Faculty Research 1990 - 1999
A comparative analysis of the murine thymic microenvironment in normal, autoimmune, and immunodeficiency states.
Document Type
Article
Publication Date
1997
Keywords
Animal, Antibodies-Monoclonal: im, Autoimmunity, Comparative-Study, Epithelium: im, Extracellular-Matrix, Immunohistochemistry, Immunologic-Deficiency-Syndromes: im, Mice, Mice-Inbred-Strains, Stromal-Cells: im, T-Lymphocytes: im, Thymus Gland
First Page
79
Last Page
89
JAX Source
Dev Immunol 1997;5(2):79-89
Abstract
It is widely accepted that the thymic microenvironment regulates normal thymopoiesis through a highly coordinated and complex series of cellular and cytokine interactions. A direct corollary of this is that abnormalities within the microenvironment could be of etiologic significance in T-cell-based diseases. Our laboratory has developed a large panel of monoclonal antibodies (mAbs) that react specifically with epithelial or nonepithelial markers in the thymus. We have taken advantage of these reagents to characterize the thymic 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, and ALY/NscJcl-aly/aly mice, and littermate control animals. We report herein that control mice, including strains of several backgrounds, have a very consistent phenotypic profile with this panel of monoclonal antibodies, including reactivity with thymic epithelial cells in 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 cortex and medulla at both the structural and cellular levels. These phenotypic data suggest that abnormalities in interactions between developing thymocytes and stromal cells characterize disease-prone mice.
Recommended Citation
Takeoka Y,
Chen SY,
Boyd RL,
Tsuneyama K,
Taguchi N,
Morita S,
Yago H,
Suehiro S,
Ansari AA,
Shultz LD,
Gershwin ME.
A comparative analysis of the murine thymic microenvironment in normal, autoimmune, and immunodeficiency states. Dev Immunol 1997;5(2):79-89