FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2414651307> ?p ?o ?g. }

• W2414651307 endingPage "1661" @default.
• W2414651307 startingPage "1651" @default.
• W2414651307 abstract "There is accumulating evidence to suggest that IgE plays a significant role in autoimmunity. The presence of circulating self-reactive IgE in patients with autoimmune disorders has been long known but, at the same time, largely understudied. However, studies have shown that the increased IgE concentration is not associated with higher prevalence for atopy and allergy in patients with autoimmune diseases, such as systemic lupus erythematosus. IgE-mediated mechanisms are conventionally known to facilitate degranulation of mast cells and basophils and promote TH2 immunity, mechanisms that are not only central to mounting an appropriate defense against parasitic worms, noxious substances, toxins, venoms, and environmental irritants but that also trigger exuberant allergic reactions in patients with allergies. More recently, IgE autoantibodies have been recognized to participate in the self-inflicted damaging immune responses that characterize autoimmunity. Such autoimmune responses include direct damage on tissue-containing autoantigens, activation and migration of basophils to lymph nodes, and, as observed most recently, induction of type 1 interferon responses from plasmacytoid dendritic cells. The importance of IgE as a central pathogenic mechanism in autoimmunity has now been clinically validated by the approval of omalizumab, an anti-IgE mAb, for patients with chronic spontaneous urticaria and for the clinical benefit of patients with bullous pemphigoid. In this review we summarize recent reports describing the prevalence of self-reactive IgE and discuss novel findings that incriminate IgE as central in the pathogenesis of inflammatory autoimmune disorders. There is accumulating evidence to suggest that IgE plays a significant role in autoimmunity. The presence of circulating self-reactive IgE in patients with autoimmune disorders has been long known but, at the same time, largely understudied. However, studies have shown that the increased IgE concentration is not associated with higher prevalence for atopy and allergy in patients with autoimmune diseases, such as systemic lupus erythematosus. IgE-mediated mechanisms are conventionally known to facilitate degranulation of mast cells and basophils and promote TH2 immunity, mechanisms that are not only central to mounting an appropriate defense against parasitic worms, noxious substances, toxins, venoms, and environmental irritants but that also trigger exuberant allergic reactions in patients with allergies. More recently, IgE autoantibodies have been recognized to participate in the self-inflicted damaging immune responses that characterize autoimmunity. Such autoimmune responses include direct damage on tissue-containing autoantigens, activation and migration of basophils to lymph nodes, and, as observed most recently, induction of type 1 interferon responses from plasmacytoid dendritic cells. The importance of IgE as a central pathogenic mechanism in autoimmunity has now been clinically validated by the approval of omalizumab, an anti-IgE mAb, for patients with chronic spontaneous urticaria and for the clinical benefit of patients with bullous pemphigoid. In this review we summarize recent reports describing the prevalence of self-reactive IgE and discuss novel findings that incriminate IgE as central in the pathogenesis of inflammatory autoimmune disorders. Five decades ago, the last of the antibody classes, IgE, was uncovered. Found only in mammals, IgE is the least abundant immunoglobulin isotype. IgE signals through 2 types of Fcε receptors (FcεRs), the high-affinity receptor FcεRI and the low-affinity receptor FcεRII. The role of IgE for host defense is mainly triggering reactions that result in protection against parasitic worms (helminths) and the expulsion of environmental substances that include toxins, venoms, irritants, and xenobiotics. Allergies represent the pathogenic detrimental response of IgE to environmental innocuous substances, commonly referred to as allergens, which in the most severe cases can result in systemic anaphylaxis and death.1Allen J.E. Maizels R.M. Diversity and dialogue in immunity to helminths.Nat Rev Immunol. 2011; 11: 375-388Crossref PubMed Scopus (613) Google Scholar, 2Galli S.J. Tsai M. Piliponsky A.M. The development of allergic inflammation.Nature. 2008; 454: 445-454Crossref PubMed Scopus (1298) Google Scholar, 3Palm N.W. Rosenstein R.K. Medzhitov R. Allergic host defences.Nature. 2012; 484: 465-472Crossref PubMed Scopus (281) Google Scholar In both these cases, IgE recognizes exogenous antigens and triggers an immunologic response associated with mast cell degranulation, which results in release of biogenic amines, lipid mediators, proteases, and cytokines. Increased IgE levels have also been reported in patients with systemic lupus erythematosus (SLE) and other autoimmune disease that are driven by the aberrant production of interferon and self-damaging autoantibodies. SLE has been characterized by a wide spectrum of autoantibodies from all 5 immunoglobulin classes that combine with autoantigens triggering self-targeted immune responses. Autoantibodies to nucleic acid–containing antigens are common in patients with SLE, and they include antibodies that react with DNA directly, nuclear histones, nuclear acidic protein antigens, Smith antigen (Sm), ribonucleoprotein, Sjögren syndrome–related antigen A (SS-A), and Sjögren syndrome–related antigen B (SS-B). The production of these autoantibodies by antibody-secreting plasma B cells fluctuates during the course of the disease and is central to disease pathogenesis. Plasma B cells that arise from B-cell proliferation and differentiation in the presence of B-cell activating factor or IL-6, secrete self-reactive autoantibodies of all subclasses, including IgE. The presence of circulating IgE autoantibodies in patients with SLE and other autoimmune diseases is not a recent discovery, having been described for the first time almost 40 years ago.4Permin H. Wiik A. The prevalence of IgE antinuclear antibodies in rheumatoid arthritis and systemic lupus erythematosus.Acta Pathol Microbiol Scand C. 1978; 86C: 245-249PubMed Google Scholar However, this area of research has made significant strides since its inception. Applying new technologies with improved sensitivities for IgE detection and the use of protein expression libraries has strongly advanced our understanding of IgE autoantibody prevalence and antigen specificity in recent years. In addition, most of the original work had focused on understanding whether IgE autoantibodies trigger allergic responses in patients, a hypothesis that has thus far not gained much traction. Instead, as will be discussed in this review, a number of more recent studies have uncovered that IgE autoantibodies are not just bystanders in patients with autoimmune diseases but rather are active contributors to disease pathogenesis. Research has shown a positive correlation between serum IgE levels and disease activity in patients with SLE compared with control subjects.5Atta A.M. Sousa C.P. Carvalho E.M. Sousa-Atta M.L. Immunoglobulin E and systemic lupus erythematosus.Braz J Med Biol Res. 2004; 37: 1497-1501Crossref PubMed Scopus (36) Google Scholar, 6Laurent J. Lagrue G. Sobel A. Increased serum IgE levels in patients with lupus nephritis.Am J Nephrol. 1986; 6: 413-414Crossref PubMed Scopus (19) Google Scholar, 7Liphaus B.L. Jesus A.A. Silva C.A. Coutinho A. Carneiro-Sampaio M. Increased IgE serum levels are unrelated to allergic and parasitic diseases in patients with juvenile systemic lupus erythematosus.Clinics. 2012; 67: 1275-1280Crossref PubMed Scopus (9) Google Scholar, 8Rebhun J. Quismorio Jr., F. Dubois E. Heiner D.C. Systemic lupus erythematosus activity and IgE.Ann Allergy. 1983; 50: 34-36PubMed Google Scholar Self-reactive IgE autoantibodies have also been described in a number of dermatologic conditions, such as bullous pemphigoid (BP), chronic spontaneous urticaria (CSU), and atopic dermatitis (AD). They either have been shown to specifically bind to self-antigens or to cross-react with environmental substances. Those self-antigens, which share IgE cross-reactivity with environmental allergens, are often referred to as “autoallergens” in the literature. In what capacity and circumstances IgE autoantibodies contribute to disease remains largely obscure, although some of their functions are starting to emerge. Successful clinical trials with omalizumab, a mAb that binds to the Fc portion of IgE and blocks its interaction with FcεR, in patients with CSU clearly indicate a pathogenic function of IgE in CSU. Similarly, patients with BP have been shown to benefit from treatment with omalizumab. Ongoing clinical research and additional clinical studies with anti-IgE therapies might shed additional light on the pathogenic activity of IgE autoantibodies in patients with autoimmune diseases. Here, we will discuss our current understanding of the role of IgE in autoimmunity and propose future areas of research. After the discovery of IgE, the scientific community focused on understanding its physiologic importance for host defense against parasitic infestations and its pathophysiologic role in allergies. However, it was shortly after its discovery that the presence of IgE autoantibodies in patients with rheumatoid arthritis and active SLE was reported, and a role in autoimmunity was postulated.4Permin H. Wiik A. The prevalence of IgE antinuclear antibodies in rheumatoid arthritis and systemic lupus erythematosus.Acta Pathol Microbiol Scand C. 1978; 86C: 245-249PubMed Google Scholar However, initial studies performed measurements of IgE autoantibodies in small cohorts by using methodologies with poor sensitivity, which underreported their prevalence. Furthermore, the incidence of increased IgE levels in patients with allergy and parasitic infestation confounded any studies linking IgE to the pathogenic mechanism of autoimmunity, making this phenomenon understudied and frequently ignored. Recently, a number of studies in diseases like SLE or pemphigus have started to reveal that IgE autoantibodies are more prevalent in autoimmunity than previously suspected, along with emerging evidence that associates IgE autoantibodies with key pathophysiologic mechanisms of autoimmunity. SLE is a syndrome affecting multiple organs, with circulating self-reactive antibodies of complex specificities. Hypergammaglobulinemia and IgG antinuclear antibodies are common laboratory findings in patients with active SLE. Several studies have shown that total IgE levels are also increased, which correlates with more severe disease manifestations.5Atta A.M. Sousa C.P. Carvalho E.M. Sousa-Atta M.L. Immunoglobulin E and systemic lupus erythematosus.Braz J Med Biol Res. 2004; 37: 1497-1501Crossref PubMed Scopus (36) Google Scholar, 6Laurent J. Lagrue G. Sobel A. Increased serum IgE levels in patients with lupus nephritis.Am J Nephrol. 1986; 6: 413-414Crossref PubMed Scopus (19) Google Scholar, 7Liphaus B.L. Jesus A.A. Silva C.A. Coutinho A. Carneiro-Sampaio M. Increased IgE serum levels are unrelated to allergic and parasitic diseases in patients with juvenile systemic lupus erythematosus.Clinics. 2012; 67: 1275-1280Crossref PubMed Scopus (9) Google Scholar, 8Rebhun J. Quismorio Jr., F. Dubois E. Heiner D.C. Systemic lupus erythematosus activity and IgE.Ann Allergy. 1983; 50: 34-36PubMed Google Scholar In studies demonstrating increased serum IgE levels, the frequency of atopy (eczema, allergic rhinitis, and asthma) did not concurrently increase in adult patients.7Liphaus B.L. Jesus A.A. Silva C.A. Coutinho A. Carneiro-Sampaio M. Increased IgE serum levels are unrelated to allergic and parasitic diseases in patients with juvenile systemic lupus erythematosus.Clinics. 2012; 67: 1275-1280Crossref PubMed Scopus (9) Google Scholar, 9Elkayam O. Tamir R. Pick A.I. Wysenbeek A. Serum IgE concentrations, disease activity, and atopic disorders in systemic lupus erythematosus.Allergy. 1995; 50: 94-96PubMed Google Scholar, 10Parks C.G. Biagini R.E. Cooper G.S. Gilkeson G.S. Dooley M.A. Total serum IgE levels in systemic lupus erythematosus and associations with childhood onset allergies.Lupus. 2010; 19: 1614-1622Crossref PubMed Scopus (22) Google Scholar, 11Wozniacka A. Sysa-Jedrzejowska A. Robak E. Samochocki Z. Zak-Prelich M. Allergic diseases, drug adverse reactions and total immunoglobulin E levels in lupus erythematosus patients.Mediators Inflamm. 2003; 12: 95-99Crossref PubMed Scopus (20) Google Scholar Even in patients with SLE with childhood onset of allergies, no association with high total IgE levels was observed.10Parks C.G. Biagini R.E. Cooper G.S. Gilkeson G.S. Dooley M.A. Total serum IgE levels in systemic lupus erythematosus and associations with childhood onset allergies.Lupus. 2010; 19: 1614-1622Crossref PubMed Scopus (22) Google Scholar In fact, all aforementioned studies and information gathered by Morton et al12Morton S. Palmer B. Muir K. Powell R.J. IgE and non-IgE mediated allergic disorders in systemic lupus erythematosus.Ann Rheum Dis. 1998; 57: 660-663Crossref PubMed Scopus (36) Google Scholar cumulatively show that frequencies of food allergy, insect allergy, allergic skin disease, and atopy were remarkably similar between patients with SLE and control subjects. The abnormal increase in IgE levels in patients with SLE prompted further investigation into their specificities. From these studies, it is now clear that at least a fraction of the circulating IgE are self-reactive, with nearly all IgE autoantibodies reported binding directly or indirectly to nucleic acids, as is also the case for the most important IgG autoantibodies found in this disease.13Zhu H. Luo H. Yan M. Zuo X. Li Q.Z. Autoantigen microarray for high-throughput autoantibody profiling in systemic lupus erythematosus.Genomics Proteomics Bioinformatics. 2015; 13: 210-218Crossref PubMed Scopus (64) Google Scholar A study of an SLE cohort that included patients from France and the United States revealed the presence of self-reactive IgE against at least 7 autoantigens, for which 65% of the subjects presented IgE autoantibodies to 1 or more of them (Table I).4Permin H. Wiik A. The prevalence of IgE antinuclear antibodies in rheumatoid arthritis and systemic lupus erythematosus.Acta Pathol Microbiol Scand C. 1978; 86C: 245-249PubMed Google Scholar, 5Atta A.M. Sousa C.P. Carvalho E.M. Sousa-Atta M.L. Immunoglobulin E and systemic lupus erythematosus.Braz J Med Biol Res. 2004; 37: 1497-1501Crossref PubMed Scopus (36) Google Scholar, 14Dema B. Pellefigues C. Hasni S. Gault N. Jiang C. Ricks T.K. et al.Autoreactive IgE is prevalent in systemic lupus erythematosus and is associated with increased disease activity and nephritis.PLoS One. 2014; 9: e90424Crossref PubMed Scopus (91) Google Scholar, 15Henault J. Riggs J.M. Karnell J.L. Liarski V.M. Li J. Shirinian L. et al.Self-reactive IgE exacerbates interferon responses associated with autoimmunity.Nat Immunol. 2016; 17: 196-203Crossref PubMed Scopus (113) Google Scholar, 16Rhyner C. Daigle I. Crameri R. Auto-reactive IgE responses to acidic ribosomal P(2) protein in systemic lupus erythematosus.Allergy. 2011; 66: 1127-1129Crossref PubMed Scopus (6) Google Scholar, 17Hatada Y. Kashiwakura J. Hayama K. Fujisawa D. Sasaki-Sakamoto T. Terui T. et al.Significantly high levels of anti-dsDNA immunoglobulin E in sera and the ability of dsDNA to induce the degranulation of basophils from chronic urticaria patients.Int Arch Allergy Immunol. 2013; 161: 154-158Crossref PubMed Scopus (66) Google Scholar, 18Dopp R. Schmidt E. Chimanovitch I. Leverkus M. Brocker E.B. Zillikens D. IgG4 and IgE are the major immunoglobulins targeting the NC16A domain of BP180 in Bullous pemphigoid: serum levels of these immunoglobulins reflect disease activity.J Am Acad Dermatol. 2000; 42: 577-583Abstract Full Text Full Text PDF PubMed Scopus (153) Google Scholar, 19Iwata Y. Komura K. Kodera M. Usuda T. Yokoyama Y. Hara T. et al.Correlation of IgE autoantibody to BP180 with a severe form of bullous pemphigoid.Arch Dermatol. 2008; 144: 41-48Crossref PubMed Scopus (107) Google Scholar, 20Concha L.B. Chang C.C. Szema A.M. Dattwyler R.J. Carlson H.E. IgE antithyroid antibodies in patients with Hashimoto's disease and chronic urticaria.Allergy Asthma Proc. 2004; 25: 293-296PubMed Google Scholar, 21Atta A.M. Santiago M.B. Guerra F.G. Pereira M.M. Sousa Atta ML. Autoimmune response of IgE antibodies to cellular self-antigens in systemic lupus erythematosus.Int Arch Allergy Immunol. 2010; 152: 401-406Crossref PubMed Scopus (44) Google Scholar, 22Dema B. Charles N. Pellefigues C. Ricks T.K. Suzuki R. Jiang C. et al.Immunoglobulin E plays an immunoregulatory role in lupus.J Exp Med. 2014; 211: 2159-2168Crossref PubMed Scopus (75) Google Scholar, 23Barone C. Bartoloni C. Gentiloni N. Grieco A. Flamini G. Systemic lupus erythematosus with only IgE-class antinuclear antibodies.Arthritis Rheum. 1981; 24: 1441-1443Crossref PubMed Scopus (6) Google Scholar, 24Messingham K.A. Noe M.H. Chapman M.A. Giudice G.J. Fairley J.A. A novel ELISA reveals high frequencies of BP180-specific IgE production in bullous pemphigoid.J Immunol Methods. 2009; 346: 18-25Crossref PubMed Scopus (75) Google Scholar, 25Messingham K.A. Onoh A. Vanderah E.M. Giudice G.J. Fairley J.A. Functional characterization of an IgE-class monoclonal antibody specific for the bullous pemphigoid autoantigen, BP180.Hybridoma (Larchmt). 2012; 31: 111-117Crossref PubMed Scopus (11) Google Scholar, 26Altrichter S. Peter H.J. Pisarevskaja D. Metz M. Martus P. Maurer M. IgE mediated autoallergy against thyroid peroxidase—a novel pathomechanism of chronic spontaneous urticaria?.PLoS One. 2011; 6: e14794Crossref PubMed Scopus (194) Google Scholar The prevalence was even greater within the subgroup of patients with active disease (83%). Levels of IgE specific for double-stranded DNA (dsDNA) showed the most significant association with disease activity and hypocomplementemia.14Dema B. Pellefigues C. Hasni S. Gault N. Jiang C. Ricks T.K. et al.Autoreactive IgE is prevalent in systemic lupus erythematosus and is associated with increased disease activity and nephritis.PLoS One. 2014; 9: e90424Crossref PubMed Scopus (91) Google Scholar This observation is further supported by our own studies showing that in a majority of patients, the level of anti-dsDNA IgE in circulation is a risk factor for SLE activity, independent of the concentration of the dsDNA-specific IgG counterpart.15Henault J. Riggs J.M. Karnell J.L. Liarski V.M. Li J. Shirinian L. et al.Self-reactive IgE exacerbates interferon responses associated with autoimmunity.Nat Immunol. 2016; 17: 196-203Crossref PubMed Scopus (113) Google Scholar All other IgE autoantibodies identified (including those against Sm, SS-A, and SS-B) correlated with disease activity.14Dema B. Pellefigues C. Hasni S. Gault N. Jiang C. Ricks T.K. et al.Autoreactive IgE is prevalent in systemic lupus erythematosus and is associated with increased disease activity and nephritis.PLoS One. 2014; 9: e90424Crossref PubMed Scopus (91) Google Scholar For some of the autoantigens described in patients with SLE, however, it is unclear whether the IgE autoantibodies formed against them are the result of autoimmunity or cross-reaction (molecular mimicry) against an allergen. This is the case for anti-ribosomal P2 IgE, which is found in patients with SLE but is also recognized as a minor allergen in patients with fungal allergy.16Rhyner C. Daigle I. Crameri R. Auto-reactive IgE responses to acidic ribosomal P(2) protein in systemic lupus erythematosus.Allergy. 2011; 66: 1127-1129Crossref PubMed Scopus (6) Google ScholarTable IIgE autoantibodies reported in patients with SLE, RA, CSU, and BPAntigen category∗Antigen category–Nucleic acid category stands for nucleic acids or for proteins that binds to nucleic acids.AntigenDisease associationPrevalenceDisease manifestationPathogenic mechanismPresence of IgG against same antigen?ReferenceNucleic acidsdsDNASLECSUSLE: 40.3% to 56.4%Lupus nephritis III: 67%Lupus nephritis IV: 82%SLE: disease activity,active nephritis,hypocomplementemiaSecretion of IFN-αYes for SLENo for CSU14Dema B. Pellefigues C. Hasni S. Gault N. Jiang C. Ricks T.K. et al.Autoreactive IgE is prevalent in systemic lupus erythematosus and is associated with increased disease activity and nephritis.PLoS One. 2014; 9: e90424Crossref PubMed Scopus (91) Google Scholar, 15Henault J. Riggs J.M. Karnell J.L. Liarski V.M. Li J. Shirinian L. et al.Self-reactive IgE exacerbates interferon responses associated with autoimmunity.Nat Immunol. 2016; 17: 196-203Crossref PubMed Scopus (113) Google Scholar, 17Hatada Y. Kashiwakura J. Hayama K. Fujisawa D. Sasaki-Sakamoto T. Terui T. et al.Significantly high levels of anti-dsDNA immunoglobulin E in sera and the ability of dsDNA to induce the degranulation of basophils from chronic urticaria patients.Int Arch Allergy Immunol. 2013; 161: 154-158Crossref PubMed Scopus (66) Google Scholar, 21Atta A.M. Santiago M.B. Guerra F.G. Pereira M.M. Sousa Atta ML. Autoimmune response of IgE antibodies to cellular self-antigens in systemic lupus erythematosus.Int Arch Allergy Immunol. 2010; 152: 401-406Crossref PubMed Scopus (44) Google Scholar, 22Dema B. Charles N. Pellefigues C. Ricks T.K. Suzuki R. Jiang C. et al.Immunoglobulin E plays an immunoregulatory role in lupus.J Exp Med. 2014; 211: 2159-2168Crossref PubMed Scopus (75) Google ScholarNucleic acidsSmSLE>7.6%Disease activity,active nephritis,hypocomplementemiaNot studiedYes14Dema B. Pellefigues C. Hasni S. Gault N. Jiang C. Ricks T.K. et al.Autoreactive IgE is prevalent in systemic lupus erythematosus and is associated with increased disease activity and nephritis.PLoS One. 2014; 9: e90424Crossref PubMed Scopus (91) Google Scholar, 21Atta A.M. Santiago M.B. Guerra F.G. Pereira M.M. Sousa Atta ML. Autoimmune response of IgE antibodies to cellular self-antigens in systemic lupus erythematosus.Int Arch Allergy Immunol. 2010; 152: 401-406Crossref PubMed Scopus (44) Google ScholarNucleic acidsSS-A/RoSLE>5.6%Disease activity,hypocomplementemiaNot studiedYes14Dema B. Pellefigues C. Hasni S. Gault N. Jiang C. Ricks T.K. et al.Autoreactive IgE is prevalent in systemic lupus erythematosus and is associated with increased disease activity and nephritis.PLoS One. 2014; 9: e90424Crossref PubMed Scopus (91) Google Scholar, 21Atta A.M. Santiago M.B. Guerra F.G. Pereira M.M. Sousa Atta ML. Autoimmune response of IgE antibodies to cellular self-antigens in systemic lupus erythematosus.Int Arch Allergy Immunol. 2010; 152: 401-406Crossref PubMed Scopus (44) Google ScholarNucleic acidsSS-B/LaSLE>3.6%Disease activity,hypocomplementemiaNot studiedYes14Dema B. Pellefigues C. Hasni S. Gault N. Jiang C. Ricks T.K. et al.Autoreactive IgE is prevalent in systemic lupus erythematosus and is associated with increased disease activity and nephritis.PLoS One. 2014; 9: e90424Crossref PubMed Scopus (91) Google Scholar, 21Atta A.M. Santiago M.B. Guerra F.G. Pereira M.M. Sousa Atta ML. Autoimmune response of IgE antibodies to cellular self-antigens in systemic lupus erythematosus.Int Arch Allergy Immunol. 2010; 152: 401-406Crossref PubMed Scopus (44) Google ScholarNucleic acidsAPEXSLE—Active nephritisNot studiedNo14Dema B. Pellefigues C. Hasni S. Gault N. Jiang C. Ricks T.K. et al.Autoreactive IgE is prevalent in systemic lupus erythematosus and is associated with increased disease activity and nephritis.PLoS One. 2014; 9: e90424Crossref PubMed Scopus (91) Google ScholarNucleic acidsMPGSLEActive nephritisNot studiedNo14Dema B. Pellefigues C. Hasni S. Gault N. Jiang C. Ricks T.K. et al.Autoreactive IgE is prevalent in systemic lupus erythematosus and is associated with increased disease activity and nephritis.PLoS One. 2014; 9: e90424Crossref PubMed Scopus (91) Google ScholarNucleic acids?CLIP4SLEActive nephritisNot studiedNo14Dema B. Pellefigues C. Hasni S. Gault N. Jiang C. Ricks T.K. et al.Autoreactive IgE is prevalent in systemic lupus erythematosus and is associated with increased disease activity and nephritis.PLoS One. 2014; 9: e90424Crossref PubMed Scopus (91) Google ScholarNucleic acidsRibosomal P2SLE31%Not studiedYes16Rhyner C. Daigle I. Crameri R. Auto-reactive IgE responses to acidic ribosomal P(2) protein in systemic lupus erythematosus.Allergy. 2011; 66: 1127-1129Crossref PubMed Scopus (6) Google ScholarNucleic acidsANASLE, RASLE: 31.5% to 81%RA: 16% to 60%Not studiedYes4Permin H. Wiik A. The prevalence of IgE antinuclear antibodies in rheumatoid arthritis and systemic lupus erythematosus.Acta Pathol Microbiol Scand C. 1978; 86C: 245-249PubMed Google Scholar, 5Atta A.M. Sousa C.P. Carvalho E.M. Sousa-Atta M.L. Immunoglobulin E and systemic lupus erythematosus.Braz J Med Biol Res. 2004; 37: 1497-1501Crossref PubMed Scopus (36) Google Scholar, 21Atta A.M. Santiago M.B. Guerra F.G. Pereira M.M. Sousa Atta ML. Autoimmune response of IgE antibodies to cellular self-antigens in systemic lupus erythematosus.Int Arch Allergy Immunol. 2010; 152: 401-406Crossref PubMed Scopus (44) Google Scholar, 24Messingham K.A. Noe M.H. Chapman M.A. Giudice G.J. Fairley J.A. A novel ELISA reveals high frequencies of BP180-specific IgE production in bullous pemphigoid.J Immunol Methods. 2009; 346: 18-25Crossref PubMed Scopus (75) Google ScholarNucleic acidsRNPSLE—Secretion of IFN-αNot studied4Permin H. Wiik A. The prevalence of IgE antinuclear antibodies in rheumatoid arthritis and systemic lupus erythematosus.Acta Pathol Microbiol Scand C. 1978; 86C: 245-249PubMed Google Scholar, 5Atta A.M. Sousa C.P. Carvalho E.M. Sousa-Atta M.L. Immunoglobulin E and systemic lupus erythematosus.Braz J Med Biol Res. 2004; 37: 1497-1501Crossref PubMed Scopus (36) Google Scholar, 15Henault J. Riggs J.M. Karnell J.L. Liarski V.M. Li J. Shirinian L. et al.Self-reactive IgE exacerbates interferon responses associated with autoimmunity.Nat Immunol. 2016; 17: 196-203Crossref PubMed Scopus (113) Google Scholar, 21Atta A.M. Santiago M.B. Guerra F.G. Pereira M.M. Sousa Atta ML. Autoimmune response of IgE antibodies to cellular self-antigens in systemic lupus erythematosus.Int Arch Allergy Immunol. 2010; 152: 401-406Crossref PubMed Scopus (44) Google ScholarNucleic acidsNucleosomeSLE—Not studiedNot studied21Atta A.M. Santiago M.B. Guerra F.G. Pereira M.M. Sousa Atta ML. Autoimmune response of IgE antibodies to cellular self-antigens in systemic lupus erythematosus.Int Arch Allergy Immunol. 2010; 152: 401-406Crossref PubMed Scopus (44) Google ScholarProteinBP230 and BP180BP70% to 90%Disease severityMast cell degranulation, cellular inflammation, destruction of hemidesmosomal integrityYes18Dopp R. Schmidt E. Chimanovitch I. Leverkus M. Brocker E.B. Zillikens D. IgG4 and IgE are the major immunoglobulins targeting the NC16A domain of BP180 in Bullous pemphigoid: serum levels of these immunoglobulins reflect disease activity.J Am Acad Dermatol. 2000; 42: 577-583Abstract Full Text Full Text PDF PubMed Scopus (153) Google Scholar, 19Iwata Y. Komura K. Kodera M. Usuda T. Yokoyama Y. Hara T. et al.Correlation of IgE autoantibody to BP180 with a severe form of bullous pemphigoid.Arch Dermatol. 2008; 144: 41-48Crossref PubMed Scopus (107) Google Scholar, 24Messingham K.A. Noe M.H. Chapman M.A. Giudice G.J. Fairley J.A. A novel ELISA reveals high frequencies of BP180-specific IgE production in bullous pemphigoid.J Immunol Methods. 2009; 346: 18-25Crossref PubMed Scopus (75) Google Scholar, 25Messingham K.A. Onoh A. Vanderah E.M. Giudice G.J. Fairley J.A. Functional characterization of an IgE-class monoclonal antibody specific for the bullous pemphigoid autoantigen, BP180.Hybridoma (Larchmt). 2012; 31: 111-117Crossref PubMed Scopus (11) Google ScholarProteinThyroid peroxidaseCSU54%Autoimmune thyroiditisNot studiedYes20Concha L.B. Chang C.C. Szema A.M. Dattwyler R.J. Carlson H.E. IgE antithyroid antibodies in patients with Hashimoto's disease and chronic urticaria.Allergy Asthma Proc. 2004; 25: 293-296PubMed Google Scholar, 26Altrichter S. Peter H.J. Pisarevskaja D. Metz M. Martus P. Maurer M. IgE mediated autoallergy against thyroid peroxidase—a novel pathomechanism of chronic spontaneous urticaria?.PLoS One. 2011; 6: e14794Crossref PubMed Scopus (194) Google ScholarProteinThyroglobulinCSU——Not studiedYes20Concha L.B. Chang C.C. Szema A.M. Dattwyler R.J. Carlson H.E. IgE antithyroid antibodies in patients with Hashimoto's disease and chronic urticaria.Allergy Asthma Proc. 2004; 25: 293-296PubMed Google ScholarANA, Anti-nuclear antibody; APEX, APEX nuclease 1; CLIP4, CAP-Gly domain–containing linker protein family member 4; MPG, N-methylpurine DNA glycosylase; RA, rheumatoid arthritis; RNP, ribonucleoprotein.∗ Antigen category–Nucleic acid category stands for nucleic acids or for proteins that binds to nucleic acids. Open table in a new tab ANA, Anti-nuclear antibody; APEX, APEX nuclease 1; CLIP4, CAP-Gly domain–containing linker protein family member 4; MPG, N-methylpurine DNA glycosylase; RA, rheumatoid arthritis; RNP, ribonucleoprotein. Interestingly, study of the French-American cohort discovered circulating IgE autoantibodies with specificities for 3 new autoantigens: APEX nuclease 1, N-methylpurine DNA glycosylase and CAP-Gly domain-containing linker protein family member 4. These autoantigens were unique in that they seemed specific for eliciting IgE autoantibodies but not autoantibodies of the IgG class.14Dema B. Pellefigues C. Hasni S. Gault N. Jiang C. Ricks T.K. et al.Autoreactive IgE is prevalent in systemic lupus erythematosus and is associated with increased disease activity and nephritis.PLoS One. 2014; 9: e90424Crossref PubMed Scopus (91) Google Scholar This is different from what has been typically described for other autoantigens for which high levels o" @default.
• W2414651307 created "2016-06-24" @default.
• W2414651307 creator A5050735223 @default.
• W2414651307 creator A5055264305 @default.
• W2414651307 creator A5068411928 @default.
• W2414651307 date "2016-06-01" @default.
• W2414651307 modified "2023-10-14" @default.
• W2414651307 title "Role of IgE in autoimmunity" @default.
• W2414651307 cites W1483040325 @default.
• W2414651307 cites W1587763349 @default.
• W2414651307 cites W1607245118 @default.
• W2414651307 cites W1788543171 @default.
• W2414651307 cites W1818618334 @default.
• W2414651307 cites W1876031798 @default.
• W2414651307 cites W1963678526 @default.
• W2414651307 cites W1967434989 @default.
• W2414651307 cites W1970667451 @default.
• W2414651307 cites W1972371826 @default.
• W2414651307 cites W1979381376 @default.
• W2414651307 cites W1979853849 @default.
• W2414651307 cites W1983076900 @default.
• W2414651307 cites W1987632693 @default.
• W2414651307 cites W1988164578 @default.
• W2414651307 cites W1991281849 @default.
• W2414651307 cites W1992361788 @default.
• W2414651307 cites W1993225559 @default.
• W2414651307 cites W1998197974 @default.
• W2414651307 cites W2002082837 @default.
• W2414651307 cites W2002366670 @default.
• W2414651307 cites W2003200425 @default.
• W2414651307 cites W2005884645 @default.
• W2414651307 cites W2006270812 @default.
• W2414651307 cites W2006772331 @default.
• W2414651307 cites W2007589345 @default.
• W2414651307 cites W2007754697 @default.
• W2414651307 cites W2008246278 @default.
• W2414651307 cites W2016896826 @default.
• W2414651307 cites W2018619428 @default.
• W2414651307 cites W2018996778 @default.
• W2414651307 cites W2019285737 @default.
• W2414651307 cites W2020636873 @default.
• W2414651307 cites W2026701592 @default.
• W2414651307 cites W2030243225 @default.
• W2414651307 cites W2030696258 @default.
• W2414651307 cites W2034314827 @default.
• W2414651307 cites W2042606815 @default.
• W2414651307 cites W2043264467 @default.
• W2414651307 cites W2045696999 @default.
• W2414651307 cites W2047803539 @default.
• W2414651307 cites W2048341078 @default.
• W2414651307 cites W2051391180 @default.
• W2414651307 cites W2053111002 @default.
• W2414651307 cites W2053283871 @default.
• W2414651307 cites W2056775918 @default.
• W2414651307 cites W2060438123 @default.
• W2414651307 cites W2070124869 @default.
• W2414651307 cites W2070147998 @default.
• W2414651307 cites W2071578751 @default.
• W2414651307 cites W2081258084 @default.
• W2414651307 cites W2081948292 @default.
• W2414651307 cites W2083694251 @default.
• W2414651307 cites W2084180208 @default.
• W2414651307 cites W2085255857 @default.
• W2414651307 cites W2087395407 @default.
• W2414651307 cites W2091129202 @default.
• W2414651307 cites W2091684082 @default.
• W2414651307 cites W2091714697 @default.
• W2414651307 cites W2093402128 @default.
• W2414651307 cites W2094424038 @default.
• W2414651307 cites W2100866375 @default.
• W2414651307 cites W2103164699 @default.
• W2414651307 cites W2115252063 @default.
• W2414651307 cites W2121663010 @default.
• W2414651307 cites W2128655309 @default.
• W2414651307 cites W2128897354 @default.
• W2414651307 cites W2133852849 @default.
• W2414651307 cites W2135301055 @default.
• W2414651307 cites W2136201313 @default.
• W2414651307 cites W2142693097 @default.
• W2414651307 cites W2144513133 @default.
• W2414651307 cites W2145361353 @default.
• W2414651307 cites W2147482491 @default.
• W2414651307 cites W2153908468 @default.
• W2414651307 cites W2155680621 @default.
• W2414651307 cites W2156414024 @default.
• W2414651307 cites W2157322085 @default.
• W2414651307 cites W2158846398 @default.
• W2414651307 cites W2159421887 @default.
• W2414651307 cites W2168079531 @default.
• W2414651307 cites W2168570572 @default.
• W2414651307 cites W2171494950 @default.
• W2414651307 cites W2218732210 @default.
• W2414651307 cites W222323509 @default.
• W2414651307 cites W2268416727 @default.
• W2414651307 cites W2300982526 @default.
• W2414651307 cites W2308059048 @default.
• W2414651307 cites W2322926965 @default.
• W2414651307 cites W2328847226 @default.

• next