CD13 is dispensable for normal hematopoiesis and myeloid cell functions in the mouse

Journal of Leukocyte Biology

Catherine O'Conor⁴  Ran Zhao³  Christina L. Grant³  Fiona Hall Fenteany³  Wolfgang Schacke³  Beata Winnicka³  Anupinder Kaur¹  Kaitlyn Vernier³  Linda H. Shapiro³  Brannen Liang³  David C. Montrose²  Flavia E. Pereira³  Daniel W. Rosenberg²  Hector L. Aguila⁴ 

[1] Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, Connecticut, USA Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, Connecticut, USA Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, Connecticut, USA;Molecular Medicine and Departments of Molecular Medicine and Departments of Molecular Medicine and Departments of;Vascular Biology and Vascular Biology and Vascular Biology and;Immunology and Immunology and Immunology and

关键词: cell differentiation;    inflammation;    aminopeptidase N;    dendritic cell;    macrophage;    adhesion molecule;   

DOI  :  10.1189/jlb.0210065

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

The robust and consistent expression of the CD13 cell surface marker on very early as well as differentiated myeloid hematopoietic cells has prompted numerous investigations seeking to define roles for CD13 in myeloid cells. To address the function of myeloid CD13 directly, we created a CD13 null mouse and assessed the responses of purified primary macrophages or DCs from WT and CD13 null animals in cell assays and inflammatory disease models, where CD13 has been implicated previously. We find that mice lacking CD13 develop normally with normal hematopoietic profiles except for an increase in thymic but not peripheral T cell numbers. Moreover, in in vitro assays, CD13 appears to be largely dispensable for the aspects of phagocytosis, proliferation, and antigen presentation that we tested, although we observed a slight decrease in actin-independent erythrocyte uptake. However, in agreement with our published studies, we show that lack of monocytic CD13 completely ablates anti-CD13-dependent monocyte adhesion to WT endothelial cells. In vivo assessment of four inflammatory disease models showed that lack of CD13 has little effect on disease onset or progression. Nominal alterations in gene expression levels between CD13 WT and null macrophages argue against compensatory mechanisms. Therefore, although CD13 is highly expressed on myeloid cells and is a reliable marker of the myeloid lineage of normal and leukemic cells, it is not a critical regulator of hematopoietic development, hemostasis, or myeloid cell function.

【 授权许可】

Unknown