Letter to editor
Antidrug antibody (ADA) formation, so-called immunogenicity, is a major issue when using anti–tumor necrosis factor (anti-TNF) therapy to treat patients with immune-mediated inflammatory diseases because it can lead to treatment failure and drug discontinuation. 1 Increasing evidence suggests that pharmacogenomics may help in identifying patients who are more prone to develop ADA to anti-TNF therapy. 2 This is of great clinical significance because preventing measures against immunogenicity should be implemented in these patients, including combination therapy with an immunomodulator (IMM). 3 Cumulative data have shown that HLA-DQ1*05 variants may be associated with a higher risk of developing ADAs to anti-TNF therapy; however, the impact of this on clinical outcomes and how to better prevent immunogenicity in these patients remains unclear.
