Kirou Kyriakos A, Mavragani Clio P, Crow Mary K
Mary Kirkland Center for Lupus Research, Department of Medicine, Hospital for Special Surgery and Weill Medical College of Cornell University, 535 East 70th Street, New York, NY 10021, USA.
Expert Rev Clin Immunol. 2007 Jul;3(4):579-88. doi: 10.1586/1744666X.3.4.579.
Type I interferon (IFN) has been implicated in the pathogenesis of systemic lupus erythematosus (SLE) since the late 1970s when elevated serum levels were noted in patients with this autoimmune disease. More recently, the ability of SLE sera to induce IFN in normal peripheral blood mononuclear cells has been noted and led to the recognition of RNA/DNA-containing immune complexes as key components of this IFN-inducing factor. Interest in the field grew with the publication of several gene expression studies that documented activation of the type I IFN pathway in patients with SLE. This activation was associated with disease activity and severity. The important implications of these advances for the management of patients with SLE are twofold. First, IFN may be a useful biomarker of disease subtype and activity and, second, IFN is a rational target for therapeutic intervention. Cautious blockade of this pathway might eliminate an important contributor to autoimmunity.
自20世纪70年代末以来，I型干扰素（IFN）就被认为与系统性红斑狼疮（SLE）的发病机制有关，当时人们注意到这种自身免疫性疾病患者的血清水平升高。最近，人们发现SLE血清能够在正常外周血单核细胞中诱导IFN，并导致含有RNA/DNA的免疫复合物被确认为这种IFN诱导因子的关键成分。随着几项基因表达研究的发表，该领域的关注度不断提高，这些研究记录了SLE患者I型IFN通路的激活情况。这种激活与疾病活动度和严重程度相关。这些进展对SLE患者管理的重要意义有两个方面。第一，IFN可能是疾病亚型和活动度的有用生物标志物；第二，IFN是治疗干预的合理靶点。谨慎阻断该通路可能消除自身免疫的一个重要促成因素。
