
Protection of PD-1 against LPS-induced endotoxemia and the underlying mechanism
YANG Li-Fen, HE Fang, ZHANG Jian, YIN Fei
Chinese Journal of Contemporary Pediatrics ›› 2010, Vol. 12 ›› Issue (10) : 812-815.
Protection of PD-1 against LPS-induced endotoxemia and the underlying mechanism
[1]Annane D, Bellissant E, Cavaillon JM. Septic shock [J]. Lancet, 2005, 365 (9453): 63-78.
[2]Karima R, Matsumoto S, Higashi H, Matsushima K. The molecular pathogenesis of endotoxic shock and organ failure [J]. Mol Med Today, 1999, 5 (3): 123-132.
[3]Keir ME, Butte MJ, Freeman GJ, Sharpe AH. PD-1 and its ligands in tolerance and immunity [J]. Annu Rev Immunol, 2008, 26: 677-704.
[4]Sharpe AH, Wherry EJ, Ahmed R, Freeman GJ. The function of programmed cell death 1 and its ligands in regulating autoimmunity and infection [J]. Nat Immunol, 2007, 8 (3): 239-245.
[5]Nishimura H, Honjo T. PD-1: an inhibitory immunoreceptor involved in peripheral tolerance [J]. Trends Immunol, 2002, 22 (5): 265-268.
[6]Nishimura H, Nose M, Hiai H, Minato N, Honjo T. Development of lupus-like autoimmune diseases by disruption of the PD-1 gene encoding an ITIM motif-carrying immunoreceptor [J]. Immunity, 1999, 11 (2): 141-151.
[7]Okazaki T, Tanaka Y, Nishio R, Mitsuiye T, Mizoguchi A, Wang J, et al. Autoantibodies against cardiac troponin I are responsible for dilated cardiomyopathy in PD-1-deficient mice [J]. Nat Med, 2003, 9 (12): 1477-1483.
[8]Nishimura H, Okazaki T, Tanaka Y, Nakatani K, Hara M, Matsumori A, et al. Autoimmune dilated cardiomyopathy in PD-1 receptor-deficient mice [J]. Science, 2001, 291(5502): 319-322.
[9]Zhao Q, Wang X, Nelin LD, Yao Y, Matta R, Manson ME, et al. MAP kinase phosphatase 1 controls innate immune responses and suppresses endotoxic shock [J]. J Exp Med, 2006, 203 (1): 131-140.
[10]Bachmaier K, Toya S, Gao X, Triantafillou T, Garrean S, Park GY, et al. E3 ubiquitin ligase Cblb regulates the acute inflammatory response underlying lung injury [J]. Nat Med, 2007, 13(8): 920-926.
[11]Wynn J, Cornell TT, Wong HR, Shanley TP, Wheeler DS. The host response to sepsis and developmental impact [J]. Pediatrics, 2010, 125 (5): 1031-1041.
[12]Peleg AY, Hooper DC. Hospital-acquired infections due to gram-negative bacteria [J]. N Engl J Med, 2010, 362 (19): 1804-1813.
[13]Gioannini TL, Weiss JP. Regulation of interactions of Gram-negative bacterial endotoxins with mammalian cells [J]. Immunol Res, 2007, 39 (1-3): 249-260.
[14]Janeway CA Jr, Medzhitov R. Innate immune recognition [J]. Annu Rev Immunol, 2002, 20: 197-216.
[15]郭萌, 李冠民, 黄清泉. 细菌内毒素研究进展 [J]. 中国实验动物学报, 2009, 17(5): 397-401.
[16]陈洁, 姜虹. TLR4信号通路与炎性反应 [J]. 医学综述, 2009,15(19): 2902-2904.
[17]Ishida Y, Agata Y, Shibahara K, Honjo T. Induced expression of PD-1, a novel member of the immunoglobulin gene superfamily, upon programmed cell death [J]. EMBO J, 1992, 11 (11): 3887-3895.
[18]Okazaki T, Honjo T. The PD-1-PD-L pathway in immunological tolerance [J]. Trends Immunol, 2006, 27 (4): 195-201.
[19]Prokunina L, Padyukov L, Bennet A, de FU, Wiman B, Prince J, et al. Association of the PD-1.3A allele of the PDCD1 gene in patients with rheumatoid arthritis negative for rheumatoid factor and the shared epitope [J]. Arthritis Rheum, 2004, 50 (6): 1770-1773.
[20]Nielsen C, Hansen D, Husby S, Jacobsen BB, Lillevang ST. Association of a putative regulatory polymorphism in the PD-1 gene with susceptibility to type 1 diabetes [J]. Tissue Antigens, 2003, 62 (6): 492-497.
[21]Kong EK, Prokunina-Olsson L, Wong WH, Lau CS, Chan TM. AlarconRiquelme M, et al. A new haplotype of PDCD1 is associated with rheumatoid arthritis in Hong Kong Chinese [J]. Arthritis Rheum, 2005, 52 (4): 1058-1062.