Open AccessOntogeny and induction of adhesion molecule expression in human fetal intestine
Author(s) -
DOAN A.,
MacDONALD T. T.,
SPENCER J.
Publication year - 1993
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1993.tb05937.x
Subject(s) - lamina propria , cell adhesion molecule , biology , vcam 1 , fetus , immunology , stromal cell , microbiology and biotechnology , cell adhesion , pathology , icam 1 , cell , epithelium , medicine , cancer research , pregnancy , genetics
SUMMARY In this study we examined the distribution of the adhesion molecules ICAM‐1, VCAM‐1 and E‐selectin in human fetal intestine, to determine whether they may have a role in the development of gut‐associated lymphoid tissue. Secondly, we studied the tempo of induction of these molecules after T cell activation in explants of human fetal intestine cultured in vitro . In the fetus from 11 to 20 weeks gestation, endothelial expression of ICAM‐1 and diffuse staining of VCAM‐1 was observed in the lamina propria. In contrast, there was intense expression of ICAM‐1 and VCAM‐1 in the developing Peyer's patches, suggesting that these molecules may be involved in the accumulation or organization of lymphoid tissue in the gut. After T cell activation in fetal intestinal explants, the expression of ICAM‐1 and VCAM‐1 was increased on most endothelial cells, leucocytes, and stromal cells in the lamina propria. Expression was maintained for at least 4 days. In contrast, the induction of E‐selectin was rapid, and the expression was transient, despite the continuing presence of activated T cells and macrophages. This suggests that other factors are required to prevent the down‐regulation of E‐selectin to maintain the sustained expression sometimes observed in vivo .