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Updated: Aug 9, 2026
Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
Comparative analysis of T-cell costimulation and CD43 activation reveals novel signaling pathways and target genes
Ivan Mattioli1, Oliver Dittrich-Breiholz, Mark Livingstone
1Department of Chemistry and Biochemistry, University of Bern, Freiestr. 3, 3012 Bern, Switzerland.
Abstract:
The CD43 lymphocyte surface receptor is involved in the regulation of lymphocyte adhesion and activation. Many CD43 functions remain controversial or unclear, and it is not known to which extent CD43 signaling pathways are shared with or distinct from those used by the T-cell receptor (TCR). Here, we systematically compared signaling events and target gene expression induced by CD43 or T-cell costimulation in primary human peripheral T cells. These studies identify nuclear factor-kappaB (NF-kappaB) p65 serine 468 as a novel inducible phosphorylation site strongly induced by T-cell costimulation and only weakly triggered by CD43 ligation. We also identified CD43 as a novel Jun N-terminal kinase (JNK) activator and a comprehensive analysis of further signaling events suggests that both stimuli use overlapping but also distinct signaling pathways. Microarray analysis of inflammatory genes shows 1 group of genes coregulated by both stimuli and 2 further groups of target genes affected solely by costimulation or primarily by CD43.
Insights
CD43 and T-cell receptor (TCR) signaling pathways in human T cells were compared. While both pathways share some signaling events, CD43 uniquely activates Jun N-terminal kinase (JNK) and distinct inflammatory gene expression.
Area of Science:
- Immunology
- Molecular Biology
- Cell Signaling
Background:
- The CD43 lymphocyte surface receptor regulates T cell adhesion and activation.
- CD43 functions and its signaling pathway overlap with the T-cell receptor (TCR) remain incompletely understood.
Purpose of the Study:
- To systematically compare signaling events and target gene expression induced by CD43 versus T-cell costimulation.
- To elucidate the distinct and shared signaling pathways utilized by CD43 and TCR.
Main Methods:
- Primary human peripheral T cells were stimulated via CD43 ligation or T-cell costimulation.
- Analysis included phosphorylation site identification (e.g., NF-kappaB p65), kinase activation (e.g., JNK), and gene expression profiling via microarrays.
Main Results:
- Identified NF-kappaB p65 serine 468 as a novel phosphorylation site strongly induced by T-cell costimulation, but weakly by CD43.
- Demonstrated CD43 as a novel activator of Jun N-terminal kinase (JNK).
- Revealed overlapping yet distinct signaling pathways for CD43 and TCR, with unique inflammatory gene expression profiles for each.
Conclusions:
- CD43 and TCR signaling pathways utilize both shared and distinct molecular mechanisms.
- CD43 engagement uniquely activates JNK and influences specific inflammatory gene sets, differentiating its role from TCR costimulation.
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