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Bcl3 Deficiency Leads to Hyperinflammation in Zebrafish
Chengjian Fan1, Nana Ai1,2, Wei Ge1,2
1Department of Biomedical Sciences, Faculty of Health Sciences, University of Macau, Avenida da Universidade, Taipa, Macau SAR, China.
Cells
|December 24, 2025
Summary
B-cell leukemia/lymphoma protein 3 (Bcl3) deficiency in zebrafish impairs immune homeostasis, causing reduced survival and increased susceptibility to infections. Restoring immune balance with dexamethasone improved outcomes, revealing Bcl3
Area of Science:
- Immunology
- Molecular Biology
- Zebrafish Model Systems
Background:
- B-cell leukemia/lymphoma protein 3 (Bcl3) is an IκB family protein regulating NF-κB transcription factors.
- Aberrant Bcl3 activity is linked to various cancers, but its role in immune homeostasis is unclear.
Purpose of the Study:
- To investigate the physiological function of Bcl3 in immune regulation using a zebrafish model.
- To elucidate Bcl3's role in maintaining immune homeostasis and organismal survival.
Main Methods:
- Generation and analysis of Bcl3 knockout zebrafish.
- Histological examination of immune organs (thymus, liver).
- Assessment of immune responses and susceptibility to bacterial/viral infections.
- Measurement of pro-inflammatory cytokine levels (il1b, il6, il8, tnfa).
- Evaluation of treatment with dexamethasone (Dex).
Main Results:
- Bcl3 deficient zebrafish showed growth retardation and reduced survival.
- Absence of Hassall bodies and hepatocellular abnormalities indicated immune organ compromise.
- Enhanced immune responses, increased infection susceptibility, and elevated pro-inflammatory cytokines were observed.
- Dexamethasone treatment reduced inflammation, downregulated cytokines, and improved survival.
Conclusions:
- Bcl3 is a critical regulator of immune activation in vivo.
- Bcl3 plays a vital role in maintaining immune homeostasis and promoting survival.
- Targeting Bcl3 pathways may offer therapeutic potential for inflammatory conditions.
