NFKB2 and Associated Diseases
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Overview of NFKB2
In humans, nuclear factor kappa B subunit 2 (NFKB2, also known as NFKB, P52/P100 subunit) is a protein encoded by the NFKB2 gene. Co-translational processing converts the p100 full-length protein of NFKB2 into the p52 active form. Depending on its dimerization partner, NFKB2 can operate as a transcriptional activator or repressor. NFKB2 is a subunit of the transcription factor complex (NF-κB) involved in the non-canonical pathway of NF-κB. Numerous cell types express the NF-κB complex, which serves as the main activator of genes involved in immune response, inflammation, differentiation, cell growth, tumorigenesis, and apoptosis.
NFKB2 in Disease
Ectopic expression of NFKB2 is associated with different diseases such as common variable immunodeficiency and cancer like lymphomagenesis and breast cancer.
- Common variable immunodeficiency
NFKB2 influences human germinal center reaction which further affects the progress of common variable immunodeficiency (CVID). CVID is a primary immune deficiency disease with typical characteristics of low levels of protective antibodies and elevated risk of infections. It has been reported that NFKB2 mutated patients are B cell deficiency before. In patients with truncating mutation of NFKB2, follicular helper and regulatory T cell subsets are decreased significantly. Besides, CXCL13 secreted by follicular helper T cells and proinflammatory cytokines such as IFNγ, IL-17, and IL-10 produced by CD4 T cells are downregulated in mutated patients. Taken together, NFKB2 influences CVID via B cells and germinal center-related T cell subsets.
Fig.1 Reduction of follicular helper and CD4+ regulatory T cells is observed in patients with NFKB2 mutation. (De Leo, 2020)
- Lymphomagenesis
NFKB2 contributes to Myc-related apoptotic response that harnesses lymphomagenesis. Deregulated c-Myc expression is considered a hallmark of several human cancers containing lymphomagenesis. According to the bioinformatics analysis, NFKB2 is a Myc repression target. In an Eμ-Myc transgenic mouse model of human Burkitt lymphoma, oncoprotein Myc inhibits NFKB2 expression at the transcriptional level, which further leads to the reduction of NFKB2 protein. NFKB2 loss contributes to Myc-driven lymphomagenesis in Eμ-Myc transgenic mice via impairing Myc-associated apoptotic response. In summary, NFKB2 can be a target for the treatment of Myc-dependent tumors.
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References
- De Leo, P.; et al. NFKB2 regulates human Tfh and Tfr pool formation and germinal center potential. Clinical Immunology. 2020, 210: 108309.
- Keller U.; et al. Myc suppression of NFKB2 accelerates lymphomagenesis. BMC cancer. 2010, 10: 1-10.
