potential to treat ischemic diseases owing to their versatile functions. However, sustaining MSC viability and therapeutic efficacy in ischemic tissues postengraftment remains a significant challenge. This is because, although MSCs are metabolically flexible, they fail to adapt to hypoxic conditions in the absence of glucose, leading to cell death. To overcome these issues, it is aimed to establish an injectable glucose delivery system using starch and amyloglucosidase embedded in alginate microgels. Here, starch/amyloglucosidase (S/A) microgels are engineered to continuously release glucose for seven days via enzymatic hydrolysis, thereby supporting MSC functions under ischemic conditions. In vitro tests under oxygen/glucose‐deprived conditions revealed that the S/A microgels not only maintained the viability and intracellular energy but also enhanced the pro‐angiogenic and immunomodulatory functions of MSCs. In vivo data further confirmed the pro‐survival and pro‐angiogenic effects of S/A microgels on MSCs following subcutaneous engraftment in mice. Overall, the developed S/A microgel significantly enhanced the survival and therapeutic potential of MSCs via sustained glucose delivery, highlighting its potential use in advancing MSC‐based therapies for ischemic conditions.
FMT rescues mice from DSS-induced colitis in a STING-dependent manner
Authors: Dan Pu, Yao Yao, Chuan Zhou, Ruixian Liu, Zhihong Wang, Yan Liu, Dandan Wang, Binbin Wang, Yaohe Wang, Zhanju Liu, Zhe Zhang, Baisui Feng
Journal: Gut Microbes (2024)

Fecal microbiota transplantation (FMT) is currently a promising therapy for inflammatory bowel disease (IBD). However, clinical studies have shown that there is an obvious individual difference in the efficacy of FMT. Therefore, it is a pressing issue to identify the factors that influence the efficacy of FMT and find ways to screen the most suitable patients for this therapy. In this work, we targeted the stimulator of interferon genes (STING), a DNA-sensing protein that regulates host-defense. By comparing the differential efficacy of FMT in mice with different expression level of STING, it is revealed that FMT therapy provides treatment for DSS-induced colitis in a STING-dependent manner. Mechanistically, FMT exerts a regulatory effect on the differentiation of intestinal Th17 cells and macrophages, splenic Th1 and Th2 cells, as well as Th1 cells of the mesenteric lymph nodes via STING, down-regulating the colonic M1/M2 and splenic Th1/Th2 cell ratios, thereby improving the imbalanced immune homeostasis in the inflamed intestine. Meanwhile, based on the 16SrDNA sequencing of mice fecal samples, STING was found to facilitate the donor strain colonization in recipients' gut, mainly
Deficiency of metabolic regulator PKM2 activates the pentose phosphate pathway and generates TCF1+ progenitor CD8+ T cells to improve immunotherapy
Authors: Geoffrey J Markowitz, Yi Ban, Diamile A Tavarez, Liron Yoffe, Enrique Podaza, Yongfeng He, Mitchell T Martin, Michael J P Crowley, Tito A Sandoval, Dingcheng Gao, M Laura Martin, Olivier Elemento, Juan R Cubillos-Ruiz, Timothy E McGraw, Nasser K Altorki, Vivek Mittal
Journal: Nature Immunology (2024)
Spatial single-cell protein landscape reveals vimentinhigh macrophages as immune-suppressive in the microenvironment of hepatocellular carcinoma
Authors: Xinyao Qiu, Tao Zhou, Shuai Li, Jianmin Wu, Jing Tang, Guosheng Ma, Shuai Yang, Ji Hu, Kaiting Wang, Siyun Shen, Hongyang Wang, Lei Chen
Journal: Nature Cancer (2024)
Identifying genetic variants that influence the abundance of cell states in single-cell data
Authors: Laurie Rumker, Saori Sakaue, Yakir Reshef, Joyce B Kang, Seyhan Yazar, Jose Alquicira-Hernandez, Cristian Valencia, Kaitlyn A Lagattuta, Annelise Mah-Som, Aparna Nathan, Joseph E Powell, Po-Ru Loh, Soumya Raychaudhuri
Journal: Nature Genetics (2024)
Enhancing the Polygenic Score Catalog with tools for score calculation and ancestry normalization
Authors: Samuel A Lambert, Benjamin Wingfield, Joel T Gibson, Laurent Gil, Santhi Ramachandran, Florent Yvon, Shirin Saverimuttu, Emily Tinsley, Elizabeth Lewis, Scott C Ritchie, Jingqin Wu, Rodrigo Cánovas, Aoife McMahon, Laura W Harris, Helen Parkinson, Michael Inouye
Journal: Nature Genetics (2024)
Identification and characterization of human GDF15 knockouts
Authors: Allan M Gurtan, Shareef Khalid, Christopher Koch, Maleeha Zaman Khan, Lindsey B Lamarche, Igor Splawski, Elizabeth Dolan, Ana M Carrion, Richard Zessis, Matthew E Clement, Zhiping Chen, Loren D Lindsley, Yu-Hsin Chiu, Ryan S Streeper, Daniel P Denning, Allison B Goldfine, Brian Doyon, Ali Abbasi, Jennifer L Harrow, Kazuhisa Tsunoyama, Makoto Asaumi, Ikuyo Kou, Alan R Shuldiner, Juan L Rodriguez-Flores, Asif Rasheed, Muhammad Jahanzaib, Muhammad Rehan Mian, Muhammad Bilal Liaqat, Syed Shahzaib Raza, Riffat Sultana, Anjum Jalal, Muhammad Hamid Saeed, Shahid Abbas, Fazal Rehman Memon, Mohammad Ishaq, John E Dominy, Danish Saleheen
Journal: Nature Metabolism (2024)
COPD-iNET: a call to the lung community for action to combat the global epidemic of COPD
Authors: Ali Önder Yildirim, Thomas M Conlon, Ian M Adcock, Reinoud Gosens, Mareike Lehmann, Theodore S Kapellos, Yohannes Tesfaigzi, Francesca Polverino, Maor Sauler, Roxana Wasnick, Enid Rose Neptune
Journal: European Respiratory Journal (2024)
Which trials do we need? Fidaxomicin plus either intravenous metronidazole or tigecycline versus vancomycin plus either intravenous metronidazole or tigecycline for fulminant Clostridioides difficile infection
Authors: G Pipitone, C Iaria, G Granata, A Cascio, A E Maraolo
Journal: Clinical Microbiology and Infection (2024)
A systematic review of antibiotic drug shortages and the strategies employed for managing these shortages
Authors: Avaneesh Kumar Pandey, Jennifer Cohn, Vrinda Nampoothiri, Uttara Gadde, Amrita Ghataure, Ashish Kumar Kakkar, Yogendra Kumar Gupta, Samir Malhotra, Oluchi Mbamalu, Marc Mendelson, Anne-Grete Märtson, Sanjeev Singh, Thomas Tängdén, Nusrat Shafiq, Esmita Charani
Journal: Clinical Microbiology and Infection (2024)
Evaluating the efficacy of whole genome sequencing in predicting susceptibility profiles for first-line antituberculosis drugs
Authors: Arash Ghodousi, Maryam Omrani, Stefania Torri, Hedyeh Teymouri, Giulia Russo, Chiara Vismara, Alberto Matteelli, Luigi Ruffo Codecasa, Daniela Maria Cirillo
Journal: Clinical Microbiology and Infection (2024)
Development and acceptability of a decision‐aid for food allergy Oral immunotherapy in children
Authors: Aikaterini Anagnostou, Elissa M. Abrams, Melanie Carver, Edmond S. Chan, Sanaz Eftekhari, Justin Greiwe, Hannah Jaffee, Jay A. Lieberman, Douglas P. Mack, S. Shahzad Mustafa, Marcus S. Shaker, David Stukus, Julie Wang, Matthew Greenhawt
Journal: Allergy (2024)

Abstract Background Limited decision‐support tools are available to help shared decision‐making (SDM) regarding food oral immunotherapy (OIT) initiation. No current tool covers all foods, forms, and pediatric ages for which OIT is offered. Methods In compliance with International Patient Decision Aid Standards criteria, this pediatric decision‐aid comparing OIT versus avoidance was developed in three stages. Nested qualitative data assessing OIT decisional needs were supplemented with evidence‐synthesis from the OIT literature to create the prototype decision‐aid content. This underwent iterative development with food allergy experts and patient advocacy stakeholders until unanimous consensus was reached regarding content, bias, readability, and utility in making a choice. Lastly, the tool underwent validated assessment of decisional acceptability, decisional conflict, and decisional self‐efficacy. Results The decision‐aid underwent 5 iterations, resulting in a 4‐page written aid (Flesch–Kincaid reading level 6.1) explaining therapy choices, risks and benefits, providing self‐rating for attribute importance for the options and self‐assessment regarding how adequate the information was in decision‐making. A total of n = 135 caregivers of food‐allergic children assessed the decision‐aid, noting good acceptability, high decisional self‐efficacy (mean score 85.9/100) and low decisional conflict (mean score 20.9/100). Information content was rated adequate and sufficient, the therapy choices wording balanced, and presented without bias for a “best choice.” Lower decisional conflict was associated with caregiver‐reported anaphylaxis. Conclusions This first pediatric OIT decision‐aid, agnostic to product, allergen, and age has good acceptability, limited bias, and is associated with low decisional conflict and high decisional self‐efficacy. It supports SDM in navigating the decision to start OIT or continue allergen avoidance.
Targeting epigenetic regulation and post-translational modification with 5-Aza-2’ deoxycytidine and SUMO E1 inhibition augments T-cell receptor therapy
Authors: Jessie S Kroonen, Anne K Wouters, Ilona J de Graaf, Dennis F G Remst, Sumit Kumar, Tassilo L A Wachsmann, Amina F A S Teunisse, Jessica P Roelands, Noel F C C de Miranda, Marieke Griffioen, Mirjam H M Heemskerk, Alfred C O Vertegaal
Journal: Journal for ImmunoTherapy of Cancer (2024)

Background Cellular immunotherapy using modified T cells offers new avenues for cancer treatment. T-cell receptor (TCR) engineering of CD8 T cells enables these cells to recognize tumor-associated antigens and tumor-specific neoantigens. Improving TCR T-cell therapy through increased potency and in vivo persistence will be critical for clinical success. Methods We evaluated a novel drug combination to enhance TCR therapy in mouse models for acute myeloid leukemia (AML) and multiple myeloma (MM). Results Combining TCR therapy with the SUMO E1 inhibitor TAK981 and the DNA methylation inhibitor 5-Aza-2’ deoxycytidine resulted in strong antitumor activity in a persistent manner against two in vivo tumor models of established AML and MM. We uncovered that the drug combination caused strong T-cell proliferation, increased cytokine signaling in T cells, improved persistence of T cells, and reduced differentiation towards exhausted phenotype. Simultaneously the drug combination enhanced immunogenicity of the tumor by increasing HLA and co-stimulation and surprisingly reducing inhibitory ligand expression. Conclusion Combining T-cell therapy with TAK981 and 5-Aza-2’ deoxycytidine may be an important step towards improved clinical outcome.
How type‐2 dendritic cells induce Th2 differentiation: Instruction, repression, or fostering T cell‐T cell communication?
Authors: Franca Ronchese, Greta R. Webb, Sotaro Ochiai, Olivier Lamiable, Maia Brewerton
Journal: Allergy (2024)

Allergic disease is caused by the activation of allergen-specific CD4+ type-2 T follicular helper cells (Tfh2) and T helper 2 (Th2) effector cells that secrete the cytokines IL-4, IL-5, IL-9, and IL-13 upon allergen encounter, thereby inducing IgE production by B cells and tissue inflammation. While it is accepted that the priming and differentiation of naïve CD4+ T cells into Th2 requires allergen presentation by type 2 dendritic cells (DC2s), the underlying signals remain unidentified. In this review we focus on the interaction between allergen-presenting DC2s and naïve CD4+ T cells in lymph node (LN), and the potential mechanisms by which DC2s might instruct Th2 differentiation. We outline recent advances in characterizing DC2 development and heterogeneity. We review mechanisms of allergen sensing and current proposed mechanisms of Th2 differentiation, with specific consideration of the role of DC2s and how they might contribute to each mechanism. Finally, we assess recent publications reporting a detailed analysis of DC-T cell interactions in LNs and how they support Th2 differentiation. Together, these studies are starting to shape our understanding of this key initial step of the allergic immune response.
Advancing the chemotherapy of tuberculous meningitis: a consensus view
Authors: Sean Wasserman, Joseph Donovan, Evelyne Kestelyn, James A Watson, Robert E Aarnoutse, James R Barnacle, David R Boulware, Felicia C Chow, Fiona V Cresswell, Angharad G Davis, Kelly E Dooley, Anthony A Figaji, Diana M Gibb, Julie Huynh, Darma Imran, Suzaan Marais, David B Meya, Usha K Misra, Manish Modi, Mihaja Raberahona, Ahmad Rizal Ganiem, Ursula K Rohlwink, Rovina Ruslami, James A Seddon, Keira H Skolimowska, Regan S Solomons, Cari J Stek, Nguyen Thuy Thuong Thuong, Reinout van Crevel, Claire Whitaker, Guy E Thwaites, Robert J Wilkinson
Journal: The Lancet Infectious Diseases (2024)
Associations of “Weekend Warrior” Physical Activity With Incident Disease and Cardiometabolic Health
Authors: Shinwan Kany, Mostafa A. Al-Alusi, Joel T. Rämö, James P. Pirruccello, Timothy W. Churchill, Steven A. Lubitz, Mahnaz Maddah, J. Sawalla Guseh, Patrick T. Ellinor, Shaan Khurshid
Journal: Circulation (2024)

BACKGROUND: Achievement of guideline-recommended levels of physical activity (≥150 minutes of moderate-to-vigorous physical activity per week) is associated with lower risk of adverse cardiovascular events and represents an important public health priority. Although physical activity commonly follows a “weekend warrior” pattern, in which most moderate-to-vigorous physical activity is concentrated in 1 or 2 days rather than spread more evenly across the week (regular), the effects of physical activity pattern across a range of incident diseases, including cardiometabolic conditions, are unknown. METHODS: We tested associations between physical activity pattern and incidence of 678 conditions in 89 573 participants (62±8 years of age; 56% women) of the UK Biobank prospective cohort study who wore an accelerometer for 1 week between June 2013 and December 2015. Models were adjusted for multiple baseline clinical factors, and P value thresholds were corrected for multiplicity. RESULTS: When compared to inactive (&lt;150 minutes moderate-to-vigorous physical activity/week), both weekend warrior (267 total associations; 264 [99%] with lower disease risk; hazard ratio [HR] range, 0.35–0.89) and regular activity (209 associations; 205 [98%] with lower disease risk; HR range, 0.41–0.88) were broadly associated with lower risk of incident disease. The strongest associations were observed for cardiometabolic conditions such as incident hypertension (weekend warrior: HR, 0.77 [95% CI, 0.73–0.80]; P =1.2×10 -27 ; regular: HR, 0.72 [95% CI, 0.68–0.77]; P =4.5×10 -28 ), diabetes (weekend warrior: HR, 0.57 [95% CI, 0.51–0.62]; P =3.9×10 -32 ; regular: HR, 0.54 [95% CI, 0.48–0.60]; P =8.7×10 -26 ), obesity (weekend warrior: HR, 0.55 [95% CI, 0.50–0.60]; P =2.4×10 -43 , regular: HR, 0.44 [95% CI, 0.40–0.50]; P =9.6×10 -47 ), and sleep apnea (weekend warrior: HR, 0.57 [95% CI, 0.48–0.69]; P =1.6×10 -9 ; regular: HR, 0.49 [95% CI, 0.39–0.62]; P =7.4×10 -10 ). When weekend warrior and regular activity were compared directly, there were no conditions for which effects differed significantly. Observations were similar when activity was thresholded at the sample median (≥230.4 minutes of moderate-to-vigorous physical activity/week). CONCLUSIONS: Achievement of measured physical activity volumes consistent with guideline recommendations is associated with lower risk for &gt;200 diseases, with prominent effects on cardiometabolic conditions. Associations appear similar whether physical activity follows a weekend warrior pattern or is spread more evenly throughout the week.
DNAJB1-PRKACA fusion drives fibrolamellar liver cancer through impaired SIK signaling and CRTC2/p300-mediated transcriptional reprogramming
Authors: Ilaria Gritti, Jinkai Wan, Vajira Weeresekara, Joel M. Vaz, Giuseppe Tarantino, Tenna Holgersen. Bryde, Vindhya Vijay, Ashwin V. Kammula, Prabhat Kattel, Songli Zhu, Phuong Vu, Marina Chan, Meng-Ju Wu, John D. Gordan, Krushna C. Patra, Vanessa S. Silveira, Robert T. Manguso, Marc N. Wein, Christopher J. Ott, Jun Qi, David Liu, Kei Sakamoto, Taranjit S. Gujral, Nabeel Bardeesy
Journal: Cancer Discovery (2024)

This work combines functional studies in model systems and examination of human tumor specimens to define a central oncogenic pathway driven by DNAJB1-PRKACA fusions in FLC. DNAJB1-PRKACA-mediated inactivation of the SIK stimulates CRTC2-p300-mediated transcription to drive tumor growth. The findings illuminate pathogenic mechanisms and inform therapeutic development.
Experts consensus on management of tooth luxation and avulsion
Authors: Ruijie Huang, Chenchen Zhou, Ling Zhan, Yuan Liu, Xian Liu, Qin Du, Jun Wang, Wei Zhao, Guangtai Song, Li-An Wu, Beizhan Jiang, Yanhong Li, Hongmei Zhang, Jing Zou
Journal: International Journal of Oral Science (2024)
An intra articular injectable Mitocelle recovers dysfunctional mitochondria in cellular organelle disorders
Authors: Min Ju Lim, Hyeryeon Oh, Jimin Jeon, Chanmi Cho, Jin Sil Lee, Yiseul Hwang, Seok Jung Kim, Jung-Soon Mo, Panmo Son, Ho Chul Kang, Won Il Choi, Siyoung Yang
Journal: Bioactive Materials (2024)
Assessing Left Atrial Dysfunction in Cardiac Amyloidosis using LA-LV Strain Slope
Authors: Fredrik Edbom, Per Lindqvist, Urban Wiklund, Björn Pilebro, Intissar Anan, Frank A Flachskampf, Sandra Arvidsson
Journal:  (2024)

Transthyretin amyloid cardiomyopathy (ATTR-CM) is an infiltrative disease of the myocardium in which extracellular deposits of amyloid cause progressive cardiac impairment. We aimed to evaluate left atrial (LA) deformation and its association with left ventricular (LV) deformation using LA-LV strain loops in patients with ATTR-CM and patients with LV hypertrophy (LVH). We hypothesized that LA strain in ATTR-CM patients is abnormal and more independent of LV strain, compared to LVH patients.
Viral antibody response predicts morbidity and mortality in alcohol-associated hepatitis
Authors: Cynthia L. Hsu, Limin Wang, Evan Maestri, Aleesha R. Jacob, Whitney L. Do, Susan Mayo, Francisco Bosques-Padilla, Elizabeth C. Verna, Juan G. Abraldes, Robert S. Brown Jr., Victor Vargas, Jose Altamirano, Juan Caballería, Debbie L. Shawcross, Alexandre Louvet, Michael R. Lucey, Philippe Mathurin, Guadalupe Garcia-Tsao, Peter Stärkel, Ramon Bataller, AlcHepNet Investigators, Xin W. Wang, Bernd Schnabl
Journal: Hepatology (2024)

Background and Aims: Alcohol-associated hepatitis (AH) is associated with very high mortality despite abstinence from alcohol; up to 40% of patients die within 6 months of diagnosis. Patients with AH are especially prone to infections, which can lead to multiorgan dysfunction and poorer prognosis. Approach and Results: We performed comprehensive serological profiling of the viral and bacterial infection history of 36 healthy controls, 48 patients with alcohol use disorder, and 224 patients with AH from 2 multicenter observational studies. We used systematic viral and bacterial epitope scanning by VirScan, a phage-display immunoprecipitation and sequencing technology that detects the peptides recognized by antibodies in patient sera, to comprehensively analyze antiviral and antibacterial antibodies and identify serologic biomarkers to predict patient outcomes. We found significant differences in the serological profiles of the 3 populations. The number of serum antibody epitopes in patients with alcohol use disorder during abstinence was increased compared with during active alcohol use. A decreased number and diversity of viral and bacterial antibody targets were detected in the sera of patients with AH, particularly those with a higher Child-Pugh score. In patients with AH, a decrease in the serum antiviral, but not antibacterial, antibody repertoire was associated with decompensation and mortality. Ninety-day mortality in AH could be predicted using a serum viral epitope signature. Conclusions: Abstinence from alcohol is associated with a significant increase in serum viral and bacterial antibody response. Decreased serum antiviral antibody repertoire is predictive of decompensation of liver disease and mortality in patients with AH.
TIPE2 protein restrains invariant NKT activation and protects against immune-mediated hepatitis in mice
Authors: Miaomiao Song, Han Wang, Xueqin Tian, Jingtao Gao, Chen Song, Yuxin Zhao, Shan Jiang, Wei Lu, Cun Guo, Yang Lv, Peiqing Zhao, Chuang Li, Xiangfeng Song, Tingmin Chang, Yunwei Lou, Hui Wang
Journal: Hepatology (2024)

Background and Aims: Concanavalin A (ConA) administration induces a rapid and severe liver injury in mice, and invariant natural killer T (iNKT) cells are recognized to be the key effector cells in this process. However, the underlying regulatory mechanisms are not well defined. Approach and Results: We found that iNKT cells constitutively expressed TIPE2 (Tumor necrosis factor-α-induced protein 8-like 2, or TNFAIPL2). Genetic TIPE2 ablation strongly sensitized mice to ConA-induced hepatitis, accompanied with hyperactivation of iNKT cells. Moreover, Tipe2 -/- mice were also more susceptible to α-galactosylceramide (αGalCer)-induced liver injury, with elevated serum ALT level and enhanced proinflammatory cytokine production. CD1d signaling blockade or iNKT cell elimination through antibodies reduced the effect of TIPE2 deficiency on liver injury. Mechanistic studies revealed that TIPE2 in iNKT cells functioned as a negative regulator, limiting iNKT cell activity and cytokine production through PIP3- AKT/mTOR pathway. TIPE2-mediated protection from liver injury was further validated by the administration of adeno-associated viruses expressing TIPE2, which effectively ameliorated ConA-induced hepatic injury. However, TIPE2 was dispensable in two other liver injury models, including D-GalN/LPS and APAP-induced hepatitis. Conclusion: Our findings reveal a new role of TIPE2 in the attenuation of iNKT cell-mediated hepatic injury. We propose that TIPE2 serves as an important regulator of immune homeostasis in the liver, and might be exploited for the therapeutic treatment of autoimmune liver diseases.