Distinct signals and immune cells drive liver pathology and glomerulonephritis in ABIN1[D485N] mice

Monocyte
DOI: 10.26508/lsa.201900533 Publication Date: 2019-11-06T21:35:11Z
ABSTRACT
We report that TLR7, IL-6, and the adaptive immune system are essential for autoimmunity glomerulonephritis but not liver pathology in mice expressing ubiquitin-binding–defective ABIN1[D485N] mutant. The blood organs of have exceptionally high numbers patrolling monocytes (pMo), which develop independently IL-6 system. They detectable months before organ seen may diagnostic potential. splenic pMo, inflammatory (iMo), neutrophils expressed levels mRNAs encoding proteins released during NETosis, together with monocyte-derived dendritic cells (MoDCs) drive mice, contribute to other organs. iMo displayed expression controlling cell division were actively dividing; this underlie increased pMo MoDC numbers, derived from iMo. An orally active IRAK4 inhibitor suppressed all facets disease phenotype prevented increase numbers.
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