Lymphatic neoangiogenesis in human kidney transplants is associated with immunologically active lymphocytic infiltrates

Renal transplant rejection is caused by a lymphocyte-rich inflammatory infiltrate that attacks cortical tubules and endothelial cells. Immunosuppressive therapy reduces the number of infiltrating cells; however, their exit routes are not known. Here a >50-fold increase of lymphatic vessel density...

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Bibliographic Details
Published in:	Journal of the American Society of Nephrology Vol. 15; no. 3; pp. 603 - 612
Main Authors:	KERJASCHKI, Dontscho, REGELE, Heinrich M, LAAKKONEN, Pirjo, PETROVA, Tatiana, LANGER, Brigitte, RAAB, Ingrid, MOOSBERGER, Isabella, NAGY-BOJARSKI, Katalyn, WATSCHINGER, Bruno, SOLEIMAN, Afschin, BIRNER, Peter, KRIEGER, Sigurd, HOVORKA, Anny, SILBERHUMER, Georg
Format:	Journal Article
Language:	English
Published:	Hagerstown, MD Lippincott Williams & Wilkins 01-03-2004
Subjects:	Adolescent Adult Aged B-Lymphocytes - immunology Biological and medical sciences Biopsy Cell Movement Female Graft Rejection - immunology Humans Kidney Transplantation - immunology Kidney Transplantation - pathology Lymphatic Vessels Male Medical sciences Middle Aged Neovascularization, Pathologic Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the urinary system T-Lymphocytes - immunology Human Nephrology Immune response Lymphatic Transplantation Kidney Urology Rejection Angiogenesis Treatment Urinary system Surgery Infiltration Neovascularization Lymphocyte
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Summary:	Renal transplant rejection is caused by a lymphocyte-rich inflammatory infiltrate that attacks cortical tubules and endothelial cells. Immunosuppressive therapy reduces the number of infiltrating cells; however, their exit routes are not known. Here a >50-fold increase of lymphatic vessel density over normal kidneys in grafts with nodular mononuclear infiltrates is demonstrated by immunohistochemistry on human renal transplant biopsies using antibodies to the lymphatic endothelial marker protein podoplanin. Nodular infiltrates are constantly associated with newly formed, Ki-67-expressing lymphatic vessels and contain the entire repertoire of T and B lymphocytes to provide specific cellular and humoral alloantigenic immune responses, including Ki-67(+) CD4(+) and CD8(+) T lymphocytes, S100(+) dendritic cells, and Ki-67(+)CD20(+) B lymphocytes and lambda- and kappa-chain-expressing plasmacytoid cells. Numerous chemokine receptor CCR7(+) cells within the nodular infiltrates seemed to be attracted by secondary lymphatic chemokine (SLC/CCL21) that is produced and released by lymphatic endothelial cells in a complex with podoplanin. From these results, it is speculated that lymphatic neoangiogenesis not only contributes to the export of the rejection infiltrate but also is involved in the maintenance of a potentially detrimental alloreactive immune response in renal transplants and provides a novel therapeutic target.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1046-6673 1533-3450
DOI:	10.1097/01.ASN.0000113316.52371.2E