Hypochlorous acid(HClO)is a critical biomolecule in living organisms,playing an essential role in numerous physiological or pathological processes.Abnormal levels of HClO in the body may lead to a series of diseases,f...Hypochlorous acid(HClO)is a critical biomolecule in living organisms,playing an essential role in numerous physiological or pathological processes.Abnormal levels of HClO in the body may lead to a series of diseases,for instance,inflammation and cancer.Thus,accurate measurement of HClO levels should be more beneficial for understanding its role in diseases and gaining a deeper insight into the pathogenesis of diseases.In this work,we designed a near-infrared two-photon fluorescent probe(HDM-Cl-HClO)for detecting fluctuations in HClO levels in inflammatory and tumor-bearing mice.Notably,the probe can respond to HClO within 5 s and trigger a brilliant red fluorescence at 660 nm.It exhibits high specificity and sensitivity for HClO.The superior spectral capability of the probe has enabled the detection of HClO levels in cells and zebrafish,as well as achieved the detection of HClO in inflammatory and tumor mice.This work not only provides a novel strategy and tool for HClO imaging in living systems,but also holds great potential for the diagnosis of inflammation and cancer.展开更多
Objectives To investigate clinical characteristics, target organ damage, and the associated risk factors of the patients aged ≥ 80 yearswith true resistant hypertension （RH）. Methods Patients aged ≥ 80 years with ...Objectives To investigate clinical characteristics, target organ damage, and the associated risk factors of the patients aged ≥ 80 yearswith true resistant hypertension （RH）. Methods Patients aged ≥ 80 years with hypertension （n = 1163） were included in this study. Theincluded participants attended a structured clinical examination and an evaluation of RH was carried out. The prevalence, clinical characteristicsand target organ damage of patients with RH were assessed. The associated clinical risk factors were analyzed by using logistic regression.Results The prevalence of RH diagnosis by 24-h ambulatory blood pressure monitoring assessment was 21.15%. End-diastolic left ven-tricular internal dimension, left ventricular mass index as well as prevalence of left ventricular hypertrophy were significantly greater in pa-tients with RH than in control group. The common carotid artery intimal media thickness, carotid walls thickness, common carotid arterydiameter and relative wall thickness were significant greater in RH group than in control. A relatively higher level of creatinine, estimatedglomerular filtration rate, microalbuminuria and retinal changes was found in RIt group than in control. A multivariate analysis showed thatpatients with a history of diabetes, higher body mass index （BMI） and lipid profiles were independent risk factors of RH. Conclusions Theprevalence of RH in patients aged ≥ 80 years was within the range of reported rates of the general population. Subjects with RH diagnosisshowed a higher occurrence of target organ damage than patients with well controlled blood pressure. Patients with diabetes, higher BMI andserum lipid profiles were independent risk factors for RH in patients aged ≥ 80 years.展开更多
BACKGROUND Globally,prostate cancer has become a major threat to men's health,with an increasing incidence and causes serious effects on the quality and length of life of patients.Despite the rapid development of ...BACKGROUND Globally,prostate cancer has become a major threat to men's health,with an increasing incidence and causes serious effects on the quality and length of life of patients.Despite the rapid development of medical technology,which provides treatments,including surgery,radiotherapy,and endocrine therapy,the treatment of patients with prostate cancer,especially with endocrine therapy,has become a major challenge in clinical treatment owing to the lengthy course of treatment,side effects of drugs,and impact of the disease on the psychological and physiological functioning of the patient,producing poor treatment adherence and a decline in quality of life.After the nursing intervention,the anxiety and depression scores of the observation group were significantly lower than those of the control group(P<0.05).The quality of life score,sexual function,and hormone function were significantly higher than those in the control group(P<0.05).CONCLUSION Case management guidance based on patient safety effectively reduced anxiety and depression in patients undergoing endocrine therapy for prostate cancer and improved their quality of life,treatment compliance,and satisfaction.展开更多
BACKGROUND Cellular senescence,a state of stable growth arrest,is intertwined with human cancers.However,characterization of cellular senescence-associated phenotypes in hepatocellular carcinoma(HCC)remains unexplored...BACKGROUND Cellular senescence,a state of stable growth arrest,is intertwined with human cancers.However,characterization of cellular senescence-associated phenotypes in hepatocellular carcinoma(HCC)remains unexplored.AIM To address this issue,we delineated cellular senescence landscape across HCC.METHODS We enrolled two HCC datasets,TCGA-LIHC and International Cancer Genome Consortium(ICGC).Unsupervised clustering was executed to probe tumor heterogeneity based upon cellular senescence genes.Least absolute shrinkage and selection operator algorithm were utilized to define a cellular senescence-relevant scoring system.TRNP1 expression was measured in HCCs and normal tissues through immunohistochemistry,immunoblotting and quantitative real-time polymerase chain reaction.The influence of TMF-regulated nuclear protein(TRNP)1 on HCC senescence and growth was proven via a series of experiments.RESULTS TCGA-LIHC patients were classified as three cellular senescence subtypes,named C1–3.The robustness and reproducibility of these subtypes were proven in the ICGC cohort.C2 had the worst overall survival,C1 the next,and C3 the best.C2 presented the highest levels of immune checkpoints,abundance of immune cells,and immunogenetic indicators.Thus,C2 might possibly respond to immunotherapy.C2 had the lowest somatic mutation rate,while C1 presented the highest copy number variations.A cellular senescence-relevant gene signature was generated,which can predict patient survival,and chemo-or immunotherapeutic response.Experimentally,it was proven that TRNP1 presented the remarkable upregulation in HCCs.TRNP1 knockdown induced apoptosis and senescence of HCC cells and attenuated tumor growth.CONCLUSION These findings provide a systematic framework for assessing cellular senescence in HCC,which decode the tumor heterogeneity and tailor the pharmacological interventions to improve clinical management.展开更多
We report the successful application of a surgical and medical co‐management(SMC)strategy in an 82‐year‐old man with hemophilia A(HA)undergoing pancreaticoduodenectomy for pancreatic head carcinoma.No major complic...We report the successful application of a surgical and medical co‐management(SMC)strategy in an 82‐year‐old man with hemophilia A(HA)undergoing pancreaticoduodenectomy for pancreatic head carcinoma.No major complications or perioperative bleeding occurred.Optimal management of HA patients undergoing major surgery requires multidisciplinary coordination to avoid postoperative complications.The SMC team integrates internists(who assess chronic disease status,adjust medications,and determine best hemostatic therapies)and surgeons(who evaluate the surgical feasibility of procedures and rely on advanced surgical skills)to improve perioperative planning to minimize complications and promote recovery.This case illustrates the utility of a shift from passive and conservative treatment to active and preventive treatment and highlights the value of SMC in many complex clinical situations.展开更多
Objective To investigate the effect of H2S on lower limb ischemia-reperfusion （LIR） induced lung injury and explore the underlying mechanism. Methods Wistar rats were randomly divided into control group, IR group, I...Objective To investigate the effect of H2S on lower limb ischemia-reperfusion （LIR） induced lung injury and explore the underlying mechanism. Methods Wistar rats were randomly divided into control group, IR group, IR＋ Sodium Hydrosulphide （NariS） group and IR＋ DL-propargylglycine （PPG） group. IR group as lung injury model induced by LIR were given 4 h reperfusion following 4 h ischemia of bilateral hindlimbs with rubber bands. NariS （0.78 mg/kg） as exogenous H2S donor and PPG （60 mg/kg） which can suppress endogenous H2S production were administrated before LIR, respectively. The lungs were removed for histologic analysis, the determination of wet-to-dry weight ratios and the measurement of mRNA and protein levels of aquaporin-1 （AQP1）, aquaporin-5 （AQP5） as indexes of water transport abnormality, and mRNA and protein levels of Toll-like receptor 4 （TLR4）, myeloid differentiation primary-response gene 88 （MyD88） and p-NF-KB as indexes of inflammation. Results LIR induced lung injury was accompanied with upregulation of TLR4-Myd88-NF-κB pathway and downregulation of AQP1/AQP5. NariS pre-treatment reduced lung injury with increasing AQP1/AQP5 expression and inhibition of TLR4-Myd88-NF-KB pathway, but PPG adjusted AO.PJAO.Ps and TLR4 pathway to the opposite side and exacerbated lung injury. Conclusion Endogenous H2S, TLR4-Myd88-NF-κB pathway and AQP1/AQP5 were involved in LIR induced lung injury. Increased H2S would alleviate lung injury and the effect is at least partially depend on the adjustment of TLR4-Myd88-NF-κB pathway and AQP1/AQP5 expression to reduce inflammatory reaction and lessen pulmonary edema.展开更多
Hutchinson-Gilford progeria syndrome(HGPS,OMIM176670)is an extremely rare,sporadic genetic syndrome with a reported prevalence of one in4-8million children worldwide.At April2012,the total number of known living child...Hutchinson-Gilford progeria syndrome(HGPS,OMIM176670)is an extremely rare,sporadic genetic syndrome with a reported prevalence of one in4-8million children worldwide.At April2012,the total number of known living children with HGPS was89worldwide,according to data from the Progeria Research Foundation.展开更多
Colorectal cancer(CRC)poses a severe global health challenge with high incidence and mortality rates.USP37 has been identified as the bona fide deubiquitinase of SND1,playing a critical role in stabilizing SND1,thereb...Colorectal cancer(CRC)poses a severe global health challenge with high incidence and mortality rates.USP37 has been identified as the bona fide deubiquitinase of SND1,playing a critical role in stabilizing SND1,thereby augmenting its oncogenic potential.The interaction between USP37 and SND1 was confirmed through extensive proteomics,ubiquitinomics,and interactomics,underscoring their synergistic effects on CRC proliferation and metastasis.Additionally,CDK1 has emerged as a pivotal regulator of USP37,phosphorylating it at threonine 631 rather than serine 628,enhancing its deubiquitinase activity,and consequently stabilizing SND1 to drive CRC malignancy further.Histological analyses of human CRC samples linked the upregulation of CDK1 and USP37 with increased SND1 levels and poor patient prognosis.High-throughput virtual screening and subsequent experimental validation identified Dacarbazine as a pharmacological inhibitor of USP37,and its inhibition disrupted SND1 stability,hindering CRC cell proliferation and metastasis.This study reveals a novel and promising molecular mechanism driving CRC progression through the CDK1-SP37-ND1 axis,highlighting the clinical importance of targeting this pathway to improve patient outcomes.展开更多
HMGA2,a pivotal transcription factor,functions as a versatile regulator implicated in the progression of diverse aggressive malignancies.In this study,mass spectrometry was employed to identify ubiquitin-specific prot...HMGA2,a pivotal transcription factor,functions as a versatile regulator implicated in the progression of diverse aggressive malignancies.In this study,mass spectrometry was employed to identify ubiquitin-specific proteases that potentially interact with HMGA2,and USP48 was identified as a deubiquitinating enzyme of HMGA2.The enforced expression of USP48 significantly increased HMGA2 protein levels by inhibiting its degradation,while the deprivation of USP48 promoted HMGA2 degradation,thereby suppressing tumor invasion and metastasis.We discovered that USP48 undergoes SUMOylation at lysine 258,which enhances its binding affinity to HMGA2.Through subsequent phenotypic screening of small molecules,we identified DUB-IN-2 as a remarkably potent pharmacological inhibitor of USP48.Interestingly,the small-molecule inhibitor targeting USP48 induces destabilization of HMGA2.Clinically,upregulation of USP48 or HMGA2 in cancerous tissues is indicative of poor prognosis for patients with colorectal cancer(CRC).Collectively,our study not only elucidates the regulatory mechanism of DUBs involved in HMGA2 stability and validates USP48 as a potential therapeutic target for CRC,but also identifies DUB-IN-2 as a potent inhibitor of USP48 and a promising candidate for CRC treatment.展开更多
The T-cell-mediated immune response is implicated in many clinical hepatic injuries, such as autoimmune hepatitis and acute virus hepatitis. CD24 is widely expressed by different immune cells and plays an important ro...The T-cell-mediated immune response is implicated in many clinical hepatic injuries, such as autoimmune hepatitis and acute virus hepatitis. CD24 is widely expressed by different immune cells and plays an important role in the pathogenesis of many autoimmune diseases. However, the role of CD24 in T-cell-mediated liver injury has not been elucidated until now. Here we showed that CD24 deficiency protects mice from concanavalin A (ConA)-induced fulminant liver injury by reducing serum interferon-γ (IFN-γ) levels. CD24 expression by hepatic T cells was markedly increased following ConA challenge. Moreover, decreased IFN-γ production by hepatic CD4^(+) T cells in CD24-deficient mice was detected, which was correlated with downregulated phosphorylation of STAT1 in hepatic tissue. In vitro experiments also supported the conclusion that CD24 deficiency impaired IFN-γ production by CD4^(+) T cells following ConA, CD3/CD28 and phorbol myristate acetate/ionomycin stimulation. Our study suggests that CD24 deficiency confers hepatoprotection by decreasing CD4^(+) T-cell-dependent IFN-γ production in vivo, which suggests that CD24 might be a potential target molecule for reducing clinical hepatitis.展开更多
基金National Natural Science Foundation of China(No.22264013)Hainan Province Clinical Medical Center(No.2021)Hainan Province Science and Technology Special Fund(No.ZDYF2024SHFZ104).
文摘Hypochlorous acid(HClO)is a critical biomolecule in living organisms,playing an essential role in numerous physiological or pathological processes.Abnormal levels of HClO in the body may lead to a series of diseases,for instance,inflammation and cancer.Thus,accurate measurement of HClO levels should be more beneficial for understanding its role in diseases and gaining a deeper insight into the pathogenesis of diseases.In this work,we designed a near-infrared two-photon fluorescent probe(HDM-Cl-HClO)for detecting fluctuations in HClO levels in inflammatory and tumor-bearing mice.Notably,the probe can respond to HClO within 5 s and trigger a brilliant red fluorescence at 660 nm.It exhibits high specificity and sensitivity for HClO.The superior spectral capability of the probe has enabled the detection of HClO levels in cells and zebrafish,as well as achieved the detection of HClO in inflammatory and tumor mice.This work not only provides a novel strategy and tool for HClO imaging in living systems,but also holds great potential for the diagnosis of inflammation and cancer.
文摘Objectives To investigate clinical characteristics, target organ damage, and the associated risk factors of the patients aged ≥ 80 yearswith true resistant hypertension （RH）. Methods Patients aged ≥ 80 years with hypertension （n = 1163） were included in this study. Theincluded participants attended a structured clinical examination and an evaluation of RH was carried out. The prevalence, clinical characteristicsand target organ damage of patients with RH were assessed. The associated clinical risk factors were analyzed by using logistic regression.Results The prevalence of RH diagnosis by 24-h ambulatory blood pressure monitoring assessment was 21.15%. End-diastolic left ven-tricular internal dimension, left ventricular mass index as well as prevalence of left ventricular hypertrophy were significantly greater in pa-tients with RH than in control group. The common carotid artery intimal media thickness, carotid walls thickness, common carotid arterydiameter and relative wall thickness were significant greater in RH group than in control. A relatively higher level of creatinine, estimatedglomerular filtration rate, microalbuminuria and retinal changes was found in RIt group than in control. A multivariate analysis showed thatpatients with a history of diabetes, higher body mass index （BMI） and lipid profiles were independent risk factors of RH. Conclusions Theprevalence of RH in patients aged ≥ 80 years was within the range of reported rates of the general population. Subjects with RH diagnosisshowed a higher occurrence of target organ damage than patients with well controlled blood pressure. Patients with diabetes, higher BMI andserum lipid profiles were independent risk factors for RH in patients aged ≥ 80 years.
文摘BACKGROUND Globally,prostate cancer has become a major threat to men's health,with an increasing incidence and causes serious effects on the quality and length of life of patients.Despite the rapid development of medical technology,which provides treatments,including surgery,radiotherapy,and endocrine therapy,the treatment of patients with prostate cancer,especially with endocrine therapy,has become a major challenge in clinical treatment owing to the lengthy course of treatment,side effects of drugs,and impact of the disease on the psychological and physiological functioning of the patient,producing poor treatment adherence and a decline in quality of life.After the nursing intervention,the anxiety and depression scores of the observation group were significantly lower than those of the control group(P<0.05).The quality of life score,sexual function,and hormone function were significantly higher than those in the control group(P<0.05).CONCLUSION Case management guidance based on patient safety effectively reduced anxiety and depression in patients undergoing endocrine therapy for prostate cancer and improved their quality of life,treatment compliance,and satisfaction.
文摘BACKGROUND Cellular senescence,a state of stable growth arrest,is intertwined with human cancers.However,characterization of cellular senescence-associated phenotypes in hepatocellular carcinoma(HCC)remains unexplored.AIM To address this issue,we delineated cellular senescence landscape across HCC.METHODS We enrolled two HCC datasets,TCGA-LIHC and International Cancer Genome Consortium(ICGC).Unsupervised clustering was executed to probe tumor heterogeneity based upon cellular senescence genes.Least absolute shrinkage and selection operator algorithm were utilized to define a cellular senescence-relevant scoring system.TRNP1 expression was measured in HCCs and normal tissues through immunohistochemistry,immunoblotting and quantitative real-time polymerase chain reaction.The influence of TMF-regulated nuclear protein(TRNP)1 on HCC senescence and growth was proven via a series of experiments.RESULTS TCGA-LIHC patients were classified as three cellular senescence subtypes,named C1–3.The robustness and reproducibility of these subtypes were proven in the ICGC cohort.C2 had the worst overall survival,C1 the next,and C3 the best.C2 presented the highest levels of immune checkpoints,abundance of immune cells,and immunogenetic indicators.Thus,C2 might possibly respond to immunotherapy.C2 had the lowest somatic mutation rate,while C1 presented the highest copy number variations.A cellular senescence-relevant gene signature was generated,which can predict patient survival,and chemo-or immunotherapeutic response.Experimentally,it was proven that TRNP1 presented the remarkable upregulation in HCCs.TRNP1 knockdown induced apoptosis and senescence of HCC cells and attenuated tumor growth.CONCLUSION These findings provide a systematic framework for assessing cellular senescence in HCC,which decode the tumor heterogeneity and tailor the pharmacological interventions to improve clinical management.
文摘We report the successful application of a surgical and medical co‐management(SMC)strategy in an 82‐year‐old man with hemophilia A(HA)undergoing pancreaticoduodenectomy for pancreatic head carcinoma.No major complications or perioperative bleeding occurred.Optimal management of HA patients undergoing major surgery requires multidisciplinary coordination to avoid postoperative complications.The SMC team integrates internists(who assess chronic disease status,adjust medications,and determine best hemostatic therapies)and surgeons(who evaluate the surgical feasibility of procedures and rely on advanced surgical skills)to improve perioperative planning to minimize complications and promote recovery.This case illustrates the utility of a shift from passive and conservative treatment to active and preventive treatment and highlights the value of SMC in many complex clinical situations.
基金supported by the Military Health Care Foundation during the 12th Five-year Plan Period(11BZ21)the Military Scientific Research Foundation during the 12th Five-year Plan Period(BWS12J051)
文摘Objective To investigate the effect of H2S on lower limb ischemia-reperfusion （LIR） induced lung injury and explore the underlying mechanism. Methods Wistar rats were randomly divided into control group, IR group, IR＋ Sodium Hydrosulphide （NariS） group and IR＋ DL-propargylglycine （PPG） group. IR group as lung injury model induced by LIR were given 4 h reperfusion following 4 h ischemia of bilateral hindlimbs with rubber bands. NariS （0.78 mg/kg） as exogenous H2S donor and PPG （60 mg/kg） which can suppress endogenous H2S production were administrated before LIR, respectively. The lungs were removed for histologic analysis, the determination of wet-to-dry weight ratios and the measurement of mRNA and protein levels of aquaporin-1 （AQP1）, aquaporin-5 （AQP5） as indexes of water transport abnormality, and mRNA and protein levels of Toll-like receptor 4 （TLR4）, myeloid differentiation primary-response gene 88 （MyD88） and p-NF-KB as indexes of inflammation. Results LIR induced lung injury was accompanied with upregulation of TLR4-Myd88-NF-κB pathway and downregulation of AQP1/AQP5. NariS pre-treatment reduced lung injury with increasing AQP1/AQP5 expression and inhibition of TLR4-Myd88-NF-KB pathway, but PPG adjusted AO.PJAO.Ps and TLR4 pathway to the opposite side and exacerbated lung injury. Conclusion Endogenous H2S, TLR4-Myd88-NF-κB pathway and AQP1/AQP5 were involved in LIR induced lung injury. Increased H2S would alleviate lung injury and the effect is at least partially depend on the adjustment of TLR4-Myd88-NF-κB pathway and AQP1/AQP5 expression to reduce inflammatory reaction and lessen pulmonary edema.
文摘Hutchinson-Gilford progeria syndrome(HGPS,OMIM176670)is an extremely rare,sporadic genetic syndrome with a reported prevalence of one in4-8million children worldwide.At April2012,the total number of known living children with HGPS was89worldwide,according to data from the Progeria Research Foundation.
基金supported by the National Natural Science Foundation of China(Nos.82103543,82303235,U19A2008 and 82373232)Fundamental Research Funds for the Central Universities(No.WK9110000159,China)+1 种基金the Natural Science Foundation of Anhui Province(No.2108085QH340,China)the China Postdoctoral Science Foundation(No.2021M693082).
文摘Colorectal cancer(CRC)poses a severe global health challenge with high incidence and mortality rates.USP37 has been identified as the bona fide deubiquitinase of SND1,playing a critical role in stabilizing SND1,thereby augmenting its oncogenic potential.The interaction between USP37 and SND1 was confirmed through extensive proteomics,ubiquitinomics,and interactomics,underscoring their synergistic effects on CRC proliferation and metastasis.Additionally,CDK1 has emerged as a pivotal regulator of USP37,phosphorylating it at threonine 631 rather than serine 628,enhancing its deubiquitinase activity,and consequently stabilizing SND1 to drive CRC malignancy further.Histological analyses of human CRC samples linked the upregulation of CDK1 and USP37 with increased SND1 levels and poor patient prognosis.High-throughput virtual screening and subsequent experimental validation identified Dacarbazine as a pharmacological inhibitor of USP37,and its inhibition disrupted SND1 stability,hindering CRC cell proliferation and metastasis.This study reveals a novel and promising molecular mechanism driving CRC progression through the CDK1-SP37-ND1 axis,highlighting the clinical importance of targeting this pathway to improve patient outcomes.
基金We extend our sincere appreciation to Mingyang Gao,Shuai Zhou,and Wenxiang Fang for their exceptional technical assistance.This research was financially supported by the National Natural Science Foundation of China(No.82103543)the Fundamental Research Funds for the Central Universities(No.WK9110000159,China)+1 种基金Natural Science Foundation of Anhui Province(No.2108085QH340,China)the Postdoctoral Science Foundation of China(No.2021M693082).
文摘HMGA2,a pivotal transcription factor,functions as a versatile regulator implicated in the progression of diverse aggressive malignancies.In this study,mass spectrometry was employed to identify ubiquitin-specific proteases that potentially interact with HMGA2,and USP48 was identified as a deubiquitinating enzyme of HMGA2.The enforced expression of USP48 significantly increased HMGA2 protein levels by inhibiting its degradation,while the deprivation of USP48 promoted HMGA2 degradation,thereby suppressing tumor invasion and metastasis.We discovered that USP48 undergoes SUMOylation at lysine 258,which enhances its binding affinity to HMGA2.Through subsequent phenotypic screening of small molecules,we identified DUB-IN-2 as a remarkably potent pharmacological inhibitor of USP48.Interestingly,the small-molecule inhibitor targeting USP48 induces destabilization of HMGA2.Clinically,upregulation of USP48 or HMGA2 in cancerous tissues is indicative of poor prognosis for patients with colorectal cancer(CRC).Collectively,our study not only elucidates the regulatory mechanism of DUBs involved in HMGA2 stability and validates USP48 as a potential therapeutic target for CRC,but also identifies DUB-IN-2 as a potent inhibitor of USP48 and a promising candidate for CRC treatment.
基金This work was supported by grants from the Army Technology Research Program of China(BWS12J051)the National Natural Science Foundation of China(31570873)+1 种基金the Shanghai Committee of Science and Technology(2015QA1404700)We thank Professor Guanhong Song and Prof.Xuetao Cao for their critical review of the manuscript.
文摘The T-cell-mediated immune response is implicated in many clinical hepatic injuries, such as autoimmune hepatitis and acute virus hepatitis. CD24 is widely expressed by different immune cells and plays an important role in the pathogenesis of many autoimmune diseases. However, the role of CD24 in T-cell-mediated liver injury has not been elucidated until now. Here we showed that CD24 deficiency protects mice from concanavalin A (ConA)-induced fulminant liver injury by reducing serum interferon-γ (IFN-γ) levels. CD24 expression by hepatic T cells was markedly increased following ConA challenge. Moreover, decreased IFN-γ production by hepatic CD4^(+) T cells in CD24-deficient mice was detected, which was correlated with downregulated phosphorylation of STAT1 in hepatic tissue. In vitro experiments also supported the conclusion that CD24 deficiency impaired IFN-γ production by CD4^(+) T cells following ConA, CD3/CD28 and phorbol myristate acetate/ionomycin stimulation. Our study suggests that CD24 deficiency confers hepatoprotection by decreasing CD4^(+) T-cell-dependent IFN-γ production in vivo, which suggests that CD24 might be a potential target molecule for reducing clinical hepatitis.
