(Journal Article): Development of lupus-like autoimmune diseases by disruption of the PD-1 gene encoding an ITIM motif-carrying immunoreceptor.
 
Nishimura H, Nose M, Hiai H, Minato N, Honjo T (Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Japan.)
 
IN: Immunity 1999; 11(2):141-151
Impact Factor(s) of Immunity: 1.545 (2004), 16.016 (2003), 17.468 (2002), 18.866 (2001)

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ABSTRACT: PD-1, a 55 kDa transmembrane protein containing an immunoreceptor tyrosine-based inhibitory motif, is induced in lymphocytes and monocytic cells following activation. Aged C57BL/6(B6)-PD-1(-/-) congenic mice spontaneously developed characteristic lupus-like proliferative arthritis and glomerulonephritis with predominant IgG3 deposition, which were markedly accelerated by introduction of a Fas mutation (lpr). Introduction of a PD-1 null mutation into the 2C-TCR (anti-H-2Ld) transgenic mice of the H-2(b/d) background resulted in the chronic and systemic graft-versus-host-like disease. Furthermore, CD8+ 2C-TCR+ PD-1(-/-) T cells exhibited markedly augmented proliferation in vitro in response to H-2d allogenic cells. Collectively, it is suggested that PD-1 is involved in the maintenance of peripheral self-tolerance by serving as a negative regulator of immune responses.

TYPE OF PUBLICATION: Original article

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