Cytokine storm in a phase 1 trial of the anti-CD28 monoclonal antibody TGN1412.

By G. Suntharalingam, M. Perry, S. Ward, S. Brett, A. Castello-Cortes, Michael D. Brunner, N. Panoskaltsis. New England Journal of Medicine, 2006

2,057 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/bd88fcb21b68bee2ff6ddf5b9105dd07c615a36d

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In Immunology

1. I. Mellman
2. J. Bluestone
3. Tasuku Honjo
4. George Coukos
5. Taku Okazaki
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7. G. Moalem-Taylor
8. B. Guy

Citations in the corpus

• The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, positive): “, 2009), although clinical trials with the Treg activator, TGN1412, led to severe adverse effects (Suntharalingam et al., 2006).”
• The Pathogenesis of Sepsis (2011, background): “The potential significance of the B7:CD28 pathway in the innate response was emphasized by a clinical trial (18) of a CD28 monoclonal agonist antibody.”
• PD-1 and PD-1 ligands: from discovery to clinical application. (2007, background): “CTLA-4 and CTLA-4‐Ig fusion protein (abatacept) have proved their efficacy in the treatment of cancer and RA, respectively (121‐124), manipulations of co-stimulatory signals can result in tragic consequences ( 125 ).”
• Current concepts in the diagnosis and management of cytokine release syndrome. (2014, background): “CRS has classically been associated with therapeutic mAb infusions, most notably anti-CD3 (OKT3), anti-CD52 (alemtuzumab),19 anti-CD20 (rituximab), and the CD28 super-agonist, TGN1412.”
• Lost in translation: animal models and clinical trials in cancer treatment. (2014, background): “In the first human clinical trials of TGN1412, the drug caused catastrophic systemic organ failure in patients, despite being administered at a sub-clinical dose that was 500 times lower than the dose found safe in animal studies [18].”
• CD28 costimulation: from mechanism to therapy (2016, background): “The experimental drug TGN1412, which had been shown in pre-clinical animal studies to induce Treg cells, caused systemic release of pro-inflammatory cytokines in six volunteers (Hünig, 2012; Suntharalingam et al., 2006).”