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Outside-to-inside signaling through transmembrane tumor necrosis factor reverses pathologic interleukin-1[beta] production and deficient apoptosis of rheumatoid arthritis monocytes
Arthritis & Rheumatism, 09/01/09

Meusch U et al. – Outside-to-inside signaling through transmembrane TNF after ligation by infliximab inhibits constitutive NF-B activation and suppresses spontaneous IL-1 production by monocytes from patients with RA.

Methods

Peripheral blood monocytes from patients with RA and healthy control subjects were incubated in the presence of anti-TNF antibody or IgG
Annexin V staining, caspase activation, poly(ADP-ribose) polymerase cleavage, and DNA staining with propidium iodide were used to analyze apoptosis
The signaling events elicited in monocytes by infliximab were analyzed by Western blotting and electromobility shift assay

Results

Peripheral blood monocytes from patients with RA were characterized by increased expression of transmembrane TNF, spontaneous in vitro production of interleukin-1 (IL-1), and a decreased rate of spontaneous ex vivo apoptosis
Incubation with infliximab induced significantly increased apoptosis in monocytes from patients with RA but not in monocytes from healthy control subjects
This apoptosis was triggered by reverse signaling of transmembrane TNF after ligation by infliximab and was independent of caspase activation. Instead, transmembrane TNF reverse signaling inhibited the constitutive NF-B activation in RA monocytes, suppressed IL-1 secretion, and normalized spontaneous in vitro apoptosis
This normalization was reversible by the addition of exogenous IL-1

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