Plants deploy sophisticated immune surveillance systems to safeguard themselves against pathogen infection,including plasma membrane-localized pattern-recognition receptors (PRRs) that initiate Pattern-Triggered Immun...Plants deploy sophisticated immune surveillance systems to safeguard themselves against pathogen infection,including plasma membrane-localized pattern-recognition receptors (PRRs) that initiate Pattern-Triggered Immunity (PTI)upon detecting pathogen-associated molecular patterns(PAMPs), and intracellular nucleotide-binding leucine-rich repeat receptors (NLRs) that induce Effector-Triggered Immunity (ETI) upon direct/indirect pathogen effector recognition. Effector-Triggered Immunity is often accompanied by a hypersensitive response (HR), which is known as rapid localized cell death at infection sites to restrict pathogen growth (Contreras et al., 2023;Jones et al., 2024). Nucleotidebinding leucine-rich repeat receptors are classified by their N-terminal domains:TIR-NLRs (TNLs), CC-NLRs (CNLs), and RPW8-NLRs (RNLs). TNLs and CNLs typically function as sensor NLRs (sNLRs) that detect pathogen effectors, while RNLs serve as helper NLRs (hNLRs) that transmit immune signals from diverse sNLRs to ultimately execute downstream resistance and trigger cell death—though some RNLs can themselves be direct targets of pathogen effectors (Contreras et al., 2023;Gong et al., 2023). The hNLRs mainly include Activated Disease Resistance 1 (ADR1), which is conserved in both dicots and monocots, and N REQUIRED GENE 1 (NRG1),which has not been identified in monocots, as well as Solanaceae-specific NLR required for cell death (NRC)-type NLRs, which are required for HR-related cell death (Contreras et al., 2023;Gong et al., 2023).展开更多
Dear Editor,To combat pathogen invasion,plants use immune receptors that detect immunogenic molecules to trigger immune responses and confer resistance.Cell-surface-resident pattern recognition receptors activate patt...Dear Editor,To combat pathogen invasion,plants use immune receptors that detect immunogenic molecules to trigger immune responses and confer resistance.Cell-surface-resident pattern recognition receptors activate pattern-triggered immunity through the perception of pathogen-associated molecular patterns(PAMPs),damage-associated molecular patterns,and phytocytokines(PCKs)(Zhou and Zhang,2020;Jones et al.,2024).展开更多
Plants are engaged in a constant battle for survival against pathogens,which triggers a multifaceted immune response characterized by pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)to prevent infec...Plants are engaged in a constant battle for survival against pathogens,which triggers a multifaceted immune response characterized by pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)to prevent infection.These two immune responses operate synergistically to enhance plant immunity.PTI is considered the first line of defense involving the recognition of pathogen-associated molecular patterns(PAMPs)by specific receptors in host cells known as pattern recognition receptors(PRRs),which initiate defense signaling.However,many pathogens often overcome the first line of defense(PTI)and successfully deploy effector proteins to promote virulence and subvert plant immunity,leading to host susceptibility.In the counter-defense,the ETI defense mechanism is activated by triggering resistance(R)genes in plants that usually encode nucleotide-binding-leucine-rich-containing(NLR)proteins.During plant-pathogen interactions,transcriptional reprogramming of defense-related genes such as pathogenesisrelated proteins and generation of reactive oxygen species(ROS)are essential for facilitating programmed cell death at the infected location to inhibit pathogen proliferation.While ROS and PR protein are critical in plant-pathogen interaction,they are not universally required or effective against all pathogens.Hence,plants’multilayer immune layer is encrypted with the compensatory activation of ETI defense response towards the failure of one component of the defense system to maintain robust immunity.展开更多
Pathogen-driven crop losses pose a significant threat to global food security.Plants deploy two primary branches of innate immunity:pathogen-associated molecular pattern-triggered immunity(PTI)and effector-triggered i...Pathogen-driven crop losses pose a significant threat to global food security.Plants deploy two primary branches of innate immunity:pathogen-associated molecular pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)(Yu et al.,2024).While PTI relies on surface-localized pattern recognition receptors,ETI is mediated by intracellular nucleotide-binding leucine-rich repeat receptors(NLRs)that directly or indirectly recognize pathogen effectors,often triggering hypersensitive cell death and systemic resistance(Yu et al.,2024).展开更多
Background： Adenoid hypertrophy （AH） is associated with pediatric chronic rhinosinusitis （pCRS）, but its role in the inflammatory process of pCRS is unclear. It is thought that innate immunity gene expression is ...Background： Adenoid hypertrophy （AH） is associated with pediatric chronic rhinosinusitis （pCRS）, but its role in the inflammatory process of pCRS is unclear. It is thought that innate immunity gene expression is disrupted in the epithelium of patients with chronic rhinosinusitis （CRS）, including antimicrobial peptides and pattern recognition receptors （PRRs）. The aim of this preliminary study was to detect the expression of innate immunity genes in epithelial cells of hypertrophic adenoids with and without pCRS to better understand their role in pCRS. Methods： Nine pCRS patients and nine simple AH patients undergoing adenoidectomy were recruited for the study. Adenoidal epithelium was isolated, and real-time quantitative polymerase chain reaction （RT-qPCR） was employed to measure relative expression levels of the following messenger RNAs in hypertrophic adenoid epithelial cells of pediatric patients with and without CRS： Human β-defensin （HBD） 2 and 3, surfactant protein （SP）-A and D, toll-like receptors 1-10, nucleotide-binding oligomerization domain （NOD）-like receptors NOD 1, NOD 2, and NACHT, LRR and PYD domains-containing protein 3, retinoic acid-induced gene 1, melanoma differentiation-associated gene 5, and nuclear factor-riB （NF-KB）. RT-qPCR data from two groups were analyzed by independent sample t-tests and Mann-Whitney U-tests. Results： The relative expression of SP-D in adenoidal epithelium ofpCRS group was significantly lower than that in AH group （pCRS 0.73 ± 0.10 vs. AH 1.21 ±0.15; P = 0.0173, t = 2.654）. The relative expression levels of all tested PRRs and NF-κB, as well as HBD-2, HBD-3, and SP-A, showed no statistically significant differences in isolated adenoidal epithelium between pCRS group and AH group. Conclusions： Down-regulated SP-D levels in adenoidal epithelium may contribute to the development of pCRS. PRRs, however, are unlikely to play a significant role in the inflammatory process ofpCRS.展开更多
Background Trichophyton rubrum （T. rubrum） represents the most important agent of dermatophytosis in humans. T. rubrum infection causes slight inflammation, and tends to be chronic and recurrent. It is suggested tha...Background Trichophyton rubrum （T. rubrum） represents the most important agent of dermatophytosis in humans. T. rubrum infection causes slight inflammation, and tends to be chronic and recurrent. It is suggested that it may result from the failure of epithelial cells to recognize T. rubrum effectively and initiate effective immune responses. The C-type lectin receptors （CLR） and toll-like receptors （TLR） are the two major pattern recognition receptors （PRRs） that recognize fungal components. Therefore, the purpose of the study was to analyze the expression of those PRRs and the cytokines in HaCaT cells stimulated with heat-inactivated T. rubrum conidia and hyphae, respectively. Methods HaCaT cells were unstimulated or stimulated with heat-inactivated T. rubrum conidia and hyphae （l×106 and 1.5×105 colony-forming unit （CFU） in 2 ml medium, respectively） for 6, 12 and 24 hours. The mRNA expression of PRRs involved in recognizing fungal pathogen-associated molecular patterns （PAMPs） and signaling molecules were measured by quantitative reverse transcription polymerase chain reaction （RT-PCR）. Meanwhile, surface toll-like receptor （TLR） 2, TLR4 and Dectin-1 were analyzed by fluorescence-activated cell sorter （FACS） 24 hours after treatment. The cytokines were detected in cell culture supernatants of HaCaT cells in 12 and 24 hours after treatment. Results HaCaT cells constitutively expressed mRNA of membrane-bound TLR1,2, 4 and 6, Dectinl and DC-SIGN, but not Dectin-2 or Mincle. Heat-killed T. rubrum did not significantly upregulate gene transcriptions of the PRRs of HaCaT cells. Heat-inactivated T. rubrum conidia significantly reduced the surface expression of TLR2 and Dectin-1, and suppressed the secretions of interferon-inducible protein-10 （IP-10） and monocyte chemotactic protein-1 （MCP-1） of HaCaT cells, while heat-killed T. rubrum hyphae significantly induced the secretions of IP-10 and MCP-I. Conclusion The cell-wall antigens of T. rubrum fail to activate transcriptional expression of PRRs and induce a lower immune response of HaCaT cells by limited cytokines secretion.展开更多
基金supported by the National Natural Science Foundation of China(32472527 and 32260653)the Guizhou Provincial General Project of the Science Foundation(ZK[2024]Key 011)+1 种基金the Guizhou Plant Bacteria and Biological Control Science and Technology Innovation Talent Team Development(Qian Ke He Talent-BQW[2025]003)the Research and Innovation Team of Guizhou University([2024]05)。
文摘Plants deploy sophisticated immune surveillance systems to safeguard themselves against pathogen infection,including plasma membrane-localized pattern-recognition receptors (PRRs) that initiate Pattern-Triggered Immunity (PTI)upon detecting pathogen-associated molecular patterns(PAMPs), and intracellular nucleotide-binding leucine-rich repeat receptors (NLRs) that induce Effector-Triggered Immunity (ETI) upon direct/indirect pathogen effector recognition. Effector-Triggered Immunity is often accompanied by a hypersensitive response (HR), which is known as rapid localized cell death at infection sites to restrict pathogen growth (Contreras et al., 2023;Jones et al., 2024). Nucleotidebinding leucine-rich repeat receptors are classified by their N-terminal domains:TIR-NLRs (TNLs), CC-NLRs (CNLs), and RPW8-NLRs (RNLs). TNLs and CNLs typically function as sensor NLRs (sNLRs) that detect pathogen effectors, while RNLs serve as helper NLRs (hNLRs) that transmit immune signals from diverse sNLRs to ultimately execute downstream resistance and trigger cell death—though some RNLs can themselves be direct targets of pathogen effectors (Contreras et al., 2023;Gong et al., 2023). The hNLRs mainly include Activated Disease Resistance 1 (ADR1), which is conserved in both dicots and monocots, and N REQUIRED GENE 1 (NRG1),which has not been identified in monocots, as well as Solanaceae-specific NLR required for cell death (NRC)-type NLRs, which are required for HR-related cell death (Contreras et al., 2023;Gong et al., 2023).
基金supported by the National Natural Science Foundation of China(32472567)the Major Basic Research Project of the Shandong Provincial Natural Science Foundation,China(ZR2024ZD07)+1 种基金and the Key R&D Program of Shandong Province,China(2024CXPT072)to S.H.by the Shandong Provincial Natural Science Foundation Youth Program,China(ZR2024MC065)to C.Y.
文摘Dear Editor,To combat pathogen invasion,plants use immune receptors that detect immunogenic molecules to trigger immune responses and confer resistance.Cell-surface-resident pattern recognition receptors activate pattern-triggered immunity through the perception of pathogen-associated molecular patterns(PAMPs),damage-associated molecular patterns,and phytocytokines(PCKs)(Zhou and Zhang,2020;Jones et al.,2024).
基金National Natural Science Foundation of China(32250410314,32250410283,32470342)Natural Science Foundation of Shanghai(24ZR1430100).
文摘Plants are engaged in a constant battle for survival against pathogens,which triggers a multifaceted immune response characterized by pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)to prevent infection.These two immune responses operate synergistically to enhance plant immunity.PTI is considered the first line of defense involving the recognition of pathogen-associated molecular patterns(PAMPs)by specific receptors in host cells known as pattern recognition receptors(PRRs),which initiate defense signaling.However,many pathogens often overcome the first line of defense(PTI)and successfully deploy effector proteins to promote virulence and subvert plant immunity,leading to host susceptibility.In the counter-defense,the ETI defense mechanism is activated by triggering resistance(R)genes in plants that usually encode nucleotide-binding-leucine-rich-containing(NLR)proteins.During plant-pathogen interactions,transcriptional reprogramming of defense-related genes such as pathogenesisrelated proteins and generation of reactive oxygen species(ROS)are essential for facilitating programmed cell death at the infected location to inhibit pathogen proliferation.While ROS and PR protein are critical in plant-pathogen interaction,they are not universally required or effective against all pathogens.Hence,plants’multilayer immune layer is encrypted with the compensatory activation of ETI defense response towards the failure of one component of the defense system to maintain robust immunity.
基金supported by the Beijing Life Science Academy(Key Laboratory)Project(2024400CB0120)the National Key Research and Development Program of China(2021YFD1400400 and 2022YFD1400800)the National Natural Science Foundation of China(32130086,32430085,and 32300123).
文摘Pathogen-driven crop losses pose a significant threat to global food security.Plants deploy two primary branches of innate immunity:pathogen-associated molecular pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)(Yu et al.,2024).While PTI relies on surface-localized pattern recognition receptors,ETI is mediated by intracellular nucleotide-binding leucine-rich repeat receptors(NLRs)that directly or indirectly recognize pathogen effectors,often triggering hypersensitive cell death and systemic resistance(Yu et al.,2024).
文摘Background： Adenoid hypertrophy （AH） is associated with pediatric chronic rhinosinusitis （pCRS）, but its role in the inflammatory process of pCRS is unclear. It is thought that innate immunity gene expression is disrupted in the epithelium of patients with chronic rhinosinusitis （CRS）, including antimicrobial peptides and pattern recognition receptors （PRRs）. The aim of this preliminary study was to detect the expression of innate immunity genes in epithelial cells of hypertrophic adenoids with and without pCRS to better understand their role in pCRS. Methods： Nine pCRS patients and nine simple AH patients undergoing adenoidectomy were recruited for the study. Adenoidal epithelium was isolated, and real-time quantitative polymerase chain reaction （RT-qPCR） was employed to measure relative expression levels of the following messenger RNAs in hypertrophic adenoid epithelial cells of pediatric patients with and without CRS： Human β-defensin （HBD） 2 and 3, surfactant protein （SP）-A and D, toll-like receptors 1-10, nucleotide-binding oligomerization domain （NOD）-like receptors NOD 1, NOD 2, and NACHT, LRR and PYD domains-containing protein 3, retinoic acid-induced gene 1, melanoma differentiation-associated gene 5, and nuclear factor-riB （NF-KB）. RT-qPCR data from two groups were analyzed by independent sample t-tests and Mann-Whitney U-tests. Results： The relative expression of SP-D in adenoidal epithelium ofpCRS group was significantly lower than that in AH group （pCRS 0.73 ± 0.10 vs. AH 1.21 ±0.15; P = 0.0173, t = 2.654）. The relative expression levels of all tested PRRs and NF-κB, as well as HBD-2, HBD-3, and SP-A, showed no statistically significant differences in isolated adenoidal epithelium between pCRS group and AH group. Conclusions： Down-regulated SP-D levels in adenoidal epithelium may contribute to the development of pCRS. PRRs, however, are unlikely to play a significant role in the inflammatory process ofpCRS.
基金This Work was supported by the grants from theFundamental Research Funds for the Central Universities （No. 10ykpy04） and the National Natural Science Foundation of China （No. 30600028）.
文摘Background Trichophyton rubrum （T. rubrum） represents the most important agent of dermatophytosis in humans. T. rubrum infection causes slight inflammation, and tends to be chronic and recurrent. It is suggested that it may result from the failure of epithelial cells to recognize T. rubrum effectively and initiate effective immune responses. The C-type lectin receptors （CLR） and toll-like receptors （TLR） are the two major pattern recognition receptors （PRRs） that recognize fungal components. Therefore, the purpose of the study was to analyze the expression of those PRRs and the cytokines in HaCaT cells stimulated with heat-inactivated T. rubrum conidia and hyphae, respectively. Methods HaCaT cells were unstimulated or stimulated with heat-inactivated T. rubrum conidia and hyphae （l×106 and 1.5×105 colony-forming unit （CFU） in 2 ml medium, respectively） for 6, 12 and 24 hours. The mRNA expression of PRRs involved in recognizing fungal pathogen-associated molecular patterns （PAMPs） and signaling molecules were measured by quantitative reverse transcription polymerase chain reaction （RT-PCR）. Meanwhile, surface toll-like receptor （TLR） 2, TLR4 and Dectin-1 were analyzed by fluorescence-activated cell sorter （FACS） 24 hours after treatment. The cytokines were detected in cell culture supernatants of HaCaT cells in 12 and 24 hours after treatment. Results HaCaT cells constitutively expressed mRNA of membrane-bound TLR1,2, 4 and 6, Dectinl and DC-SIGN, but not Dectin-2 or Mincle. Heat-killed T. rubrum did not significantly upregulate gene transcriptions of the PRRs of HaCaT cells. Heat-inactivated T. rubrum conidia significantly reduced the surface expression of TLR2 and Dectin-1, and suppressed the secretions of interferon-inducible protein-10 （IP-10） and monocyte chemotactic protein-1 （MCP-1） of HaCaT cells, while heat-killed T. rubrum hyphae significantly induced the secretions of IP-10 and MCP-I. Conclusion The cell-wall antigens of T. rubrum fail to activate transcriptional expression of PRRs and induce a lower immune response of HaCaT cells by limited cytokines secretion.
