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Effector-triggered immunity (ETI) is one of the pathways, along with the pattern-triggered immunity (PTI) pathway, by which the innate immune system recognises pathogenic organisms and elicits a protective immune response. ETI is elicited when an effector protein secreted by a pathogen into the host cell is successfully recognised by the host.
The innate immune system or nonspecific immune system [1] is one of the two main immunity strategies in vertebrates (the other being the adaptive immune system). The innate immune system is an alternate defense strategy and is the dominant immune system response found in plants, fungi, prokaryotes, and invertebrates (see Beyond vertebrates). [2 ...
An immune response is a physiological reaction which occurs within an organism in the context of inflammation for the purpose of defending against exogenous factors. These include a wide variety of different toxins, viruses, intra- and extracellular bacteria, protozoa, helminths, and fungi which could cause serious problems to the health of the host organism if not cleared from the body.
If pathogens successfully evade the innate response, vertebrates possess a second layer of protection, the adaptive immune system, which is activated by the innate response. [3] Here, the immune system adapts its response during an infection to improve its recognition of the pathogen.
This allows the innate immune system to recognize pathogens and thus, protect the host from infection. [ 3 ] : 494 Although the term "PAMP" is relatively new, the concept that molecules derived from microbes must be detected by receptors from multicellular organisms has been held for many decades, and references to an "endotoxin receptor" are ...
Given the diversity of effectors, they affect a wide variety of intracellular processes. The T3SS effectors of pathogenic E. coli, Shigella, Salmonella, and Yersinia regulate actin dynamics to facilitate their own attachment or invasion, subvert endocytic trafficking, block phagocytosis, modulate apoptotic pathways, and manipulate innate immunity as well as host responses.
“The discovery that tau phosphorylation can act as a protective mechanism against HSV-1 infection suggests that enhancing this immune response could help mitigate the impact of viral infections ...
Adenovirus, herpes simplex virus, HSV-1 and HSV-2, as well as the negative-stranded RNA virus, vesicular stomatitis virus (VSV), have been shown to be able to activate a STING-dependent innate immune response. [14] STING deficiency in mice led to lethal susceptibility to HSV-1 infection due to the lack of a successful type I interferon response ...