The complement receptor 3, CR3 (CD11b/CD18), on T lymphocytes: activation-dependent up-regulation and regulatory
C Wagner1, G M Hänsch, S Stegmaier
1Institut für Immunologie der Universität Heidelberg, Heidelberg, Germany.
European Journal of Immunology
|April 12, 2001
Summary
Complement receptor 3 (CR3) expression increases on T cells upon activation, suggesting a regulatory role in T cell responses. This finding offers new insights into T cell function and CR3
Area of Science:
- Immunology
- Cell Biology
Background:
- Complement receptor 3 (CR3; CD11b/CD18) is primarily found on leukocytes like NK cells, monocytes, and neutrophils.
- While T cells typically express low levels of CD11b, particularly CD8+ cells, its expression can be modulated.
Purpose of the Study:
- To investigate the expression and functional role of CR3 (CD11b/CD18) on T lymphocytes.
- To determine if CR3 expression on T cells is activation-dependent and influences T cell proliferation and cytokine release.
Main Methods:
- Flow cytometry was used to analyze CD11b expression on peripheral T lymphocytes and T cell lines.
- T cell proliferation and IL-2 release were measured following stimulation with anti-CD3/IL-2 or mononuclear cells/mitogen, with and without CR3-targeting antibodies or ligands.
Main Results:
- CD11b expression was significantly upregulated on both CD4+ and CD8+ T cells upon stimulation, reaching up to 28% in peripheral T cells and 90% in T cell lines.
- The majority of CD11b+ T cells also expressed CD56.
- Inhibition of CR3 function using antibodies or ligands suppressed anti-CD3-induced T cell proliferation and IL-2 release, whereas CR3-negative T cell lines were unaffected.
Conclusions:
- T cell expression of CR3 is activation-dependent.
- CR3 plays a regulatory role in T cell proliferation and IL-2 production, highlighting its functional significance in T cell responses.
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