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Inhibiting HLA–B27 homodimer–driven immune cell inflammation in spondylarthritis

✍ Scribed by Sravan K. Payeli; Simon Kollnberger; Osiris Marroquin Belaunzaran; Markus Thiel; Kirsty McHugh; Joanna Giles; Jacqueline Shaw; Sascha Kleber; Anna Ridley; Isabel Wong-Baeza; Sarah Keidel; Kimiko Kuroki; Katsumi Maenaka; Andreas Wadle; Christoph Renner; Paul Bowness

Book ID
115550483
Publisher
John Wiley and Sons
Year
2012
Tongue
English
Weight
684 KB
Volume
64
Category
Article
ISSN
0004-3591

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## Abstract ## Objective HLA–B27 is capable of forming in vitro a heavy‐chain homodimer structure lacking β~2~‐microglobulin. We undertook this study to ascertain if patients with spondylarthritis express β~2~‐microglobulin–free HLA–B27 heavy chains in the form of homodimers and receptors for HLA–

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## Abstract ## Objective HLA–B27/human β~2~‐microglobulin–transgenic (B27‐transgenic) rats, a model of spondylarthritis (SpA), develop spontaneous colitis and arthritis under conventional conditions. CD4+ T cells are pivotal in the development of inflammation in B27‐transgenic rats. This study was