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Accurate models of antigen processing have implications for the study of basic immunology as well as for the design of peptide-based vaccines and other immunotherapies.
We have deployed our QSAR prediction models via MHCPred [16]; subsequently supplementing this with sophisticated models of antigen presentation [17]; deployed via EpiJen [18].
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Supported by animal models of antigen-induced autoimmunity, the rationale of HSCT is to time-shift the clinical autoimmunity to an earlier period, restoring self-tolerance.
For example, Belvisi et al. [19] showed that in preclinical models of antigen-induced airway eosinophilia and Sephadex-induced lung edema using Brown Norway rats, ciclesonide showed comparable efficacy with fluticasone, although ciclesonide was 7 9-fold less potent in terms of ED50.
Increasing the strength of signal or presence of IL-2 can override the Treg-mediated suppression, which we show in the context of three different in vitro models of antigen-specific T cell activation.
In vivo studies highlighted a crucial role for S100a8/a9 in the promotion of inflammation [ 18] and inflammation-induced carcinogenesis [ 19] by using S100a9 -/- animals in models of antigen-induced arthritis and colon carcinogenesis, respectively.
Indeed in vivo studies with S100a9 -/- animals highlighted a crucial role for S100a8/a9 in the promotion of inflammation and inflammation-induced carcinogenesis in models of antigen-induced arthritis and colon carcinogenesis, respectively [ 18, 19].
Otherwise, compound 4e presented a dose-dependent analgesic effect in a model of antigen (mBSA -induced arthritis and anti-inflamBSA -inducedle in carthritisn induced pandedema, indicating its potential as a new antiarthritis profilepe.
This integrated model of antigen processing provided the unique insight that HLA class I alleles apparently constitute two separate classes: those that are TAP-efficient for peptide loading (HLA-B27, -A3, and -A24) and those that are TAP-inefficient (HLA-A2, -B7, and -B8).
We previously published a method of measuring in vivo delayed type hypersensitivity using a mouse model of antigen and immune response transfer that is inhibited by TGF-β1.[18] Wild-type mice (C57BL/6) were tested for DTH responses using a transfer DTH assay.
To compare the therapeutic effects of hIL-10, vIL-10, and mut.hIL-10 in a rabbit knee model of antigen induced arthritis, disease was induced by intra-articular injection of OVA into the knees of OVA immunized rabbits.
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