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ApoL1 and the Immune Response of Patients with Systemic Lupus Erythematosus

  • Systemic Lupus Erythematosus (G Tsokos, Section Editor)
  • Published:
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Abstract

Purpose of Review

Systemic lupus erythematosus (SLE) confers up to a 50-fold increased risk of cardiovascular disease (CVD), and African Americans with SLE experience accelerated damage accrual and doubled cardiovascular risk when compared to their European American counterparts.

Recent Findings

Genome-wide association studies have identified a substantial signal at 22q13, now assigned to variation at apolipoprotein L1 (APOL1), which has associated with progressive nondiabetic nephropathy, cardiovascular disease, and many immune-associated renal diseases, including lupus nephritis.

Summary

We contend that alterations in crucial APOL1 intracellular pathways may underpin associated disease states based on structure-functional differences between variant and ancestral forms. While ancestral APOL1 may be a key driver of autophagy, nonconserved primary structure changes result in a toxic gain of function with attenuation of autophagy and an unsupervised pore-forming feature. Thus, the divergent intracellular biological pathways of ancestral and variant APOL1 may explain a worsened prognosis as demonstrated in SLE.

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Acknowledgements

This work was supported by a Rheumatology Research Foundation Scientist Development Award to ADB. Submission fulfills a requirement of the Masters Programs in Clinical Investigation to ADB.

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Correspondence to Ashira D. Blazer.

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This article does not contain any primary studies with human or animal subjects performed by the authors.

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This article is part of the Topical Collection on Systemic Lupus Erythematosus

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Blazer, A.D., Clancy, R.M. ApoL1 and the Immune Response of Patients with Systemic Lupus Erythematosus. Curr Rheumatol Rep 19, 13 (2017). https://doi.org/10.1007/s11926-017-0637-9

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  • DOI: https://doi.org/10.1007/s11926-017-0637-9

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