Exact(3)
Cytosolic DNA arising from intracellular pathogens triggers a powerful innate immune response1,2.
Tattoli, I. et al. Amino acid starvation induced by invasive bacterial pathogens triggers an innate host defense program.
HIV, as other pathogens, triggers the proliferation of immune cells.
Similar(57)
Chronic infections by bacterial pathogens trigger airway inflammation and structural lung damage, beginning in the early life and influencing the later stage of the disease [2].
While Caenorhabditis elegans specifically responds to infection by the up-regulation of certain genes, distinct pathogens trigger the expression of a common set of genes.
Indeed, there are now examples of pathogens triggering down-regulation of host genes (e.g. [48]); this is clearly an area that merits further investigation.
For example, pathogens trigger the expression of proinflammatory cytokines and chemokines via the activation of Toll-like receptors (TLR) by pathogen-associated molecular patterns (PAMP) like LPS, lipopeptides or bacterial DNA [8].
We show here that both genes are also redundantly required in defense against pathogens triggered by MeJA.
Several studies have tried to identify potent infectious pathogens triggering temporal arteritis [ 37, 38] and some case series have suggested a potential relation between vasculitis and cancer [ 23].
These pathogens trigger plant defence and immune responses through mechanisms involving respectively, phytohormones like salicylic acid (SA), a key modulator of SAR, and jasmonic acid/ethylene pathways [ 21].
As aggregates comprise a large number of individual protein molecules, there is the potential for the surface to display a "repetitive" array of epitopes that may be seen by the immune system as resembling the external surfaces of pathogens, triggering the pattern recognition receptors (Toll-like receptors) on APCs.
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