Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Dec 15;23(24):15998.
doi: 10.3390/ijms232415998.

Unraveling the Link between Interferon-α and Systemic Lupus Erythematosus: From the Molecular Mechanisms to Target Therapies

Affiliations
Review

Unraveling the Link between Interferon-α and Systemic Lupus Erythematosus: From the Molecular Mechanisms to Target Therapies

Barbara Infante et al. Int J Mol Sci. .

Abstract

Systemic lupus erythematosus (SLE) is a chronic, systemic autoimmune disease with a wide range of clinical expressions. The kidney is often affected, usually within 5 years of the onset of SLE, and lupus nephropathy (LN) carries a high risk for increased morbidity. The clinical heterogeneity of the disease is accompanied by complex disturbances affecting the immune system with inflammation and tissue damage due to loss of tolerance to nuclear antigens and the deposition of immune complexes in tissues. Several studies have reported that in human SLE, there is an important role of the Type-I-interferons (INF) system suggested by the upregulation of INF-inducible genes observed in serial gene expression microarray studies. This review aims to describe the transduction pathways of Type-I-interferons, in particular INFα, and its immune-regulatory function in the pathogenesis of SLE and, in particular, in LN. In addition, recent novelties concerning biologic therapy in LN will be discussed.

Keywords: interferon-α; lupus nephropathy; systemic lupus erytrematosus; type-I interferons.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Summary of the main regulators of INFα in SLE.
Figure 2
Figure 2
Regulation of INFα production by plasmacytoid DCs.

References

    1. Eloranta M.-L., Rönnblom L. Cause and Consequences of the Activated Type I Interferon System in SLE. J. Mol. Med. 2016;94:1103–1110. doi: 10.1007/s00109-016-1421-4. - DOI - PMC - PubMed
    1. Barber M.R.W., Drenkard C., Falasinnu T., Hoi A., Mak A., Kow N.Y., Svenungsson E., Peterson J., Clarke A.E., Ramsey-Goldman R. Global Epidemiology of Systemic Lupus Erythematosus. Nat. Rev. Rheumatol. 2021;17:515–532. doi: 10.1038/s41584-021-00668-1. - DOI - PMC - PubMed
    1. Pons-Estel G.J., Alarcón G.S., Scofield L., Reinlib L., Cooper G.S. Understanding the Epidemiology and Progression of Systemic Lupus Erythematosus. Semin. Arthritis Rheum. 2010;39:257–268. doi: 10.1016/j.semarthrit.2008.10.007. - DOI - PMC - PubMed
    1. Rose T., Dörner T. Drivers of the Immunopathogenesis in Systemic Lupus Erythematosus. Best Pract. Res. Clin. Rheumatol. 2017;31:321–333. doi: 10.1016/j.berh.2017.09.007. - DOI - PubMed
    1. Maselli A., Conti F., Alessandri C., Colasanti T., Barbati C., Vomero M., Ciarlo L., Patrizio M., Spinelli F.R., Ortona E., et al. Low Expression of Estrogen Receptor β in T Lymphocytes and High Serum Levels of Anti-Estrogen Receptor α Antibodies Impact Disease Activity in Female Patients with Systemic Lupus Erythematosus. Biol. Sex Differ. 2016;7:3. doi: 10.1186/s13293-016-0057-y. - DOI - PMC - PubMed

MeSH terms