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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 201, Supplement 682
The 90th Annual Meeting of The German Physiological Society
3/26/2011-3/29/2011
Regensburg, Germany


RESIDENT CARDIAC IMMUNE CELLS AND EXPRESSION OF CD39 AND CD73
Abstract number: P089

*Borg1 N., Bonner1 F., Bongardt1 S., Schrader1 J.

CD39 and CD73 are ectoenzymes expressed on immune cells catalysing the extracellular degradation of ATP to adenosine. We analysed the expression of CD39 and CD73 on leukocytes present in mouse cardiac tissue and blood under unstressed conditions. Leukocytes of mouse myocardial tissue were extracted in a multi-step procedure including Langendorff perfusion, enzymatic digestion and centrifugation. Blood immune cells were isolated from retro-orbital blood after lysis of erythrocytes. Expression analysis of CD39 and CD73 was performed by flow cytometry (BD FACS Canto II). We found that already the unstressed heart contains 3,21 ±1,60 x 105 leukocytes consisting of T-cells (4,1 %), B-cells (6 %), natural killer cells (0,5 %), granulocytes (1,6 %), monocytes (7 %), makrophages and dendritic cells (together 78 %). T-cells are the dominant cell population expressing CD73, whereas the expression of CD73 on myeloid cells is generally low. An opposite expression pattern was found for CD39 with highest expression on myeloid cells. The expression pattern of CD39 and CD73 on leukocytes in the heart was similar to that in blood. However, the percentage of T-cells expressing CD73 and their expression level was higher in blood as compared to cardiac tissue. We conclude that the normal heart already contains significant amounts of T-cells, B-cells, granulocytes and monocytes, the most prominent fraction being dendritic cells and macrophages. Because of the inverse expression of CD73 and CD39 on lymphatic and myeloid cells it appears that both cells types operate together in the extracellular degradation of ATP to adenosine.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 201, Supplement 682 :P089

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