INTRODUCTION Tuberculosis(TB)remains a widespread and serious infectious disease caused by the chronic pathogen Mycobacterium tuberculosis(Mtb),leading to approximately 10 million new cases and 1.5 million deaths annu...INTRODUCTION Tuberculosis(TB)remains a widespread and serious infectious disease caused by the chronic pathogen Mycobacterium tuberculosis(Mtb),leading to approximately 10 million new cases and 1.5 million deaths annually[1].Notably,the continuous emergence of drug-resistantMtb strains and co-infection with human immunodeficiency virus(HIV)further pose significant challenges to TB prevention and treatment,necessitating an innovative breakthrough in TB control.Vaccination is the most economical and effective approach to preventing and controlling infectious diseases.However,Bacillus Calmette-Guérin(BCG)is currently the only licensed vaccine available for TB,protecting meningeal and disseminated TB in children,but failing to protect adolescents and adults,who are the primary transmitters of TB.Moreover,BCG cannot prevent the progression of latent TB infection(LTBI)to active TB,and its protective efficacy wanes over time[2,3].Against this backdrop,efforts to develop more effective TB vaccines have been ongoing.展开更多
The major innate immune cell types involved in tuberculosis(TB)infection are macrophages,dendritic cells(DCs),neutrophils and natural killer(NK)cells.These immune cells recognize the TB-causing pathogen Mycobacterium ...The major innate immune cell types involved in tuberculosis(TB)infection are macrophages,dendritic cells(DCs),neutrophils and natural killer(NK)cells.These immune cells recognize the TB-causing pathogen Mycobacterium tuberculosis(Mtb)through various pattern recognition receptors(PRRs),including but not limited to Toll-like receptors(TLRs),Nod-like receptors(NLRs)and C-type lectin receptors(CLRs).Upon infection by Mtb,the host orchestrates multiple signaling cascades via the PRRs to launch a variety of innate immune defense functions such as phagocytosis,autophagy,apoptosis and inflammasome activation.In contrast,Mtb utilizes numerous exquisite strategies to evade or circumvent host innate immunity.Here we discuss recent research on major host innate immune cells,PRR signaling,and the cellular functions involved in Mtb infection,with a specific focus on the host’s innate immune defense and Mtb immune evasion.A better understanding of the molecular mechanisms underlying host–pathogen interactions could provide a rational basis for the development of effective anti-TB therapeutics.展开更多
Helicobacter pylori (H.pylori) has co-evolved with humans to be transmitted from person to person and to colonize the stomach persistently.A well-choreographed equilibrium between the bacterial effectors and host resp...Helicobacter pylori (H.pylori) has co-evolved with humans to be transmitted from person to person and to colonize the stomach persistently.A well-choreographed equilibrium between the bacterial effectors and host responses permits microbial persistence and health of the host,but confers a risk for serious diseases including gastric cancer.During its long coexistence with humans,H.pylori has developed complex strategies to limit the degree and extent of gastric mucosal damage and in? ammation,as well as immune effector activity.The present editorial thus aims to introduce and comment on major advances in the rapidly developing area of H.pylori/human gastric mucosa interaction (and its pathological sequelae),which is the result of millennia of co-evolution of,and thus of reciprocal knowledge between,the pathogen and its human host.展开更多
In a recent publication in Nature,Sakoguchi et al.reveal a long-sought missing link between pathogen-derived ligands and activating human natural killer(NK)cell receptors.1 The study identifies a clade of Plasmodium f...In a recent publication in Nature,Sakoguchi et al.reveal a long-sought missing link between pathogen-derived ligands and activating human natural killer(NK)cell receptors.1 The study identifies a clade of Plasmodium falciparum(P.falciparum)repetitive interspersed family(RIFIN)proteins that not only bind to the inhibitory KIR2DL1 receptor but,strikingly,also engage the activating KIR2DS1 receptor,thereby offering new insight into NK cell regulation in malaria and expanding our understanding of host–pathogen interaction in innate immune responses.展开更多
Plants can be infected by multiple pathogens concurrently in natural systems. However,pathogen–pathogen interactions have rarely been studied. In addition to the oomycete Phytophthora sojae, fungi such as Fusarium sp...Plants can be infected by multiple pathogens concurrently in natural systems. However,pathogen–pathogen interactions have rarely been studied. In addition to the oomycete Phytophthora sojae, fungi such as Fusarium spp. also cause soybean root rot. In a 3-year field investigation, we discovered that P. sojae and Fusarium spp. frequently coexisted in diseased soybean roots. Out of 336 P. sojae–soybean–Fusarium combinations,more than 80% aggravated disease. Different Fusarium species all enhanced P. sojae infection when co-inoculated on soybean. Treatment with Fusarium secreted non-proteinaceous metabolites had an effect equal to the direct pathogen coinoculation. By screening a Fusarium graminearum mutant library, we identified Fusarium promoting factor of Phytophthora sojae infection 1(Fpp1),encoding a zinc alcohol dehydrogenase. Fpp1 is functionally conserved in Fusarium and contributes to metabolite-mediated infection promotion, in which vitamin B6(VB6) produced by Fusarium is key. Transcriptional and functional analyses revealed that Fpp1 regulates two VB6 metabolism genes, and VB6 suppresses expression of soybean disease resistance-related genes. These results reveal that co-infection with Fusarium promotes loss of P. sojae resistance in soybean, information that will inform the sustainable use of diseaseresistant crop varieties and provide new strategies to control soybean root rot.展开更多
基金supported by the National Key Research and Development Program of China(2022YFC2302900 and 2021YFA1300200 to C.H.L.and J.W.)the National Natural Science Foundation of China(82330069 to C.H.L.and 82372653 to J.W.)+4 种基金the State Key Laboratory of Medical Proteomics(SKLPK202001,SKLPO202003,and SKLP-X202401 to C.H.L.)the CAS Project for Young Scientists in Basic Research(YSBR-010 to J.W.)Youth Innovation Promotion Association CAS(Y2022036 to J.W.)Shenzhen Medical Research Fund(B2302035 to C.H.L.)Guangzhou National Laboratory(GZNL2024A01023 to C.H.L.).
文摘INTRODUCTION Tuberculosis(TB)remains a widespread and serious infectious disease caused by the chronic pathogen Mycobacterium tuberculosis(Mtb),leading to approximately 10 million new cases and 1.5 million deaths annually[1].Notably,the continuous emergence of drug-resistantMtb strains and co-infection with human immunodeficiency virus(HIV)further pose significant challenges to TB prevention and treatment,necessitating an innovative breakthrough in TB control.Vaccination is the most economical and effective approach to preventing and controlling infectious diseases.However,Bacillus Calmette-Guérin(BCG)is currently the only licensed vaccine available for TB,protecting meningeal and disseminated TB in children,but failing to protect adolescents and adults,who are the primary transmitters of TB.Moreover,BCG cannot prevent the progression of latent TB infection(LTBI)to active TB,and its protective efficacy wanes over time[2,3].Against this backdrop,efforts to develop more effective TB vaccines have been ongoing.
基金the National Key Research and Development Program of China(Grant Nos.2017YFA0505900 and 2017YFD0500300)the National Basic Research Programs of China(Grant No.2014CB74440)+2 种基金the National Natural Science Foundation of China(Grant Nos.81371769 and 81571954)the Strategic Priority Research Program of the Chinese Academy of Sciences(Grant No.XDPB03)the Youth Innovation Promotion Association CAS(Grant No.Y12A027BB2).
文摘The major innate immune cell types involved in tuberculosis(TB)infection are macrophages,dendritic cells(DCs),neutrophils and natural killer(NK)cells.These immune cells recognize the TB-causing pathogen Mycobacterium tuberculosis(Mtb)through various pattern recognition receptors(PRRs),including but not limited to Toll-like receptors(TLRs),Nod-like receptors(NLRs)and C-type lectin receptors(CLRs).Upon infection by Mtb,the host orchestrates multiple signaling cascades via the PRRs to launch a variety of innate immune defense functions such as phagocytosis,autophagy,apoptosis and inflammasome activation.In contrast,Mtb utilizes numerous exquisite strategies to evade or circumvent host innate immunity.Here we discuss recent research on major host innate immune cells,PRR signaling,and the cellular functions involved in Mtb infection,with a specific focus on the host’s innate immune defense and Mtb immune evasion.A better understanding of the molecular mechanisms underlying host–pathogen interactions could provide a rational basis for the development of effective anti-TB therapeutics.
基金Supported by University of Pavia(Fondo d'Ateneo per la Ricercato Ricci V)+1 种基金Second University of Naples(CIRANAD to Romano M)
文摘Helicobacter pylori (H.pylori) has co-evolved with humans to be transmitted from person to person and to colonize the stomach persistently.A well-choreographed equilibrium between the bacterial effectors and host responses permits microbial persistence and health of the host,but confers a risk for serious diseases including gastric cancer.During its long coexistence with humans,H.pylori has developed complex strategies to limit the degree and extent of gastric mucosal damage and in? ammation,as well as immune effector activity.The present editorial thus aims to introduce and comment on major advances in the rapidly developing area of H.pylori/human gastric mucosa interaction (and its pathological sequelae),which is the result of millennia of co-evolution of,and thus of reciprocal knowledge between,the pathogen and its human host.
文摘In a recent publication in Nature,Sakoguchi et al.reveal a long-sought missing link between pathogen-derived ligands and activating human natural killer(NK)cell receptors.1 The study identifies a clade of Plasmodium falciparum(P.falciparum)repetitive interspersed family(RIFIN)proteins that not only bind to the inhibitory KIR2DL1 receptor but,strikingly,also engage the activating KIR2DS1 receptor,thereby offering new insight into NK cell regulation in malaria and expanding our understanding of host–pathogen interaction in innate immune responses.
基金supported by grants from the National Natural Science Foundation of China (3217237431721004)the China Agriculture Research System (CARS-004-PS14)。
文摘Plants can be infected by multiple pathogens concurrently in natural systems. However,pathogen–pathogen interactions have rarely been studied. In addition to the oomycete Phytophthora sojae, fungi such as Fusarium spp. also cause soybean root rot. In a 3-year field investigation, we discovered that P. sojae and Fusarium spp. frequently coexisted in diseased soybean roots. Out of 336 P. sojae–soybean–Fusarium combinations,more than 80% aggravated disease. Different Fusarium species all enhanced P. sojae infection when co-inoculated on soybean. Treatment with Fusarium secreted non-proteinaceous metabolites had an effect equal to the direct pathogen coinoculation. By screening a Fusarium graminearum mutant library, we identified Fusarium promoting factor of Phytophthora sojae infection 1(Fpp1),encoding a zinc alcohol dehydrogenase. Fpp1 is functionally conserved in Fusarium and contributes to metabolite-mediated infection promotion, in which vitamin B6(VB6) produced by Fusarium is key. Transcriptional and functional analyses revealed that Fpp1 regulates two VB6 metabolism genes, and VB6 suppresses expression of soybean disease resistance-related genes. These results reveal that co-infection with Fusarium promotes loss of P. sojae resistance in soybean, information that will inform the sustainable use of diseaseresistant crop varieties and provide new strategies to control soybean root rot.
