Skip to main content

Advertisement

SpringerLink
Log in

Therapeutic Approaches to Type I Interferonopathies

  • Pediatric Rheumatology (S Ozen, Section Editor)
  • Published:
Current Rheumatology Reports Aims and scope Submit manuscript

Abstract

Purpose of Review

To review recent scientific advances and therapeutic approaches in the expanding field of type I interferonopathies.

Summary

Type I interferonopathies represent a genetically and phenotypically heterogenous group of disorders of the innate immune system caused by constitutive activation of antiviral type I interferon (IFN). Clinically, type I interferonopathies are characterized by autoinflammation and varying degrees of autoimmunity or immunodeficiency. The elucidation of the underlying genetic causes has revealed novel cell-intrinsic mechanisms that protect the organism against inappropriate immune recognition of self nucleic acids by cytosolic nucleic acid sensors. The type I IFN system is subject to a tight and complex regulation. Disturbances of its checks and balances can spark an unwanted immune response causing uncontrolled type I IFN signaling. Novel mechanistic insight into pathways that control the type I IFN system is providing opportunities for targeted therapeutic approaches by repurposing drugs such as Janus kinase inhibitors or reverse transcriptase inhibitors.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1
Fig. 2

Similar content being viewed by others

References

Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance

  1. Manthiram K, Zhou Q, Aksentijevich I, Kastner DL. The monogenic autoinflammatory diseases define new pathways in human innate immunity and inflammation. Nat Immunol. 2017;18:832–42.

    Article  PubMed  CAS  Google Scholar 

  2. • Schlee M, Hartmann G. Discriminating self from non-self in nucleic acid sensing. Nat Rev Immunol. 2016;16:566–80. Excellent and comprehensive review on nucleic acid-sensing mechanisms.

    Article  PubMed  CAS  Google Scholar 

  3. Ivashkiv LB, Donlin LT. Regulation of type I interferon responses. Nat Rev Immunol. 2014;14:36–49.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  4. Crow YJ. Type I interferonopathies: a novel set of inborn errors of immunity. Ann N Y Acad Sci. 2011;1238:91–8.

    Article  PubMed  CAS  Google Scholar 

  5. Lee-Kirsch MA. The type I interferonopathies. Annu Rev Med. 2017;68:297–315.

    Article  PubMed  CAS  Google Scholar 

  6. Rodero MP, Tesser A, Bartok E, Rice GI, Della Mina E, Depp M, et al. Type I interferon-mediated autoinflammation due to DNase II deficiency. Nat Commun. 2017;8:2176.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  7. Aicardi J, Goutieres F. A progressive familial encephalopathy in infancy with calcifications of the basal ganglia and chronic cerebrospinal fluid lymphocytosis. Ann Neurol. 1984;15:49–54.

    Article  PubMed  CAS  Google Scholar 

  8. Crow YJ, Chase DS, Lowenstein Schmidt J, Szynkiewicz M, Forte GMA, Gornall HL, et al. Characterization of human disease phenotypes associated with mutations in TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, ADAR, and IFIH1. Am J Med Genet A. 2015;167A:296–312.

    Article  PubMed  CAS  Google Scholar 

  9. Ramantani G, Kohlhase J, Hertzberg C, Innes AM, Engel K, Hunger S, et al. Expanding the phenotypic spectrum of lupus erythematosus in Aicardi-Goutieres syndrome. Arthritis Rheum. 2010;62:1469–77.

    Article  PubMed  CAS  Google Scholar 

  10. Ramantani G, Hausler M, Niggemann P, Wessling B, Guttmann H, Mull M, et al. Aicardi-Goutieres syndrome and systemic lupus erythematosus (SLE) in a 12-year-old boy with SAMHD1 mutations. J Child Neurol. 2011;26:1425–8.

    Article  PubMed  Google Scholar 

  11. Cuadrado E, Vanderver A, Brown KJ, Sandza A, Takanohashi A, Jansen MH, et al. Aicardi–Goutières syndrome harbours abundant systemic and brain-reactive autoantibodies. Ann Rheum Dis. 2014;74:1931–9. https://doi.org/10.1136/annrheumdis-2014-205396.

    Article  PubMed  CAS  Google Scholar 

  12. Rice GI, Forte GM, Szynkiewicz M, Chase DS, Aeby A, Abdel-Hamid MS, et al. Assessment of interferon-related biomarkers in Aicardi-Goutieres syndrome associated with mutations in TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, and ADAR: a case-control study. Lancet Neurol. 2013;12:1159–69.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  13. Crow YJ, Hayward BE, Parmar R, Robins P, Leitch A, Ali M, et al. Mutations in the gene encoding the 3′-5′ DNA exonuclease TREX1 cause Aicardi-Goutieres syndrome at the AGS1 locus. Nat Genet. 2006;38:917–20.

    Article  PubMed  CAS  Google Scholar 

  14. Crow YJ, Leitch A, Hayward BE, Garner A, Parmar R, Griffith E, et al. Mutations in genes encoding ribonuclease H2 subunits cause Aicardi-Goutieres syndrome and mimic congenital viral brain infection. Nat Genet. 2006;38:910–6.

    Article  PubMed  CAS  Google Scholar 

  15. Rice GI, Bond J, Asipu A, Brunette RL, Manfield IW, Carr IM, et al. Mutations involved in Aicardi-Goutieres syndrome implicate SAMHD1 as regulator of the innate immune response. Nat Genet. 2009;41:829–32.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  16. Rice GI, Kasher PR, Forte GM, Mannion NM, Greenwood SM, Szynkiewicz M, et al. Mutations in ADAR1 cause Aicardi-Goutieres syndrome associated with a type I interferon signature. Nat Genet. 2012;44:1243–8.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  17. Rice GI, Del Toro DY, Jenkinson EM, Forte GM, Anderson BH, Ariaudo G, et al. Gain-of-function mutations in IFIH1 cause a spectrum of human disease phenotypes associated with upregulated type I interferon signaling. Nat Genet. 2014;46:503–9.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  18. Yang YG, Lindahl T, Barnes DE. Trex1 exonuclease degrades ssDNA to prevent chronic checkpoint activation and autoimmune disease. Cell. 2007;131:873–86.

    Article  PubMed  CAS  Google Scholar 

  19. •• Wolf C, Rapp A, Berndt N, Staroske W, Schuster M, Dobrick-Mattheuer M, et al. RPA and Rad51 constitute a cell intrinsic mechanism to protect the cytosol from self DNA. Nat Commun. 2016;7:11752. This study demonstrates that TREX1 is a cytosolic tail-anchored DNase lining the outer nuclear membrane to degrade self DNA leaking from the nucleus into the cytosol.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  20. •• Stetson DB, Ko JS, Heidmann T, Medzhitov R. Trex1 prevents cell-intrinsic initiation of autoimmunity. Cell. 2008;134:587–98. This paper demonstrates that self DNA derived from reverse-transcribed retroelements accumulates in TREX1-deficient mice.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  21. Ablasser A, Hemmerling I, Schmid-Burgk JL, Behrendt R, Roers A, Hornung V. TREX1 deficiency triggers cell-autonomous immunity in a cGAS-dependent manner. J Immunol. 2014;192:5993–7.

    Article  PubMed  CAS  Google Scholar 

  22. Gray EE, Treuting PM, Woodward JJ, Stetson DB. Cutting edge: cGAS is required for lethal autoimmune disease in the Trex1-deficient mouse model of Aicardi-Goutieres syndrome. J Immunol. 2015;195:1939–43.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  23. Reijns MA, Rabe B, Rigby RE, Mill P, Astell KR, Lettice LA, et al. Enzymatic removal of ribonucleotides from DNA is essential for mammalian genome integrity and development. Cell. 2012;149:1008–22.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  24. Hiller B, Achleitner M, Glage S, Naumann R, Behrendt R, Roers A. Mammalian RNase H2 removes ribonucleotides from DNA to maintain genome integrity. J Exp Med. 2012;209:1419–26.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  25. Sparks JL, Chon H, Cerritelli SM, Kunkel TA, Johansson E, Crouch RJ, et al. RNase H2-initiated ribonucleotide excision repair. Mol Cell. 2012;47:980–6.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  26. Kind B, Muster B, Staroske W, Herce HD, Sachse R, Rapp A, et al. Altered spatio-temporal dynamics of RNase H2 complex assembly at replication and repair sites in Aicardi-Goutieres syndrome. Hum Mol Genet. 2014;23:5950–60.

    Article  PubMed  CAS  Google Scholar 

  27. Gunther C, Kind B, Reijns MA, Berndt N, Martinez-Bueno M, Wolf C, et al. Defective removal of ribonucleotides from DNA promotes systemic autoimmunity. J Clin Invest. 2015;125:413–24.

    Article  PubMed  Google Scholar 

  28. Mackenzie KJ, Carroll P, Lettice L, Tarnauskaitė Ž, Reddy K, Dix F, et al. Ribonuclease H2 mutations induce a cGAS/STING-dependent innate immune response. EMBO J. 2016;35:831–44.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  29. Pokatayev V, Hasin N, Chon H, Cerritelli SM, Sakhuja K, Ward JM, et al. RNase H2 catalytic core Aicardi-Goutières syndrome-related mutant invokes cGAS-STING innate immune-sensing pathway in mice. J Exp Med. 2016;213:329–36.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  30. Goldstone DC, Ennis-Adeniran V, Hedden JJ, Groom HC, Rice GI, Christodoulou E, et al. HIV-1 restriction factor SAMHD1 is a deoxynucleoside triphosphate triphosphohydrolase. Nature. 2011;480:379–82.

    Article  PubMed  CAS  Google Scholar 

  31. Lahouassa H, Daddacha W, Hofmann H, Ayinde D, Logue EC, Dragin L, et al. SAMHD1 restricts the replication of human immunodeficiency virus type 1 by depleting the intracellular pool of deoxynucleoside triphosphates. Nat Immunol. 2012;13:223–8.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  32. Tungler V, Staroske W, Kind B, Dobrick M, Kretschmer S, Schmidt F, et al. Single-stranded nucleic acids promote SAMHD1 complex formation. J Mol Med (Berl). 2013;91:759–70.

    Article  CAS  Google Scholar 

  33. Beloglazova N, Flick R, Tchigvintsev A, Brown G, Popovic A, Nocek B, et al. Nuclease activity of the human SAMHD1 protein implicated in the Aicardi-Goutieres syndrome and HIV-1 restriction. J Biol Chem. 2013;288:8101–10.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  34. Ryoo J, Choi J, Oh C, Kim S, Seo M, Kim SY, et al. The ribonuclease activity of SAMHD1 is required for HIV-1 restriction. Nat Med. 2014;20:936–41.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  35. Kretschmer S, Wolf C, Konig N, Staroske W, Guck J, Hausler M, et al. SAMHD1 prevents autoimmunity by maintaining genome stability. Ann Rheum Dis. 2014;

  36. Clifford R, Louis T, Robbe P, Ackroyd S, Burns A, Timbs AT, et al. SAMHD1 is mutated recurrently in chronic lymphocytic leukemia and is involved in response to DNA damage. Blood. 2014;123:1021–31.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  37. Liddicoat BJ, Piskol R, Chalk AM, Ramaswami G, Higuchi M, Hartner JC, et al. RNA editing by ADAR1 prevents MDA5 sensing of endogenous dsRNA as nonself. Science. 2015;349:1115–20.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  38. Lee-Kirsch MA, Gong M, Schulz H, Ruschendorf F, Stein A, Pfeiffer C, et al. Familial chilblain lupus, a monogenic form of cutaneous lupus erythematosus, maps to chromosome 3p. Am J Hum Genet. 2006;79:731–7.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  39. Rice G, Newman WG, Dean J, Patrick T, Parmar R, Flintoff K, et al. Heterozygous mutations in TREX1 cause familial chilblain lupus and dominant Aicardi-Goutieres syndrome. Am J Hum Genet. 2007;80:811–5.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  40. Lee-Kirsch MA, Chowdhury D, Harvey S, Gong M, Senenko L, Engel K, et al. A mutation in TREX1 that impairs susceptibility to granzyme A-mediated cell death underlies familial chilblain lupus. J Mol Med. 2007;85:531–7.

    Article  PubMed  CAS  Google Scholar 

  41. Ravenscroft JC, Suri M, Rice GI, Szynkiewicz M, Crow YJ. Autosomal dominant inheritance of a heterozygous mutation in SAMHD1 causing familial chilblain lupus. Am J Med Genet A. 2011;155A:235–7.

    Article  PubMed  Google Scholar 

  42. •• König N, Fiehn C, Wolf C, Schuster M, Cura Costa E, Tüngler V, et al. Familial chilblain lupus due to a gain-of-function mutation in STING. Ann Rheum Dis. 2016; First description, together with reference [52••], of clinical efficacy of JAK inhibition in type I IFN-mediated autoinflammation.

  43. •• Liu Y, Jesus AA, Marrero B, Yang D, Ramsey SE, Montealegre Sanchez GA, et al. Activated STING in a vascular and pulmonary syndrome. N Engl J Med. 2014;371:507–18. First description of TMEM173 mutations in patients with severe autoinflammation, acral vasculitis, and pulmonary disease. This study also demonstrates suppression of type I IFN activation in patient cells in vitro.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  44. Jeremiah N, Neven B, Gentili M, Callebaut I, Maschalidi S, Stolzenberg MC, et al. Inherited STING-activating mutation underlies a familial inflammatory syndrome with lupus-like manifestations. J Clin Invest. 2014;124:5516–20.

    Article  PubMed  PubMed Central  Google Scholar 

  45. Agarwal AK, Xing C, DeMartino GN, Mizrachi D, Hernandez MD, Sousa AB, et al. PSMB8 encoding the β5i proteasome subunit is mutated in joint contractures, muscle atrophy, microcytic anemia, and panniculitis-induced lipodystrophy syndrome. Am J Hum Genet. 2010;87:866–72.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  46. Liu Y, Ramot Y, Torrelo A, Paller AS, Si N, Babay S, et al. Mutations in proteasome subunit beta type 8 cause chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature with evidence of genetic and phenotypic heterogeneity. Arthritis Rheum. 2012;64:895–907.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  47. Brehm A, Liu Y, Sheikh A, Marrero B, Omoyinmi E, Zhou Q, et al. Additive loss-of-function proteasome subunit mutations in CANDLE/PRAAS patients promote type I IFN production. J Clin Invest. 2015;125:4196–211.

    Article  PubMed  PubMed Central  Google Scholar 

  48. O’Shea JJ, Schwartz DM, Villarino AV, Gadina M, McInnes IB, Laurence A. The JAK-STAT pathway: impact on human disease and therapeutic intervention. Annu Rev Med. 2015;66:311–28.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  49. Assi R, Verstovsek S, Daver N. “JAK-ing” up the treatment of primary myelofibrosis: building better combination strategies. Curr Opin Hematol. 2017;24:115–24.

    Article  PubMed  CAS  Google Scholar 

  50. Jagasia M, Zeiser R, Arbushites M, Delaite P, Gadbaw B, von Bubnoff N. Ruxolitinib for the treatment of patients with steroid-refractory GVHD: an introduction to the REACH trials. Immunotherapy. 2018;10:391–402.

    Article  PubMed  CAS  Google Scholar 

  51. Smolen JS, Landewé R, Bijlsma J, Burmester G, Chatzidionysiou K, Dougados M, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2016 update. Ann Rheum Dis. 2017;76:960–77.

    Article  PubMed  Google Scholar 

  52. •• Frémond M-L, Rodero MP, Jeremiah N, Belot A, Jeziorski E, Duffy D, et al. Efficacy of the Janus kinase 1/2 inhibitor ruxolitinib in the treatment of vasculopathy associated with TMEM173-activating mutations in 3 children. J Allergy Clin Immunol. 2016;138:1752–5. See annotation for reference [42••].

    Article  PubMed  CAS  Google Scholar 

  53. Seo J, Kang J-A, Suh DI, Park E-B, Lee C-R, Choi SA, et al. Tofacitinib relieves symptoms of stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy caused by 2 de novo variants in TMEM173. J Allergy Clin Immunol. 2017;139:1396–1399.e12.

    Article  PubMed  CAS  Google Scholar 

  54. Tüngler V, König N, Günther C, Engel K, Fiehn C, Smitka M, et al. Response to: “JAK inhibition in STING-associated interferonopathy” by Crow et al. Ann Rheum Dis. 2016;75:e76.

    Article  PubMed  Google Scholar 

  55. Sanchez GAM, Reinhardt A, Ramsey S, Wittkowski H, Hashkes PJ, Berkun Y, et al. JAK1/2 inhibition with baricitinib in the treatment of autoinflammatory interferonopathies. J Clin Invest. 2018;pii: 98814. https://doi.org/10.1172/JCI98814. [Epub ahead of print]

  56. Kim H, Brooks KM, Tang CC, Wakim P, Blake M, Brooks SR, et al. Pharmacokinetics, pharmacodynamics, and proposed dosing of the oral JAK1 and JAK2 inhibitor baricitinib in pediatric and young adult CANDLE and SAVI patients. Clin Pharmacol Ther. 2017;

  57. Yan N, Regalado-Magdos AD, Stiggelbout B, Lee-Kirsch MA, Lieberman J. The cytosolic exonuclease TREX1 inhibits the innate immune response to human immunodeficiency virus type 1. Nat Immunol. 2010;11:1005–13.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  58. Kassiotis G, Stoye JP. Immune responses to endogenous retroelements: taking the bad with the good. Nat Rev Immunol. 2016;16:207–19.

    Article  PubMed  CAS  Google Scholar 

  59. • Beck-Engeser GB, Eilat D, Wabl M. An autoimmune disease prevented by anti-retroviral drugs. Retrovirology. 2011;8:91. First description of a therapeutic effect of antiretroviral therapy with RT inhibitors in TREX1-deficient mice.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  60. •• Thomas CA, Tejwani L, Trujillo CA, Negraes PD, Herai RH, Mesci P, et al. Modeling of TREX1-dependent autoimmune disease using human stem cells highlights L1 accumulation as a source of neuroinflammation. Cell Stem Cell. 2017;21:319–331.e8. This study demonstrates enhanced LINE-retroelement activity in human reprogrammed neurons from AGS patients with TREX1 deficiency.

    Article  PubMed  CAS  PubMed Central  Google Scholar 

  61. Ballana E, Esté JA. SAMHD1: at the crossroads of cell proliferation, immune responses, and virus restriction. Trends Microbiol. 2015;23:680–92.

    Article  PubMed  CAS  Google Scholar 

  62. Ahmad S, Mu X, Yang F, Greenwald E, Park JW, Jacob E, et al. Breaching self-tolerance to Alu duplex RNA underlies MDA5-mediated inflammation. Cell. 2018;172:797–810.e13.

    Article  PubMed  CAS  Google Scholar 

  63. •• Achleitner M, Kleefisch M, Hennig A, Peschke K, Polikarpova A, Oertel R, et al. Lack of Trex1 causes systemic autoimmunity despite the presence of antiretroviral drugs. J Immunol Baltim. 2017;199:2261–9. This study demonstrates a lack of therapeutic effect of antiretroviral treatment with RT inhibitors in TREX1-deficient mice.

    Article  CAS  Google Scholar 

  64. Reverse Transcriptase Inhibitors in AGS - Full Text View - ClinicalTrials.gov [Internet]. [cited 2018 Feb 18]. Available from: https://clinicaltrials.gov/ct2/show/NCT02363452.

  65. Lee-Kirsch MA, Gong M, Chowdhury D, Senenko L, Engel K, Lee YA, et al. Mutations in the gene encoding the 3′-5′ DNA exonuclease TREX1 are associated with systemic lupus erythematosus. Nat Genet. 2007;39:1065–7.

    Article  PubMed  CAS  Google Scholar 

  66. Namjou B, Kothari PH, Kelly JA, Glenn SB, Ojwang JO, Adler A, et al. Evaluation of the TREX1 gene in a large multi-ancestral lupus cohort. Genes Immun. 2011;12:270–9.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  67. An J, Briggs TA, Dumax-Vorzet A, Alarcón-Riquelme ME, Belot A, Beresford M, et al. Tartrate-resistant acid phosphatase deficiency in the predisposition to systemic lupus erythematosus. Arthritis Rheumatol. 2017 69(1):131–142. https://doi.org/10.1002/art.39810

  68. Khamashta M, Merrill JT, Werth VP, Furie R, Kalunian K, Illei GG, et al. Sifalimumab, an anti-interferon-α monoclonal antibody, in moderate to severe systemic lupus erythematosus: a randomised, double-blind, placebo-controlled study. Ann Rheum Dis. 2016;75:1909–16.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  69. Furie R, Khamashta M, Merrill JT, Werth VP, Kalunian K, Brohawn P, et al. Anifrolumab, an anti-interferon-α receptor monoclonal antibody, in moderate-to-severe systemic lupus erythematosus. Arthritis Rheumatol Hoboken NJ. 2017;69:376–86.

    Article  CAS  Google Scholar 

  70. Frémond M-L, Uggenti C, Van Eyck L, Melki I, Bondet V, Kitabayashi N, et al. Brief report: blockade of TANK-binding kinase 1/IKKɛ inhibits mutant stimulator of interferon genes (STING)-mediated inflammatory responses in human peripheral blood mononuclear cells. Arthritis Rheumatol Hoboken NJ. 2017;69:1495–501.

    Article  CAS  Google Scholar 

  71. Peschke K, Achleitner M, Frenzel K, Gerbaulet A, Ada SR, Zeller N, et al. Loss of Trex1 in dendritic cells is sufficient to trigger systemic autoimmunity. J Immunol. 2016;197:2157–66.

    Article  PubMed  CAS  Google Scholar 

Download references

Funding

This work was supported by the Deutsche Forschungsgemeinschaft (Clinical Research Unit 249; LE 1074/4-2 to M.L.-K and TU 421/1-2 to V.T.).

Author information

Authors and Affiliations

  1. Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany

    Marc Bienias, Normi Brück, Constanze Griep, Christine Wolf, Stefanie Kretschmer, Barbara Kind, Victoria Tüngler, Reinhard Berner & Min Ae Lee-Kirsch

Authors
  1. Marc Bienias
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Normi Brück
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Constanze Griep
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Christine Wolf
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Stefanie Kretschmer
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Barbara Kind
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Victoria Tüngler
    View author publications

    You can also search for this author in PubMed Google Scholar

  8. Reinhard Berner
    View author publications

    You can also search for this author in PubMed Google Scholar

  9. Min Ae Lee-Kirsch
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Min Ae Lee-Kirsch.

Ethics declarations

Conflict of Interest

The authors declare that they have no conflict of interest.

Human and Animal Rights and Informed Consent

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

Additional information

This article is part of the Topical Collection on Pediatric Rheumatology

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Bienias, M., Brück, N., Griep, C. et al. Therapeutic Approaches to Type I Interferonopathies. Curr Rheumatol Rep 20, 32 (2018). https://doi.org/10.1007/s11926-018-0743-3

Download citation

  • Published:

  • DOI: https://doi.org/10.1007/s11926-018-0743-3

Keywords

Search

Navigation