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. Author manuscript; available in PMC: 2010 Nov 1.
Published in final edited form as: Am J Transplant. 2009 Nov;9(11):2479–2484. doi: 10.1111/j.1600-6143.2009.02801.x

Figure 1.

Figure 1

Representative sections of proximal coronary arteries from transplanted hearts with elastic tissue stain. Group number refers to group labeling from Table I. (a,b,d,e,f) B6.RAG1−/− into CB6F1.RAG1−/−, (c) CB6F1.RAG isograft. a) no treatment (grp1), normal artery; b) MEM alone (grp2), normal artery; d) LCMV (grp6), d.28, early lesion; e) LCMV (grp3), d.56, late lesion; f) LCMV + anti-NK1.1 (grp5), d.56, artery clear; c) LCMV isograft (grp4), normal artery. Marked neointimal and adventitial hypercellularity is present at day 28 (d) while later lesion at day 56 (e) has increased fibrosis and reduced cellularity. Depletion of NK cells (f) blocked formation of intimal lesions. Immunoperoxidase stained proximal coronaries of B6.RAG−/− → CB6F1.RAG−/− LCMV inoculated hearts sacrificed at day 28 using anti-Ly49G2 (g), anti-∝SMA (h) and anti-CD16/32 (i). Several Ly49G2+ cells (NK cells) are shown to be present within the neointima (arrows). SMA+ cells (smooth muscle cells or myofibroblast) comprise the major cell type in the neointima. The media smooth muscle is also positive. Numerous CD16/32+ cells with the appearance of macrophages in the adventitia and in the neointima. Coronary vessel walls indicated by △.