Clinical and epidemiological research therapy with high-dose steroids; however, the number of patients who received such rescue therapy is probably too low to inﬂuence the ﬁndings. Only one 12-week period of withdrawal was evalu- ated, so the impact of multiple treatment interruptions cannot be determined. However, 12 weeks is felt to be a representative length of withdrawal in clinical practice and is therefore clinically relevant. Furthermore, patients who did not experience any change in disease activity (DAS28 reduction <0.6 from baseline to day 78) were not randomised to the withdrawal period and entered the LTE directly. Such patients could be expected to be at a higher risk of immunogenicity, given the link between clinical response and immunogenicity seen with some biological agents.8 13 14 20 In this study a comparable immunogenicity proﬁle was seen for these patients in the LTE to that seen for patients randomised and treated; this will be examined further in a future report. It should be noted that the analyses presented here are based on as-observed data which are vulnerable to drop-outs. However, patient retention in this study was high. Lastly, the DAS28 results were based on CRP, which may yield higher responses than the DAS28 (erythrocyte sedimentation rate); however, CRP has been well validated as an outcome measure to assess disease activity21 and is increasingly used in clinical trials. In summary, 3-month interruption with subsequent reintro- duction of SC abatacept was associated with overall low immu- nogenicity, a ﬁnding consistent with that found with intravenous abatacept. Furthermore, this stop–start schedule was well toler- ated and did not have a negative effect on efﬁcacy. These ﬁndings are important considerations for the clinical use of SC abatacept. Acknowledgements The authors thank Eve Guichard, Medicus International, for editorial support. Funding This study was sponsored and editorial support funded by Bristol-Myers Squibb. Competing interests JK has received research grants from Bristol-Myers Squibb, Pﬁzer, Abbott, Vertex, Astra Zeneca, Chelsea, Lilly, Roche, Centocor, Merck, Amgen, UCB, Aventis and has participated in speakers’ bureaux for Amgen, Bristol-Myers Squibb, Novartis Pharmaceuticals Corporation and UCB. GG has received research grants from Pﬁzer, Genentech, Roche, Forest, Cephalon, Regeneron, Centocor, Bristol- Myers Squibb and New England Research Associates, has participated in a speakers’ bureau for Bristol-Myers Squibb and has received consulting fees from Bristol-Myers Squibb. IS has received consulting fees and honoraria from, and has participated in a speakers’ bureau for, Bristol-Myers Squibb. MR and IL have no competing interests to declare. CL has received clinical research grants from, and has participated in speakers’ bureaux for, Bristol-Myers Squibb. SG, RP, ID and MP are full-time employees of, and stockholders in, Bristol-Myers Squibb. Ethics approval The study was approved by Institutional Review Board/Independent Ethics Committee and informed consent was given by patients. Provenance and peer review Not commissioned; externally peer reviewed. REFERENCES 1. Haggerty HG, Abbott MA, Reilly TP, et al. Evaluation of immunogenicity of the T cell costimulation modulator abatacept in patients treated for rheumatoid arthritis. J Rheumatol 2007;34:2365–73. 2. Schellekens H. Factors inﬂuencing the immunogenicity of therapeutic proteins. Nephrol Dial Transplant 2005;20(Suppl 6):vi3–9. 3. Emi Aikawa N, de Carvalho JF, Artur Almeida Silva C, et al. 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