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We have shown that exosomes activate CD8+ T cells, indicating that antigens present on exosomes can be processed through the class I MHC presentation pathway.
Therefore, alternative vaccine delivery systems, which enable introduction of nonreplicating antigen into the MHC class I presentation pathway, are sought.
The classical antigen presentation pathway consists of two monomorphic (proteasome and TAP) and one polymorphic components (MHC Class I).
Under the host selection pressure HIV evolves rapidly to override crucial steps in the antigen presentation pathway.
In mammals, the DM molecules are encoded by the major histocompatibility complex (MHC) and execute key functions in the class II antigen presentation pathway.
It is commonly believed that delivery of antigen into the class I antigen presentation pathway is a limiting factor in the clinical translation of DNA vaccines.
Herpesviruses manage to dodge this immune response by hampering one of the central hinges of human adaptive immunity, the major histocompatibility complex (MHC) class I antigen presentation pathway.
This review focuses on the diverse mechanisms of viral evasion of the MHC class I antigen presentation pathway with particular emphasis on viruses of veterinary importance.
Second, viruses inhibit the MHC class II antigen presentation pathway by affecting the stability or intracellular sorting of class II proteins.
The trimolecular complex consisting of the class I heavy chain, β2-microglobulin and the peptide are generated by the MHC class I antigen presentation pathway.
Overall our results highlight key tissue-specific differences in transgene presentation pathway requirements of importance for the design of rAAV-based T cell-inducing vaccines.
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