Abstract
Systemic lupus erythematosus (SLE) is characterized by multisystem inflammation and production of autoantibodies, which can generate immune complexes and may cause tissue damage through the recognition of an autoantigen. Although many factors have been proposed, such as genetic factors, environmental factors, hormonal action, viruses, and dysregulation of cytokine production, the cause of this disease is not well understood. It has been reported that the levels of interferon (IFN)-α in the sera of some SLE patients are elevated and that IFN-α induces maturation of monocytes into highly active antigen-presenting dendritic cells (DCs). We analyzed the association between IFN-α genotype and the risk of SLE to clarify whether IFN-α plays a central role in susceptibility to SLE. The results showed that no IFN-α genotype was significantly associated with the risk of SLE.
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References
Wallace DJ (2002) The clinical presentation of systemic lupus erythematosus. In: Wallace DJ, Hahn BH (eds) Dubois’ lupus erythematosus, 6th edn. Lippincott Williams & Wilkins, Philadelphia
Rozzo SJ, Allard JD, Choubey D, et al. (2001) Evidence for an interferon-inducible gene, Ifi202, in the susceptibility to systemic lupus. Immunity 15:435–443
Wakeland EK, Liu K, Graham RR, Behrens TW (2001) Delineating the genetic basis of systemic lupus erythematosus. Immunity 15:397–408
Harley JB, Moser KL, Gaffner PM, Berrens TW (1998) The genetics of human systemic lupus erythematosus. Curr Opin Immunol 10:690-696
Vyse TJ, Kotzin BL (1996) Genetic basis of systemic lupus erythematosus. Curr Opin Immunol 8:843-851
De Maeyer E, De Maeyer-Guignard J (1998) Type I interferons. Int Rev Immunol 17:53–73
Ioannou Y, Isenberg DA (2000) Current evidence for the induction of autoimmune rheumatic manifestations by cytokine therapy. Arthritis Rheum 43:1431-1442
Fukuyama S, Kajiwara E, Suzuki M, et al. (2000) Systemic lupus erythematosus after alpha-interferon therapy for chronic hepatitis C: a case report and review of the literature. Am J Gastroenterol 95:310-312
Blanco P, Palicka AK, Gill M, Pascual V, Banchereau J (2001) Induction of dendric cell differentiation by IFN-α in systemic lupus erythematosus. Science 294:1540–1543
Akahoshi M, Ishihara M, Remus N, et al. (2004) Association between IFNA genotype and the risk of sarcoidosis. Hum Genet 114:503–509
Baechler EC, Batliwalla FM, Karypis G, et al. (2003) Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus. Proc Natl Acad Sci U S A 100:2610–2615
Bennett L, Palucka A, Aree E, et al. (2003) Interferon and granulopoiesis signatures in systemic lupus erythematosus blood. J Exp Med 197:711–723
Roberts RM, Liu L, Guo Q, et al. (1998) The evolution of the type I interferons. J Interferon Cytokine Res 18:805-816
Golovleva I, Kandefer-Szerszen M, Beckman L, Lundgren E (1996) Polymorphism in the interferon-α gene family. Am J Hum Genet 59:570-578
Hermann P, Rubio M, Nakajima T, Delespesse G, Sarfati M (1998) IFN-α priming of human monocytes differentially regulates gram-positive and gram-negative bacteria-induced IL-10 release and selectively enhances IL-12p70, CD80, and MHC class I expression. J Immunol 161:2011-2018
Peng SL, Moslehi J, Craft J (1997) Roles of interferon-γ and interleukin-4 in murine lupus. J Clin Invest 99:1936–1946
Acknowledgement
We thank Ms. Yuko Furukawa for her skillful technical assistance. We are especially grateful to Dr. Motosuke Hanada for his encouragement and helpful advice.
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Nakashima, H., Matsuno, S., Akahoshi, M. et al. Association between IFNA genotype and the risk of systemic lupus erythematosus. Clin Rheumatol 24, 38–40 (2005). https://doi.org/10.1007/s10067-004-0966-8
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DOI: https://doi.org/10.1007/s10067-004-0966-8