Effector-triggered Immunity
Effector-triggered Immunity - Related Videos
08:45
Assay for Pathogen-Associated Molecular Pattern (PAMP)-Triggered Immunity (PTI) in Plants
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Cited by 23 •
2009
A cell death-based assay for PTI in Nicotiana benthamiana plants is described.
12:23
Analysis of Yersinia enterocolitica Effector Translocation into Host Cells Using Beta-lactamase Effector Fusions
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Cited by 5 •
2015
Effector translocation into host cells via a type III secretion system is a common virulence strategy among gram-negative bacteria. A beta-lactamase effector fusion based assay for quantitative analysis of translocation was applied. In Yersinia infected cells, conversion of a FRET reporter by the beta-lactamase is monitored using laser scanning microscopy.
02:16
Intranasal Immunization with BCG in a Mouse Model
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2025
This video demonstrates intranasal BCG immunization in mice, activating both innate and adaptive immune responses, leading to the development of lung-resident memory T cells and effector B cells, thus enhancing protection against Mycobacterium infections.
03:03
Measuring the Activation of Fc-Mediated Effector Functions by HA Antibodies
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2025
This video demonstrates an assay measuring the antibody-mediated activation of T cell effector functions. Adding an influenza virus hemagglutinin (HA)-specific monoclonal antibody to transfected mammalian cells expressing HA results in the formation of immune complexes with HA. Upon introducing engineered T cells expressing Fc receptors and a luciferase reporter, the T cells are activated by the antibody-HA complexes, and this activation is detected by adding a luciferase substrate and...
08:39
Electroporation of Functional Bacterial Effectors into Mammalian Cells
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Cited by 7 •
2015
Electroporation was used to insert purified bacterial virulence effector proteins directly into living eukaryotic cells. Protein localization was monitored by confocal immunofluorescence microscopy. This method allows for studies on trafficking, function, and protein-protein interactions using active exogenous proteins, avoiding the need for heterologous expression in eukaryotic cells.
FAQs
Recognition of an effector, or of the change it causes in a host process, activates signaling inside the plant cell. This signaling promotes defense-gene expression and can produce a strong, localized response rather than a general reaction throughout the plant. The resulting activity helps restrict pathogen spread near the initially affected cells.
A pathogen-derived effector does not need to be recognized only as a foreign molecule. Its disruption of a host process can also provide the signal that activates immunity. This expands the ways intracellular receptors can identify infection and links pathogen activity to targeted defense signaling, even when recognition focuses on the consequence of effector action.
Basal defenses provide an initial layer of protection, but some pathogens can overcome them through effector activity. ETI adds a stronger and more targeted response when host cells detect those effectors or their effects. Comparing these layers helps explain why pathogen effectors are important determinants of infection success and plant resistance.
Localized hypersensitive cell death can occur after intracellular immune receptors activate ETI. Because the response is concentrated near affected cells, it may limit the area available for pathogen spread rather than producing unrestricted tissue damage. Its occurrence also serves as a visible outcome of strong immune activation during bacterial, fungal, or oomycete infection.
The response is relevant to infections caused by bacteria, fungi, and oomycetes. These pathogens may deliver effectors that alter host processes, creating targets for intracellular immune recognition. Studying ETI across these infection types helps connect particular pathogen strategies with the plant defense responses that restrict their spread and contribute to disease resistance.
Research can identify the intracellular immune receptors involved in recognition and the pathogen effector targets or effects that activate them. Those findings provide a basis for designing strategies to strengthen plant resistance. The broader goal is to engineer durable disease resistance, particularly against pathogens that can overcome basal defenses during infection.