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Cell-type-restricted anti-cytokine therapy: TNF inhibition from one pathogenic source. | LitMetric

Cell-type-restricted anti-cytokine therapy: TNF inhibition from one pathogenic source.

Proc Natl Acad Sci U S A

Laboratory of Molecular Mechanisms of Immunity, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow 119991, Russia; Laboratory of Experimental Immunology, Lobachevsky State University of Nizhny Novgorod, Nizhny Novgorod 603950, Russia; Research Group Inflammation Biology, German Rheumatism Research Center, a Leibniz Institute, 10117 Berlin, Germany; Department of Immunology, Faculty of Biology and Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow 199991, Russia;

Published: March 2016

AI Article Synopsis

  • Overexpression of TNF is linked to various autoimmune diseases, making anti-TNF therapy effective in treating these conditions.
  • Researchers developed MYSTI, a bispecific antibody that targets myeloid cells and binds to TNF, to specifically inhibit TNF from these cells.
  • In tests on TNF humanized mice, MYSTI showed enhanced protection against liver damage compared to traditional systemic TNF inhibitors, indicating a promising targeted treatment for conditions driven by macrophage-derived TNF.

Article Abstract

Overexpression of TNF contributes to pathogenesis of multiple autoimmune diseases, accounting for a remarkable success of anti-TNF therapy. TNF is produced by a variety of cell types, and it can play either a beneficial or a deleterious role. In particular, in autoimmunity pathogenic TNF may be derived from restricted cellular sources. In this study we evaluated the feasibility of cell-type-restricted TNF inhibition in vivo. To this end, we engineered MYSTI (Myeloid-Specific TNF Inhibitor)--a recombinant bispecific antibody that binds to the F4/80 surface molecule on myeloid cells and to human TNF (hTNF). In macrophage cultures derived from TNF humanized mice MYSTI could capture the secreted hTNF, limiting its bioavailability. Additionally, as evaluated in TNF humanized mice, MYSTI was superior to an otherwise analogous systemic TNF inhibitor in protecting mice from lethal LPS/D-Galactosamine-induced hepatotoxicity. Our results suggest a novel and more specific approach to inhibiting TNF in pathologies primarily driven by macrophage-derived TNF.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4801281PMC
http://dx.doi.org/10.1073/pnas.1520175113DOI Listing

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