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Classically activated macrophages (M1) exhibit a pro-inflammatory role, mediating host defense against microorganisms or tumor cells; whereas alternatively activated macrophages (M2) perform a range of physiological processes, including inflammation, wound repair and tissue remodeling.
Of note, vaccination with facultatively intracellular pathogens, like B. henselae, could also depend on effective T-cell memory for mediating host defense and production of specific antibodies.
It has now become clear that the TLR-dependent innate immune response is essential in mediating host defense to infection and to infection-related inflammation and tissue remodeling [7], [8].
Symbiotic microbes may represent a particularly promising source because microbial symbioses are widespread [e.g., [22]], largely unexplored for natural products [cf. [5]; but see [16]], and often involve the exchange of small molecules between symbionts and hosts [cf. [16]], including compounds mediating host defense [e.g., [11], [17] [19]].
Despite its importance in mediating host defense against bacterial infection, IL-22 may paradoxically lead to pathological inflammation and thus promote tumorigenesis.
Another notable interesting enzyme is D-dopachrome tautomerase, the functional homolog of macrophage migration inhibitory factor [ 222], which could be involved in mediating host defense mechanism.
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An immunologist whose research has contributed to the understanding of the precise mechanisms of how white blood cells respond to chemical signals to mediate host defense or tissue damage, Snyderman accepted his first faculty appointment at Duke in 1972.
Another mechanism by which SP-A can mediate host defense is via direct modulation of alveolar macrophage function.
Therefore, these cells may directly mediate host defense even before foreign antigen-specific T cells have differentiated.
The mucosal epithelium is not a simple passive barrier; it also mediates host defenses by secreting mucus, defensins, and complement proteins 16. HIV-1 can activate the different complement cascade pathways, which all converge at the cleavage of C3, but HIV-1 can escape complement-mediated lysis as the virions incorporate host proteins that will cleave activated C3 into inactivated iC3b 17.
We show that the Caenorhabditis elegans receptors CED-1 and C03F11.3, and their mammalian orthologues, the scavenger receptors SCARF1 and CD36, mediate host defense against two prototypic fungal pathogens, Cryptococcus neoformans and Candida albicans.
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