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Multicolor Flow Cytometry Analyses of Cellular Immune Response in Rhesus Macaques
Published on: April 23, 2010
Polymorphism for RhT3, a CD3-like cell surface antigen, expressed on rhesus monkey T lymphocytes.
Immunology
|December 1, 1986
Summary
The FN18 antibody targets RhT3, a rhesus monkey T-cell antigen similar to human CD3. This RhT3 antigen exhibits polymorphism, likely due to an autosomal dominant trait affecting its epitope expression, not causing immunodeficiency.
Area of Science:
- Immunology
- Primate genetics
Background:
- The FN18 monoclonal antibody identifies RhT3, a rhesus monkey homologue of the human CD3 antigen found on mature T cells.
- RhT3 exhibits polymorphism, with FN18 showing reactivity in only a portion of the rhesus monkey population.
Purpose of the Study:
- To investigate the genetic basis and functional implications of RhT3 polymorphism in rhesus monkeys.
- To determine the inheritance pattern and potential association of RhT3 expression with immune status.
Main Methods:
- Immunofluorescent staining of peripheral blood lymphocytes using the FN18 antibody.
- Analysis of RhT3 expression in relation to sex, age, MHC class I expression, and T-cell numbers.
- Family studies to elucidate inheritance patterns.
- Intracellular staining and cell proliferation assays with mitogens.
Main Results:
- FN18 non-reactivity (negative phenotype) was observed in 2.7% of the rhesus monkey population and appeared to be a stable trait.
- RhT3 non-expression was not linked to immunodeficiency, sex, age, or MHC class I expression.
- Family studies suggested an autosomal dominant inheritance pattern for RhT3 expression.
- Functional T-cell assays indicated that RhT3 molecules are present and functional even in FN18 non-reactive animals.
- Intracellular staining revealed polymorphism at the epitope level.
Conclusions:
- RhT3 polymorphism in rhesus monkeys is likely determined by an autosomal dominant gene.
- The observed polymorphism affects the epitope recognized by FN18 and does not impair T-cell function or cause immunodeficiency.
- This finding contributes to understanding T-cell antigen variability in non-human primates.
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