A Comparative Analysis of the Murine Thymic Microenvironment in Normal, Autoimmune, and Immunodeficiency StatesReport as inadecuate

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Developmental Immunology - Volume 5 1997, Issue 2, Pages 79-89

Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, School of Medicine, Davis, California 95616, USA

Institute of Bio-Active Science, Nippon Zoki Pharmaceutical Co. Ltd., Yashiro, Hyogo 673-14, Japan

Department of Pathology and Immunology, Monash University, Prahran, Victoria 3181, Australia

Department of Pathology, Emory University, School of Medicine, Atlanta, Georgia 30322, USA

Jackson Laboratory, Bar Harbor, Maine 04609, USA

Department of Pathology, Toyama City Hospital, Imaizumi, Toyama 939, Japan

Received 14 October 1996; Accepted 10 December 1996

Copyright © 1997 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


It is widely accepted that the thymic microenvironment regulates normal thymopoiesisthrough a highly coordinated and complex series of cellular and cytokine interactions. A directcorollary of this is that abnormalities within the microenvironment could be of etiologicsignificance in T-cell-based diseases. Our laboratory has developed a large panel ofmonoclonal antibodies mAbs that react specifically with epithelial or nonepithelialmarkers in the thymus. We have taken advantage of these reagents to characterize thethymic microenvironment of several genetic strains of mice, including BALB-cJ,C57BL-6J, NZB-BlnJ, SM-J, NOD-Ltz, NOD-Ltz-scid-sz, C57BL-6J-Hcphme-Hcphme, andALY-NscJcl-aly-aly mice, and littermate control animals. We report herein that controlmice, including strains of several backgrounds, have a very consistent phenotypic profilewith this panel of monoclonal antibodies, including reactivity with thymic epithelial cellsin the cortex, the medulla and the corticomedullary junction, and the extracellular matrix.In contrast, the disease-prone strains studied have unique, abnormal staining of thymic cortexand medulla at both the structural and cellular levels. These phenotypic data suggestthat abnormalities in interactions between developing thymocytes and stromal cells characterizedisease-prone mice.

Author: Yuichi Takeoka, Shao-Yuan Chen, Richard L. Boyd, Koichi Tsuneyama, Nobuhisa Taguchi, Shinji Morita, Hisashi Yago, Seishi Suehiro,

Source: https://www.hindawi.com/


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