Reduced expression of CD99 and functional disturbance in anencephalic cortical thymocytes

In a significant proportion of cases, anencephaly is associated with thymic enlargement, suggesting a possibility that anencephalic fetuses have a functional disturbance in thymocyte differentiation and development. In this report, we demonstrated that CD99 expression was consistently reduced in cor...

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Bibliographic Details
Published in:Virchows Archiv : an international journal of pathology 1999-05, Vol.434 (5), p.443-449
Main Authors: SHIN, Y. K, LEE, G. K, KOOK, M. C, JUNG, K. C, KIM, J. R, SONG, H. G, PARK, S. H, CHI, J. G
Format: Article
Language:English
Subjects:
12E7 Antigen
Anencephaly - metabolism
Anencephaly - pathology
Antigens, CD - biosynthesis
Antigens, CD - immunology
Apoptosis
Biological and medical sciences
Cell Adhesion Molecules - biosynthesis
Cell Adhesion Molecules - immunology
Cell Aggregation
Down-Regulation
Fetus - pathology
Gestational Age
Humans
Immunohistochemistry
Malformations of the nervous system
Medical sciences
Neurology
T-Lymphocytes - metabolism
T-Lymphocytes - pathology
Thymus Gland - metabolism
Thymus Gland - pathology
Thymus Hyperplasia - metabolism
Thymus Hyperplasia - pathology
Tropical medicine
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Summary:In a significant proportion of cases, anencephaly is associated with thymic enlargement, suggesting a possibility that anencephalic fetuses have a functional disturbance in thymocyte differentiation and development. In this report, we demonstrated that CD99 expression was consistently reduced in cortical thymocytes of all anencephalic fetuses. In addition, the CD99-dependent aggregation of immature cortical thymocytes was almost completely impaired and apoptosis of thymocytes was markedly reduced in several cases. These results are in agreement with previous findings that CD99 regulates the aggregation and apoptosis of various types of cells. These data strongly suggest that functional disturbance of thymocytes and thymic hyperplasia are related to the reduced expression of CD99 molecule in anencephalic fetuses.
ISSN:0945-6317
1432-2307
DOI:10.1007/s004280050364