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CD30 ligation induces nuclear factor-kappa B activation in human T cell lines
P P McDonald1, M A Cassatella, A Bald
1Department of General Pathology, University of Verona, Italy.
European Journal of Immunology
|October 1, 1995
Summary
Anti-CD30 monoclonal antibodies rapidly activate nuclear factor-kappa B (NF-kappa B) signaling in CD30+ cells. This activation involves NF-kappa B complexes containing p50 and p65 RelA, crucial for short-term cellular responses.
Area of Science:
- Immunology
- Molecular Biology
- Cell Signaling
Background:
- CD30 is a receptor within the tumor necrosis factor/nerve growth factor receptor superfamily.
- CD30 expression is found on certain immune cells, including T helper cells and Hodgkin's disease-derived cell lines.
Purpose of the Study:
- To investigate the effect of agonistic anti-CD30 monoclonal antibodies on nuclear factor-kappa B (NF-kappa B) activation.
- To determine the kinetics and components of NF-kappa B complexes induced by CD30 ligation.
Main Methods:
- Incubation of L540 cells and human T helper clones with agonistic anti-CD30 monoclonal antibodies (mAbs).
- Gel retardation assays to detect NF-kappa B DNA binding activities in nuclear extracts.
- Analysis of NF-kappa B complex composition.
Main Results:
- Agonistic anti-CD30 mAbs rapidly induced NF-kappa B DNA binding activity within 20 minutes, sustained for up to 6 hours.
- An isotype-matched antibody did not induce NF-kappa B activation, confirming specificity.
- NF-kappa B activation correlated with CD30 expression levels on T helper clones.
- Induced NF-kappa B complexes contained p50 NF-kappa B1 and p65 RelA.
Conclusions:
- CD30 ligation triggers rapid and sustained activation of NF-kappa B signaling.
- NF-kappa B nuclear translocation and activation are early cellular responses to CD30 engagement.
- The findings elucidate a key signaling pathway downstream of CD30.