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IL-23 secreted by activated macrophages and dendritic cells has been shown to enhance the production of the most critical cytokine, IFN-γ, in mediating host protection against T. gondii infection.
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Innate immunity can activate autophagy to mediate host protection in vivo.
To assess if Caspase-1 and Pycard together mediate host protection in the context of inflammasome activation, we investigated the contribution of Caspase-1 during Mtb infection.
In order to define potential molecular mechanisms of T helper cell mediated host protection in intracerebral viral infection, we screened the expression profile of highly purified CD4+ effector T cells isolated from the CNS of VV challenged wild type vs α4 CKO mice for molecules directly involved in virus defense.
During infection, SIGNR3 is expressed in lung phagocytes and interacts with Mtb bacilli and mycobacterial surface glycoconjugates and mediates host protection by inducing secretion of protective cytokines including TNF α and IL-6 [ 94, 95].
Biondo, C. et al. The interleukin-1β/CXCL1/2/neutrophil axis mediates host protection against group B streptococcal infection.
TPL2-ERK1/2 signaling pathway mediates host protection against Mtb infection through negative regulation of type I IFN production [ 198].
IAPs were described critical in mediating host cell viability.
Our results provide new insights on how Wolbachia affects its hosts through mediating host miRNAs.
GP1 mediates host cell attachment and receptor recognition, whereas GP2 mediates fusion of the viral and host membranes8,9,10,11,12.
The autophagy gene ATG5 mediates autophagosome-independent host protection.
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