Expression of CD21 and CD23 during human fetal development
Thornton, Catherine A., Holloway, Judith A. and Warner, John O. (2002) Expression of CD21 and CD23 during human fetal development. Pediatric Research, 52, (2), 245-250. (doi:10.1203/01.PDR.0000023172.89966.50).
Full text not available from this repository.
Neonates produce lower levels of IgE compared with adults. Diminished IL-4 production and impaired up-regulation of CD40L by neonatal T cells could explain this, however other regulators of IgE production, such as CD21 and CD23, could contribute to reduced circulating IgE levels during fetal development. Heparinized blood samples were collected from adults and from the umbilical cord at premature and term births. Whole blood flow cytometry was used to assess the percentage of T (CD3+) and B (CD19+) lymphocytes expressing CD21 and/or CD23 at 26–29 (n = 3), 30–33 (n = 7), 34–37 (n = 5), and >37 (n = 11) wk of gestation, as well as in adults (n = 15). Plasma-soluble CD21 was also measured. At term, the percentage of CD21+ and CD23+ B cells was comparable to the adult, however, the percentage of cells positive for each of these surface antigens was decreased significantly before term. The percentage of T cells expressing CD21 from all gestations was significantly higher than the adult and the percentage positive decreased with increasing gestational age. Conversely, soluble CD21 levels increased with increasing gestation to be comparable to the adult by term. Thus, it is unlikely that altered expression of CD21 and CD23 on B cells contributes to the low level of IgE in the neonatal circulation unless functional differences occur or a lack of processing to the soluble form is important in regulating IgE production. However the abundance of CD21-positive T cells could alter the T- and B-cell interaction necessary for IgE switching by B cells and, thereby, especially with impaired IL-4 production, limit IgE production.
|Subjects:||Q Science > QH Natural history > QH301 Biology
R Medicine > RJ Pediatrics
|Divisions:||University Structure - Pre August 2011 > School of Medicine > Infection, Inflammation and Repair
|Date Deposited:||28 Apr 2006|
|Last Modified:||01 Jun 2011 11:24|
|Contributors:||Thornton, Catherine A. (Author)
Holloway, Judith A. (Author)
Warner, John O. (Author)
|Contact Email Address:||firstname.lastname@example.org|
|RDF:||RDF+N-Triples, RDF+N3, RDF+XML, Browse.|
Actions (login required)