Involvement of NF-κB Signaling Pathway in the Pathogenesis of Systemic Lupus Erythematosus
Systemic lupus erythematosus is autoimmune disease characterised by a myriad of immune system aberrations that involve B-cells, T-cells, and cells of the monocytic lineage, resulting in polyclonal B-cell activation, increased numbers of antibody producing cells, hypergammaglobulinemia, autoantibody production, and immune complex formation.
It appears that excessive and uncontrolled T-cell help in the differentiation
and activation of autoantibody forming B-cells is probably a final common pathway.
B-cell activation is abnormal in patients with SLE. The number of B-cells at all stages
of activation is increased in the peripheral blood of patients with active SLE.2
Abnormalities in T-cell function are also evident in patients with SLE.
The total number of peripheral blood T-cells is usually reduced,
probably because of the effects of antilymphocyte antibodies
there is a skewing of T-cell function towards B-cell help, leading to
enhanced antibody production.
The NF-κB/Rel family includes NF-κB1, NF-κB2, p65, RelB, and c-Rel.
Most members of this family can homodimerize, as well as form heterodimers with each other.
In addition, the IκB family also includes the precursor proteins of NF-κB1 and NF-κB2, p105
and p100, which contain a C-terminal IκB-like structure and inhibit the nuclear translocation
of specific NF-κB members.
Nephrol Open J. 2016; 2(1): 9-13. doi: 10.17140/NPOJ-2-112