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. 2018 Sep 20;38(11):2691–2705. doi: 10.1161/ATVBAHA.118.311689

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© 2018 The Authors.

Arteriosclerosis, Thrombosis, and Vascular Biology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 6. — Colocalization of complement factor C4 with several retinal cell types. A, Twelve-mo-old Tspan12 ECKO retinal cross-sections stained with anti-C4 and IB4. Split and merged channels are shown. Arrows indicate blood vessels decorated with C4. B, Colocalization of extravasated IgG and C4 on a subset of retinal cells and on the borders of cystoid lesions in the mutant tissue. C, Rod-bipolar cell spacing seems increased in the mutant tissue. The section shows also 1 or 2 C4-decorated Müller glia cells, which were recognized by their extensions towards the outer limiting membrane (arrow). D, Disorganized Müller cells in the mutant tissue. Sox9 marks nuclei of Müller glia. Arrow highlights a C4-decorated cell which was recognized as amacrine cell based on cell body location and cell shape. E, Partial colocalization of C4 with microglia marker IBA-1. PKC indicates protein kinase C; and Sox9, SRY-box 9.