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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.
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Gene silencing of APL1C completely abolishes Rel1-mediated host protection against P. berghei, and thus the presence of APL1C is required for this protection.
These results, further supported by expression studies [ 8], showed that the aphid immune system greatly differs from that of other well studied insects and it was hypothesized that aphids compensate for a deficient immune system by symbiont-mediated host protection and an extraordinary reproduction rate [ 8].
Likewise, for antibody-mediated host protection against lethal challenge (e.g., with a toxin or pathogen), B may be equated with the observed fractional host survival (i.e., proportion of surviving hosts) due to binding by antibody (e.g., antitoxin or pathogen-neutralizing antibody), such that B0 is again unity (corresponding to complete protection against lethality).
Studies in mice deficient in ATG5 in phagocytes revealed that this autophagy gene was required for IFN-γ-mediated in vivo host protection likely because ATG5 was required for the induction of IFN-γ-dependent anti-microbial activity in macrophages [13].
The autophagy gene ATG5 mediates autophagosome-independent host protection.
Infection with the intracellular protozoan parasite T. cruzi elicits a strong CD8+ T-cell-mediated IFN- γ response that is necessary for host protection.
In the host, IFN- γ always stimulates cell-mediated immune responses that are critical for the development of host protection against pathogenic intracellular microorganisms.
Interestingly, some researchers have shown that in the absence of circulating antibody, Fc receptor mediated internalization of L. mexicana in mouse phagocytes is compromised, leading to increased host protection.
Therefore, since it is likely that a Th1 response, in addition to the recruitment of myeloid cells, is important for host protection against ehrlichial infection, our data suggests that MyD88-mediated recognition of ehrlichiae is important for optimal induction of Th1 immune responses.
Type 2 immunity is essential for host protection against parasitic nematode infection while is detrimental in certain type 2-mediated inflammatory pathologies.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com