A NONDELETIONAL MECHANISM OF PERIPHERAL TOLERANCE IN T-CELL RECEPTOR TRANSGENIC MICE
Details
Publication Year 1991-12,Volume 88,Issue #24,Page 11421-11425
Journal Title
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Publication Type
Journal Article
Abstract
To investigate tolerance to extrathymic self molecules, we produced two groups of transgenic mice: one expressed the major histocompatibility complex molecule H-2K(b) in pancreatic beta-cells, and the other expressed rearranged T-cell receptor genes encoding an anti-H-2K(b) receptor. The transgenic T-cell receptor genes were shown to confer the correct specificity and to be expressed appropriately. T cells bearing this receptor were activated by H-2K(b) in vitro and in vivo, and they underwent negative selection in mice expressing H-2K(b) in the thymus. To determine the fate and function of these anti-H-2K(b) T cells in mice expressing H-2K(b) exclusively in the periphery, the two groups of transgenic mice were mated to produce double transgenic offspring. In these, transgene-expressing T cells were present in both thymus and periphery. Persisting T cells had not down-regulated either their antigen-specific receptors or their CD8 molecules. Despite the persistence of large numbers of potentially reactive T cells, the mice were tolerant of H-2K(b) in that they could not reject H-2K(b)-bearing skin grafts, although they did reject third-party grafts. The results show that peripheral T-cell tolerance, unlike that imposed in the thymus, does not involve deletion of T cells. The existence of T cells bearing receptors specific for self components raises the possibility that aberrant activation of such cells may lead to the development of autoimmune disease.
Publisher
NATL ACAD SCIENCES
Keywords
CLASS-II MHC; PANCREATIC BETA-CELLS; ANTIGEN RECEPTOR; EXPRESSION; MOLECULES; DELETION; REARRANGEMENT; INACTIVATION; SELECTION; GENES
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Creation Date: 1991-12-01 12:00:00
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