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Expression of CD21 and CD23 during human fetal development
Catherine A Thornton1, Judith A Holloway, John O Warner
1Allergy and Inflammation Sciences, School of Medicine, University of Southampton, SO16 6YD, UK. caj@soton.ac.uk
Pediatric Research
|August 1, 2002
Summary
Neonates have lower immunoglobulin E (IgE) due to fewer CD21 and CD23 expressing B cells before term. However, increased CD21 on T cells may also limit IgE production.
Area of Science:
- Immunology
- Neonatal Immunology
- Cellular Immunology
Background:
- Neonates exhibit lower immunoglobulin E (IgE) levels than adults.
- This reduction may be linked to diminished interleukin-4 (IL-4) production and impaired CD40 ligand (CD40L) upregulation by neonatal T cells.
- Other factors like CD21 and CD23 expression on lymphocytes could influence IgE levels during fetal development.
Purpose of the Study:
- To investigate the expression patterns of CD21 and CD23 on T and B lymphocytes in relation to gestational age.
- To assess plasma-soluble CD21 levels across different gestational ages.
- To determine the potential contribution of CD21 and CD23 expression to reduced neonatal IgE levels.
Main Methods:
- Collection of heparinized blood samples from adults and umbilical cords at various gestational ages (premature and term births).
- Whole blood flow cytometry to analyze CD21 and CD23 expression on T (CD3+) and B (CD19+) lymphocytes.
- Measurement of plasma-soluble CD21 concentrations.
Main Results:
- At term, B cell expression of CD21 and CD23 was similar to adults, but significantly lower before term.
- T cells exhibited higher CD21 expression across all gestations compared to adults, decreasing with advancing gestational age.
- Soluble CD21 levels increased with gestation, reaching adult levels by term.
Conclusions:
- Altered CD21 and CD23 expression on B cells is unlikely to be the primary cause of low neonatal IgE, unless functional differences or processing issues are involved.
- The high abundance of CD21-positive T cells in neonates might impair T- and B-cell interactions crucial for IgE switching, potentially limiting IgE production, especially with concurrent IL-4 deficiency.