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Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
T lymphocytes mediate immunologic control of C3 gene expression
M B Goldman1, M A Knovich, J N Goldman
1Department of Medicine, Pennsylvania State University College of Medicine, Hershey.
Immunologic control of C3 gene expression involves T lymphocytes (CD4+ and CD8+). This suppression requires an inducing antibody and is blocked by anti-Thy-1.2, highlighting a complex regulatory network.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Tissue macrophages can immunologically control complement component 3 (C3) gene expression.
- Previous studies indicated that spleen fragment treatment with anti-C3 antibody can achieve C3 gene suppression.
Purpose of the Study:
- To elucidate the cellular requirements for anti-C3 antibody-mediated suppression of C3 gene expression.
- To investigate the role of T lymphocytes and other cellular components in regulating C3 gene expression.
Main Methods:
- Treatment of spleen fragments with anti-C3 antibody.
- Utilized anti-Thy-1.2 monoclonal antibody to block T cell activity.
- Depletion of CD4+ and CD8+ T lymphocyte subpopulations.
- Experimentation with cholera toxin to elevate intracellular cyclic adenosine monophosphate (cAMP) levels.
Main Results:
- C3 suppression necessitates the involvement of both CD4+ and CD8+ T lymphocytes.
- Pretreatment with anti-Thy-1.2 antibody abrogated the suppressive effect of anti-C3 antibody.
- Selective reduction of either CD4+ or CD8+ T cells prevented C3 suppression.
- Elevated intracellular cAMP levels via cholera toxin partially mimicked T cell-mediated suppression.
Conclusions:
- A regulatory network involving specific inducing antibodies and both CD4+ and CD8+ T cell subsets is essential for suppressing C3 gene expression.
- This regulatory mechanism shares similarities with networks controlling murine immunoglobulin allotype suppression.
- The findings reveal a complex interplay between humoral and cellular immunity in regulating complement gene expression.
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