CD46 knock-out using CRISPR/Cas9 editing of hTERT immortalized human cells modulates complement activation.

ABSTRACT: The kidney is especially sensitive to diseases associated with overactivation of the complement system. While most of these diseases affect kidney glomeruli and the microvasculature, there is also evidence for tubulointerstitial deposition of complement factors. Complement inactivating factors on cell membranes comprise CD55, CD59 and CD46, which is also termed membrane cofactor protein (MCP). CD46 has been described as localized to glomeruli, but especially also to proximal tubular epithelial cells (RPTECs). However, human cell culture models to assess CD46 function on RPTECs are still missing. Therefore, we here performed gene editing of RPTEC/TERT1 cells generating a monoclonal CD46-/- cell line that did not show changes of the primary cell like characteristics. In addition, factor I an

SUBMITTER: Wieser M 

PROVIDER: S-EPMC6453361 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature