Association of endogenous anti–interferon‐α autoantibodies with decreased interferon‐pathway and disease activity in patients with systemic lupus erythematosus
dc.contributor.author | Morimoto, Alyssa M. | en_US |
dc.contributor.author | Flesher, Donna Thibault | en_US |
dc.contributor.author | Yang, Jihong | en_US |
dc.contributor.author | Wolslegel, Kristen | en_US |
dc.contributor.author | Wang, Xiangdan | en_US |
dc.contributor.author | Brady, Ann | en_US |
dc.contributor.author | Abbas, Alexander R. | en_US |
dc.contributor.author | Quarmby, Valerie | en_US |
dc.contributor.author | Wakshull, Eric | en_US |
dc.contributor.author | Richardson, Bruce C. | en_US |
dc.contributor.author | Townsend, Michael J. | en_US |
dc.contributor.author | Behrens, Timothy W. | en_US |
dc.date.accessioned | 2011-11-10T15:38:30Z | |
dc.date.available | 2012-10-01T18:34:42Z | en_US |
dc.date.issued | 2011-08 | en_US |
dc.identifier.citation | Morimoto, Alyssa M.; Flesher, Donna Thibault; Yang, Jihong; Wolslegel, Kristen; Wang, Xiangdan; Brady, Ann; Abbas, Alexander R.; Quarmby, Valerie; Wakshull, Eric; Richardson, Bruce; Townsend, Michael J.; Behrens, Timothy W. (2011). "Association of endogenous anti–interferon‐α autoantibodies with decreased interferon‐pathway and disease activity in patients with systemic lupus erythematosus." Arthritis & Rheumatism 63(8): 2407-2415. <http://hdl.handle.net/2027.42/87110> | en_US |
dc.identifier.issn | 0004-3591 | en_US |
dc.identifier.issn | 1529-0131 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/87110 | |
dc.description.abstract | Objective Numerous observations implicate interferon‐α (IFNα) in the pathophysiology of systemic lupus erythematosus (SLE); however, the potential impact of endogenous anti‐IFNα autoantibodies (AIAAs) on IFN‐pathway and disease activity is unclear. The aim of this study was to characterize IFN‐pathway activity and the serologic and clinical profiles of AIAA‐positive patients with SLE. Methods Sera obtained from patients with SLE (n = 49), patients with rheumatoid arthritis (n = 25), and healthy control subjects (n = 25) were examined for the presence of AIAAs, using a biosensor immunoassay. Serum type I IFN bioactivity and the ability of AIAA‐positive sera to neutralize IFNα activity were determined using U937 cells. Levels of IFN‐regulated gene expression in peripheral blood were determined by microarray, and serum levels of BAFF, IFN‐inducible chemokines, and other autoantibodies were measured using immunoassays. Results AIAAs were detected in 27% of the serum samples from patients with SLE, using a biosensor immunoassay. Unsupervised hierarchical clustering analysis identified 2 subgroups of patients, IFN low and IFN high , that differed in the levels of serum type I IFN bioactivity, IFN‐regulated gene expression, BAFF, anti–ribosomal P, and anti‐chromatin autoantibodies, and in AIAA status. The majority of AIAA‐positive patients had significantly lower levels of serum type I IFN bioactivity, reduced downstream IFN‐pathway activity, and lower disease activity compared with the IFN high patients. AIAA‐positive sera were able to effectively neutralize type I IFN activity in vitro. Conclusion Patients with SLE commonly harbor AIAAs. AIAA‐positive patients have lower levels of serum type I IFN bioactivity and evidence for reduced downstream IFN‐pathway and disease activity. AIAAs may influence the clinical course in SLE by blunting the effects produced by IFNα. | en_US |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.title | Association of endogenous anti–interferon‐α autoantibodies with decreased interferon‐pathway and disease activity in patients with systemic lupus erythematosus | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Geriatrics | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Ann Arbor VA Hospital, Ann Arbor, Michigan and University of Michigan, Ann Arbor | en_US |
dc.contributor.affiliationother | Genentech, South San Francisco, California | en_US |
dc.contributor.affiliationother | Amgen, South San Francisco, California | en_US |
dc.contributor.affiliationother | Department of Bioanalytical Research and Development MS‐38, Genentech, 1 DNA Way, South San Francisco, CA 94080 | en_US |
dc.identifier.pmid | 21506093 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/87110/1/30399_ftp.pdf | |
dc.identifier.doi | 10.1002/art.30399 | en_US |
dc.identifier.source | Arthritis & Rheumatism | en_US |
dc.identifier.citedreference | Pestka S, Krause CD, Walter MR. Interferons, interferon‐like cytokines, and their receptors. Immunol Rev 2004; 202: 8 – 32. | en_US |
dc.identifier.citedreference | Ronnblom L, Eloranta ML, Alm GV. The type I interferon system in systemic lupus erythematosus [review]. Arthritis Rheum 2006; 54: 408 – 20. | en_US |
dc.identifier.citedreference | Hooks JJ, Jordan WG, Cuppos T, Montsopoulos TH, Fauci AS, Notkins AL. Multiple interferons in the circulation of patients with systemic lupus erythematosus and vasculitis. Arthritis Rheum 1982; 25: 396 – 400. | en_US |
dc.identifier.citedreference | Preble OT, Black RJ, Friedman RM, Klippel JH, Vilcek J. Systemic lupus erythematosus: presence in human serum of an unusual acid‐labile leukocyte interferon. Science 1982; 216: 429 – 31. | en_US |
dc.identifier.citedreference | Blanco P, Palucka AK, Gill M, Pascual V, Banchereau J. Induction of dendritic cell differentiation by IFN‐α in systemic lupus erythematosus. Science 2001; 294: 1540 – 3. | en_US |
dc.identifier.citedreference | Bengtsson AA, Sturfelt G, Truedsson L, Blomberg J, Alm G, Vallin GH, et al. Activation of type I interferon system in systemic lupus erythematosus correlates with disease activity but not with antiretroviral antibodies. Lupus 2000; 9: 664 – 71. | en_US |
dc.identifier.citedreference | Dall'Era MC, Cardarelli PM, Preston BT, Witte A, Davis JC. Type I interferon correlates with clinical and serologic manifestations of systemic lupus erythematosus. Ann Rheum Dis 2005; 64: 1692 – 7. | en_US |
dc.identifier.citedreference | Kirou KA, Lee C, George S, Louca K, Peterson MG, Crow MK. Activation of the interferon‐α pathway identifies a subgroup of systemic lupus erythematosus patients with distinct serologic features and active disease. Arthritis Rheum 2005; 52: 1491 – 503. | en_US |
dc.identifier.citedreference | Hua J, Kirou K, Lee C, Crow MK. Functional assay of type I interferon in systemic lupus erythematosus plasma and association with anti‐RNA binding protein autoantibodies. Arthritis Rheum 2006; 54: 1906 – 16. | en_US |
dc.identifier.citedreference | Schilling PJ, Kurzrock R, Kantarjian H, Gutterman J, Talpaz M. Development of systemic lupus erythematosus after interferon therapy for chronic myelogenous leukemia. Cancer 1991; 68: 1536 – 7. | en_US |
dc.identifier.citedreference | Mehta ND, Hooberman AL, Vokes EE, Neeley S, Cootler S. 35‐year‐old patient with chronic myelogenous leukemia developing systemic lupus erythematosus after α‐interferon therapy. Am J Hematol 1992; 41: 141. | en_US |
dc.identifier.citedreference | Baechler EC, Barliwalla FM, Karypis G, Gaffney PM, Ortmann WA, Espe KJ, et al. Interferon‐inducible gene expression signature in peripheral blood cells of patients with severe lupus. Proc Natl Acad Sci U S A 2003; 100: 2610 – 5. | en_US |
dc.identifier.citedreference | Bennett L, Palucka AK, Arce E, Cantrell V, Borvak J, Banchereau J, et al. Interferon and granulopoiesis signatures in systemic lupus erythematosus blood. J Exp Med 2003; 197: 711 – 23. | en_US |
dc.identifier.citedreference | Crow MK. Interferon‐α: A new target for therapy in systemic lupus erythematosus? [review]. Arthritis Rheum 2003; 48: 2395 – 301. | en_US |
dc.identifier.citedreference | McBride JM, Wallace DJ, Yao Z, Morimoto A, Jiang J, Maciuca R, et al. Dose‐dependent modulation of interferon regulated genes with administration of single and repeat doses of rontalizumab in a phase I, placebo controlled, double blind, dose escalation study in SLE. Arthritis Rheum 2009; 60 Suppl 10: S775. | en_US |
dc.identifier.citedreference | Yao Y, Richman L, Higgs BW, Morehouse CA, de los Reyes M, Brohawn P, et al. Neutralization of interferon‐α/β–inducible genes and downstream effect in a phase I trial of an anti–interferon‐α monoclonal antibody in systemic lupus erythematosus. Arthritis Rheum 2009; 60: 1785 – 96. | en_US |
dc.identifier.citedreference | Tan EM, Cohen AS, Fries JF, Masi AT, McShane DJ, Rothfield NF, et al. The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 1982; 25: 1271 – 7. | en_US |
dc.identifier.citedreference | Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF, Cooper NS, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988; 31: 315 – 24. | en_US |
dc.identifier.citedreference | Mire‐Sluis AR, Barrett YC, Devanarayan V, Koren E, Liu H, Maia M, et al. Recommendations for the design and optimization of immunoassays used in the detection of host antibodies against biotechnology products. J Immunol Methods 2004; 289: 1 – 16. | en_US |
dc.identifier.citedreference | Eisen MB, Spellman PT, Brown PO, Botstein D. Cluster analysis and display of genome‐wide expression patterns. Proc Natl Acad Sci U S A 1998; 95: 14863 – 8. | en_US |
dc.identifier.citedreference | Saldanha AJ. Java Treeview: extensible visualization of microarray data. Bioinformatics 2004; 20: 3246 – 8. | en_US |
dc.identifier.citedreference | Bombardier C, Gladman DD, Urowitz MB, Caron D, Chang DH, and the Committee on Prognosis Studies in SLE. Derivation of the SLEDAI: a disease activity index for lupus patients. Arthritis Rheum 1992; 35: 630 – 40. | en_US |
dc.identifier.citedreference | Swanson SJ, Ferbas J, Mayeux P, Casadevall N. Evaluation of methods to detect and characterize antibodies against recombinant human erythropoietin. Nephron Clin Pract 2004; 96: 88 – 95. | en_US |
dc.identifier.citedreference | Lofgren JA, Dhandapani S, Pennucci JJ, Abbott CM, Nytych DT, Kaliyaperumal A, et al. Comparing ELISA and surface plasmon resonance for assessing clinical immunogenicity of panitumumab. J Immunol 2007; 178: 7467 – 72. | en_US |
dc.identifier.citedreference | Jabs WJ, Hennig C, Zawatzky R, Kirchner H. Failure to detect antiviral activity in serum and plasma of healthy individuals displaying high activity in ELISA for IFN‐α and IFN‐β. J Interferon Cytokine Res 1999; 19: 463 – 9. | en_US |
dc.identifier.citedreference | Panem S, Check IJ, Henriksen D, Vilcek J. Antibodies to α‐interferon in a patient with systemic lupus erythematosus. J Immunol 1982; 129: 1 – 3. | en_US |
dc.identifier.citedreference | Sibbitt WL, Gibbs DL, Kenny C, Bankhurst AD, Searles RP, Ley KD. Relationship between circulating interferon and anti‐interferon antibodies and impaired natural killer cell activity in systemic lupus erythematosus. Arthritis Rheum 1985; 28: 624 – 9. | en_US |
dc.identifier.citedreference | Von Wussow P, Jakschies D, Hartung K, Deicher H. Presence of interferon and anti‐interferon in patients with systemic lupus erythematosus. Rheumatol Int 1988; 8: 225 – 30. | en_US |
dc.identifier.citedreference | Slavikova M, Schmeisser H, Kontsekova E, Mateicka F, Borecky L, Kontsek P. Incidence of autoantibodies against type I and type II interferons in a cohort of systemic lupus erythematosus patients in Slovakia. J Interferon Cytokine Res 2003; 23: 143 – 7. | en_US |
dc.identifier.citedreference | Litinskiy MB, Nardelli B, Hilbert DM, He B, Schaffer A, Casali P, et al. DCs induce CD40‐independent immunoglobulin class switching through BLyS and APRIL. Nat Immunol 2002; 3: 822 – 9. | en_US |
dc.identifier.citedreference | Gottenberg JE, Cagnard N, Lucchesi C, Letourneur F, Mistou S, Lazure TS, et al. Activation of IFN pathways and plasmacytoid dendritic cell recruitment in target organs of primary Sjogren's syndrome. Proc Natl Acad Sci U S A 2006; 103: 2770 – 5. | en_US |
dc.identifier.citedreference | Mackay F, Woodcock SA, Lawton P, Ambrose C, Baetscher M, Schneider P, et al. Mice transgenic for BAFF develop lymphocytic disorders along with autoimmune manifestations. J Exp Med 1999; 190: 1697 – 710. | en_US |
dc.identifier.citedreference | Petri M, Singh S, Tesfasyone H, Dedrick R, Fry K, Lai PG, et al. Longitudinal expression of type I interferon responsive genes in systemic lupus erythematosus. Lupus 2009; 18: 980 – 9. | en_US |
dc.identifier.citedreference | Stohl W, Metyas S, Tan SM, Cheema GS, Oamar B, Xu D, et al. B Lymphocyte stimulator overexpression in patients with systemic lupus erythematosus. Arthritis Rheum 2003; 48: 3475 – 86. | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
Files in this item
Remediation of Harmful Language
The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.
Accessibility
If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.