In both lupus and asthma, NF-kappaB stimulates differentiation of monocytes into dendritic cells
Dendritic cells stimulate the immune system by presenting antigens (foreign particles) to other immune cells and by causing the release of pro-inflammatory cytokines. It is believed that dendritic cells may play an important role in autoimmune disease.
The serum from patients with lupus causes monocytes to transform into dendritic cells and is associated with increased NF-kB activation.
The serum from patients with asthma also causes monocytes to transform into dendritic cells and is associated with increased NF-kB activation.
Inhibition of NF-kB contributes to T cell tolerance – by which is meant tolerance to self. When “tolerant” T cells do not attack self. T cell intolerance may lead to autoimmune disease.
- Something in the blood (sera) of both asthmatic patients and lupus patients is causing monocytes to become dendritic cells and express higher levels of active NF-kappaB.
- Activated NF-kB contributes to the intolerance of T cells, which may lead to autoimmune disease.
- Inhibition of NF-kB contributes to restoration of normal function, both in asthma and in lupus.
Targeted NF-kappaB inhibition of asthmatic serum-mediated human monocyte-derived dendritic cell differentiation in a transendothelial trafficking model.
Summary of the abstract
We have shown that selective inhibition of NF-kB in dendritic cells contributes to T cell tolerance.
Here we demonstrated for the first time that asthmatic serum facilitated monocyte maturation associated with increased NF-kB activation.
Furthermore, selective blockade of NF-kB led to increased cell death and and decreased levels of activated T-cells and IL-12, but not IL-10 in asthmatic serum, accompanied by reduced proliferation of T cells.