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Báo cáo y học: "CTLA-4 polymorphism and primary Sjögren’s syndrome: authors’ response Corinne Miceli-Richard, Jacques-Eric Gottenberg and Xavier Mariette"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: CTLA-4 polymorphism and primary Sjögren’s syndrome: authors’ response Corinne Miceli-Richard, Jacques-Eric Gottenberg and Xavier Mariette. | Available online http arthritis-research.eom content 9 3 402 Letter CTLA-4 polymorphism and primary Sjogren s syndrome authors response Corinne Miceli-Richard Jacques-Eric Gottenberg and Xavier Mariette Rhumatologie Institut Pour la Santé et la Recherche Médicale INSERM U802 Université Paris-Sud 11 Hôpital Bicêtre Assistance Publique-Hôpitaux de Paris AP-HP Le Kremlin Bicêtre France Corresponding author Xavier Mariette xavier.mariette@bct.aphp.fr Published 5 June 2007 Arthritis Research Therapy 2007 9 402 doi 10.1186 ar2199 This article is online at http arthritis-research.com content 9 3 402 2007 BioMed Central Ltd See related research article by Gottenberg et al. http arthritis-research.com content 9 2 R24 and related letter by Lester et al. http arthritis- research.com content 9 3 401 We thank Dr Lester and colleagues 1 for their interest in our recent article 2 and for their comments. As underlined by Lester and colleagues 1 replication cohorts are of primary importance in genetic association studies. With regard to primary Sjogren s syndrome pSS however it is difficult to collect a very large group of patients and our cohort of pSS patients even though it comprised 281 patients remains somehow of moderate size when compared with other cohorts of patients with closely related auto-immune diseases such as lupus. This observation leads us all to be very careful with the reported findings from pSS genetic association studies. The objective of our discussion was not to suggest that our results could be interpreted meaningfully against those of Downie-Doyle and colleagues 3 but to highlight the fact that contradictory results could be observed if small populations of patients and controls are analyzed. As discussed in our manuscript 2 the at-risk allele found in our first cohort of patients CTLA-4 49A G A has been reported to be protective in various auto-immune diseases. These results naturally prompted us to confirm the findings in a second cohort of patients. The