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SWNTs were shown to activate major histocompatibility complex (MHC) class I pathway of antigen antibody response system resulting in the appearance of an edematous aspect after one week.
After 1 week, only single-walled carbon nanotubes (SWNTs) activated major histocompatibility complex (MHC) class I pathway of antigen antibody response system (higher CD4+/CD8+ value), resulting in the appearance of an edematous aspect.
As the generation of Salmonella antigens for MHC class II molecules is an efficient process in infected B cells, we tested whether BCR-mediated phagocytosis also leads to cross-presentation of Salmonella antigens via the MHC class I pathway of B cells and whether this elicits a cytotoxic T cell response against Salmonella-infected cells.
Because these phenotypes cannot be explained by the established inhibitory functions, additional mechanisms by which HCMV modulates the class I pathway of antigen presentation are likely to exist.
The i.p. administration of LPS activates the MHC Class I pathway of antigen processing in concordance with previous studies with LPS-activated trout macrophages [ 8].
After the translation process, the produced protein can enter in the class I pathway of immunologic presentation process for activation of CD8+ T cells or participate of cross-priming process for CD4+ T cells [ 27].
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These have the ability to introduce the recombinant gene product into the MHC class-I pathway of antigen presentation and therefore prime cytotoxic T cells as well as generate humoral immunity [22] [24].
Thus, TRAF6 contributes to effective elimination of RNA viruses that activate MDA5 pathway as well as those activate RIG-I pathway through production of sufficient amount of type I IFN.
The known PPIs are compared across datasets in two ways: (i) pathway enrichment and (ii) presence of interologs.
(i) The pathway of pollution to hypertension was explained through the route of stress to hypertension while the adulteration of food through obesity to hypertension.
One of them, TRIM25, has been implicated in the RIG-I pathway by regulating the capability of RIG-I to activate type I IFN [ 26, 27].
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