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Random complex mixtures of polypeptides such as glatiramer acetate (GA) were among the first to be applied as immunodulators that take into account T cell degeneracy.
Our results suggest that reactivity to hLFA1 peptide in peripheral blood may be the result of T cell degeneracy.
Our results suggest that reactivity to the hLFA1 peptide in peripheral blood may be the result of T cell degeneracy.
An additional, and in our opinion better explanation, is that reactivity to the hLFA1 peptide in peripheral blood is in large part the result of T cell degeneracy.
And their immediate disappearance in the later stages of infection in resistant genotype libraries and continued expression in susceptible genotypes supports a hypothesis that continual expression of this protein may lead to mitochondrial dysfunction and subsequent cell degeneracy.
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Pathogen-specific memory T cells, by virtue of the inherent degeneracy of T-cell receptor recognition of peptide:major histocompatibility complex ligands, may exhibit cross reactivity with allogeneic peptide:major histocompatibility complexes and thereby mediate graft rejection.
However, in this essay we discuss an alternative aspect of degeneracy in T cell recognition: the notion that peptides can assume different "registers" in the groove of a single MHC molecule, as first suggested and demonstrated by Sercarz and co-workers (reviewed in [J. autoimmun. 16 (2001) 201]).
Also for each case, the calculated current-voltage characteristic per super-cell shows that the spin degeneracy in the system is obviously broken and the current becomes strongly spin dependent.
In particular, we discuss two new insights: degeneracy among CD8 T cells appears to be substantially less than among CD4 T cells, and T cell clones characterized by a high affinity TCR interaction with a given pMHC complex are less degenerate than lower avidity T cells that require higher levels of pMHC complex for their activation.
Limited success with antigen-specific immunotherapies has led to the identification of novel approaches which consider the degeneracy of the T cell response, i.e. their ability to respond to multiple antigenic peptides.
Based on results from this model, we hypothesize, due to the considerable degeneracy in the T cell repertoire, that induction of full-blown autoimmune disease via molecular mimicry is a tightly regulated process requiring multiple factors related to the pathogen expressing the potential mimic epitope.
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