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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:2273.)
© 2007 American Heart Association, Inc.

Editorial

Prevention of Tissue Death by Killer Cells?

The Role of the Immune System in Arteriogenesis

Wolfgang Schaper

From the Department of Experimental Cardiology, Max-Planck-Institute, Bad Nauheim, Germany.

Correspondence to Wolfgang Schaper, Max-Planck-Institute, Department of Experimental Cardiology, Parkstrasse 1, Bad Nauheim D-61231, Germany. E-mail w.schaper@kerckhoff.mpg.de

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Based on the observation that mouse strains differing in lymphocyte-mediated immune responses differed also markedly in collateral density, in their ability to develop a collateral circulation, in remodeling and the expression of VEGF-A after femoral artery occlusion, previously reported by Scholz et al,¹ Chalothorn,² and Helisch et al,³ van Weel et al had set out to test the role of lymphocytes in arteriogenesis.⁴ They found that NK-cells and CD4 cells are important for collateral vessel growth and that substitution in animals deficient for these cells accelerated collateral development. These elegant studies, using mouse genetics as well as antibody-based deletion experiments, provide a solution to a long smoldering discussion about the role of lymphocytes in arteriogenesis as well as in angiogenesis. As early as 1976 Klintworth and collaborators⁵ showed that angiogenesis in response to corneal injury was associated with an influx of leukocytes. The causal relationship was proven by irradiation to depress the bone marrow leading to impaired angiogenesis. The contribution of subsets of leukocytes was difficult to discern at the time because only morphological markers were available. Lymphocytes were believed to play a lesser role compared with the unfractionated leukocyte population. We could show in 1971 that leukocytes played a role in arteriogenesis because they invaded the wall of developing coronary collaterals,⁶ and a systematic study published in 1976⁷ identified these cells as monocytes. These findings were later supplemented by increased endothelial expression of monocyte chemoattractant protein 1 and by increased expression of adhesion molecules. The role of the monocyte . . . [Full Text of this Article]

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