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Publication Detail
Anti-TNF drives regulatory T cell expansion by paradoxically promoting membrane TNF-TNFRII binding in rheumatoid arthritis
The interplay between inflammatory and regulatory pathways orchestrate an effective immune response that provides protection from pathogens whilst limiting injury to host tissue. TNF is a pivotal inflammatory cytokine but there is conflicting evidence as to whether it boosts or inhibits regulatory T cells (Treg). Here we show that the therapeutic anti-TNF antibody adalimumab, but not the soluble TNF receptor etanercept, paradoxically promoted the interaction between monocytes and Treg isolated from patients with rheumatoid arthritis (RA). Adalimumab bound to monocyte membrane TNF from RA patients and unexpectedly enhanced its expression but also its binding to TNFRII expressed on Treg. As a consequence adalimumab expanded functional Foxp3+ Treg equipped to suppress Th17 through an IL-2/STAT5 dependent mechanism. Our data not only highlight the beneficial effect of membrane TNF on Treg numbers during chronic inflammation but in addition reveals how a therapeutic antibody that is thought to act by simply blocking its target can enhance the regulatory properties of this pro-inflammatory cytokine.
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