کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3342419 | 1214285 | 2007 | 5 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Anti-alpha-actinin antibodies: A new marker of lupus nephritis Anti-alpha-actinin antibodies: A new marker of lupus nephritis](/preview/png/3342419.png)
The exact role of anti-ds (double stranded) DNA antibodies in the pathogenesis of kidney injury in lupus nephritis remains a focus of continuing investigation. One theory explaining the pathogenicity of anti-dsDNA antibodies in lupus nephritis is direct cross-reactivity with renal antigens. Several years ago, α-actinin was identified as a major cross-reactive target for pathogenic anti-dsDNA antibodies in murine SLE. Indeed, binding of a nephritogenic murine anti-dsDNA antibody was stronger to the α-actinin derived from a lupus prone mouse mesangial cell line as compared to α-actinin in a non-autoimmune mouse mesangial cell line. Furthermore, we recently showed that immunization of non-autoimmune mice with α-actinin induces anti-chromatin antibodies, glomerular IgG deposition and proteinuria. In humans, anti-α-actinin autoantibodies (Ab) were associated with anti-dsDNA Ab in SLE. In those patients, anti-α-actinin rather than anti-dsDNA Ab were significantly associated with glomerulonephritis and disease activity. The anti-α-actinin reactivity was associated with high avidity anti-dsDNA Ab. Moreover, the anti-α-actinin response was related to the actin-binding site of α-actinin. Taken together, these studies indicate that detection of anti-α-actinin Ab, in association with anti-dsDNA Ab, may constitute a new marker in lupus nephritis.
Journal: Autoimmunity Reviews - Volume 6, Issue 7, August 2007, Pages 464–468