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Dahle, Charlotte
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Publications (10 of 49) Show all publications
Ahmad, A., Heijke, R., Eriksson, P., Wirestam, L., Kechagias, S., Dahle, C. & Sjöwall, C. (2021). Autoantibodies associated with primary biliary cholangitis are common among patients with systemic lupus erythematosus even in the absence of elevated liver enzymes. Clinical and Experimental Immunology, 203(1), 22-31
Open this publication in new window or tab >>Autoantibodies associated with primary biliary cholangitis are common among patients with systemic lupus erythematosus even in the absence of elevated liver enzymes
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2021 (English)In: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. 203, no 1, p. 22-31Article in journal (Refereed) Published
Abstract [en]

Knowledge of concomitant autoimmune liver diseases (AILD) is more detailed in primary Sjogrens syndrome (pSS) compared to systemic lupus erythematosus (SLE). Herein, the prevalence of autoantibodies associated with autoimmune hepatitis (AIH) and primary biliary cholangitis (PBC) was investigated in stored sera from patients with SLE (n = 280) and pSS (n = 114). Antibodies against mitochondria (AMA), liver-kidney microsomal (LKM) antigen, smooth muscle (SMA) and anti-nuclear antibodies (ANA) were analysed with immunofluorescence microscopy. In addition, AILD-associated autoantibodies were tested with immunoblot. Prior to sampling, eight SLE (2 center dot 9%) and three pSS (2 center dot 6%) cases were diagnosed with AILD. Among SLE-cases without known AILD (n = 272), 26 (9 center dot 6%) had PBC-associated autoantibodies, 15 (5 center dot 5%) AIH-associated autoantibodies (excluding ANA) and one serological overlap. Most subjects with PBC-associated autoantibodies had liver enzymes within reference limits (22 of 27, 81%) or mild laboratory cholestasis (two of 27, 7 center dot 4%), while one fulfilled the diagnostic PBC-criteria. AMA-M2 detected by immunoblot was the most common PBC-associated autoantibody in SLE (20 of 272, 7 center dot 4%). The prevalence of SMA (4 center dot 4%) was comparable with a healthy reference population, but associated with elevated liver enzymes in four of 12 (25%), none meeting AIH-criteria. The patient with combined AIH/PBC-serology had liver enzymes within reference limits. Among pSS cases without known AILD (n = 111), nine (8 center dot 1%) had PBC-associated, 12 (10 center dot 8%) AIH-associated autoantibodies and two overlapped. PBC-associated autoantibodies were found as frequently in SLE as in pSS but were, with few exceptions, not associated with laboratory signs of liver disease. Overall, AILD-associated autoantibodies were predominantly detected by immunoblot and no significant difference in liver enzymes was found between AILD autoantibody-negative and -positive patients.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2021
Keywords
autoantibodies; autoimmune hepatitis; primary biliary cholangitis; Sjogrens syndrome; systemic lupus erythematosus
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:liu:diva-170539 (URN)10.1111/cei.13512 (DOI)000573490000001 ()32910463 (PubMedID)2-s2.0-85091690857 (Scopus ID)
Note

Funding Agencies|Swedish Rheumatism Association; Region ostergotland (ALF grants); Swedish Society of Medicine; King Gustaf Vs 80-year Anniversary foundation; King Gustaf V and Queen Victorias Freemasons foundation

Available from: 2020-10-16 Created: 2020-10-16 Last updated: 2025-02-11Bibliographically approved
Tjernberg, A. R., Woksepp, H., Sandholm, K., Johansson, M., Dahle, C., Ludvigsson, J. F., . . . Ekdahl, K. N. (2020). Celiac disease and complement activation in response to Streptococcus pneumoniae. European Journal of Pediatrics, 179, 133-140
Open this publication in new window or tab >>Celiac disease and complement activation in response to Streptococcus pneumoniae
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2020 (English)In: European Journal of Pediatrics, ISSN 0340-6199, E-ISSN 1432-1076, Vol. 179, p. 133-140Article in journal (Refereed) Published
Abstract [en]

Individuals with celiac disease (CD) are at increased risk of invasive pneumococcal disease (IPD). The aim of this study was to explore whether the complement response to Streptococcus pneumoniae differed according to CD status, and could serve as an explanation for the excess risk of IPD in CD. Twenty-two children with CD and 18 controls, born 1999-2008, were included at Kalmar County Hospital, Sweden. The degree of complement activation was evaluated by comparing levels of activation products C3a and sC5b-9 in plasma incubated for 30 min with Streptococcus pneumoniae and in non-incubated plasma. Complement analyses were performed with enzyme-linked immunosorbent assay (ELISA). Pneumococcal stimulation caused a statistically significant increase in C3a as well as sC5b-9 in both children with CD and controls but there was no difference in response between the groups. After incubation, C3a increased on average 4.6 times and sC5b-9 22 times in both the CD and the control group (p = 0.497 and p = 0.724 respectively). Conclusion: Complement response to Streptococcus pneumoniae seems to be similar in children with and without CD and is thus unlikely to contribute to the increased susceptibility to invasive pneumococcal disease in CD.

Place, publisher, year, edition, pages
SPRINGER, 2020
Keywords
Coeliac; Pneumococcal; Infection; Innate immunity; MBL
National Category
Pediatrics
Identifiers
urn:nbn:se:liu:diva-162327 (URN)10.1007/s00431-019-03490-w (DOI)000494392200001 ()31691001 (PubMedID)
Note

Funding Agencies|Medical Research Council of Southeast Sweden [658741]; Region Kalmar County; Swedish Research CouncilSwedish Research Council [522-2A09-195, 2016-2075-5.1, 2018-04087]; Swedish Celiac Society; Fulbright Commission; Linnaeus University; Norwegian Research CouncilResearch Council of Norway [274332]; Orebro University

Available from: 2019-11-28 Created: 2019-11-28 Last updated: 2021-03-30
Håkansson, I., Ernerudh, J., Vrethem, M., Dahle, C. & Ekdahl, K. N. (2020). Complement activation in cerebrospinal fluid in clinically isolated syndrome and early stages of relapsing remitting multiple sclerosis. Journal of Neuroimmunology, 340, Article ID 577147.
Open this publication in new window or tab >>Complement activation in cerebrospinal fluid in clinically isolated syndrome and early stages of relapsing remitting multiple sclerosis
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2020 (English)In: Journal of Neuroimmunology, ISSN 0165-5728, E-ISSN 1872-8421, Vol. 340, article id 577147Article in journal (Refereed) Published
Abstract [en]

To assess if markers of complement activation are associated with disease activity, C1q, C3, C3a and sC5b-9 levels in plasma and cerebrospinal fluid (CSF) were determined in 41 patients with clinically isolated syndrome (CIS) or remitting multiple sclerosis (RRMS), in a prospective longitudinal four-year cohort study. C1q in CSF (CSF-C1q) was significantly higher in patients than in controls. Baseline CSF-C1q and CSF-C3a correlated with several neuroinflammatory markers and neurofilament light chain levels. Baseline CSF-C3a correlated with the number of T2 lesions at baseline and new T2 lesions during follow-up. Baseline CSF-C3a was also significantly higher in patients with (n = 21) than in patients without (n = 20) signs of disease activity according to the NEDA-3 concept during one year of follow-up (p ≤ .01) Study results support that complement activation is involved in MS pathophysiology and that CSF-C3a carries prognostic information.

Place, publisher, year, edition, pages
Elsevier, 2020
Keywords
Complement system, C1q, C3a, Multiple sclerosis, Clinically isolated syndrome, Disease activity
National Category
Neurology Clinical Medicine Clinical Laboratory Medicine
Identifiers
urn:nbn:se:liu:diva-163143 (URN)10.1016/j.jneuroim.2020.577147 (DOI)000514757300005 ()
Note

Funding agencies:  Medical Research Council of Southeast Sweden (FORSS); NEURO Sweden; Swedish Research CouncilSwedish Research Council [K2013-61X-22310-01-4, 2016-2075-5.1]; ALF grants, Region Ostergotland; Linnaeus University

Available from: 2020-01-16 Created: 2020-01-16 Last updated: 2025-02-18Bibliographically approved
Dadfa, E., Furuhjelm, C., Nilsson, J., Dahle, C. & Garred, P. (2020). Fatal pneumococcus meningitis in a child with complement factor ficolin-3 deficiency [Letter to the editor]. Journal of Allergy and Clinical Immunology: In Practice, 8(2), 778-779
Open this publication in new window or tab >>Fatal pneumococcus meningitis in a child with complement factor ficolin-3 deficiency
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2020 (English)In: Journal of Allergy and Clinical Immunology: In Practice, ISSN 2213-2198, E-ISSN 2213-2201, Vol. 8, no 2, p. 778-779Article in journal, Letter (Other academic) Published
Abstract [en]

n/a

Place, publisher, year, edition, pages
Elsevier, 2020
National Category
Immunology
Identifiers
urn:nbn:se:liu:diva-164038 (URN)10.1016/j.jaip.2019.07.039 (DOI)000512964500055 ()31408713 (PubMedID)2-s2.0-85071333557 (Scopus ID)
Note

Funding Agencies|Danish Research Council for Independent ResearchDet Frie Forskningsrad (DFF) [DFF-6110-00489]; Svend Andersen Research Foundation; Novo Nordisk Research FoundationNovo Nordisk Foundation; Rigshospitalet

Available from: 2020-03-04 Created: 2020-03-04 Last updated: 2021-04-19Bibliographically approved
Tsymala, I., Nigritinou, M., Zeka, B., Schulz, R., Niederschick, F., Matkovic, M., . . . Bradl, M. (2020). Induction of aquaporin 4-reactive antibodies in Lewis rats immunized with aquaporin 4 mimotopes. Acta neuropathologica communications, 8(1), Article ID 49.
Open this publication in new window or tab >>Induction of aquaporin 4-reactive antibodies in Lewis rats immunized with aquaporin 4 mimotopes
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2020 (English)In: Acta neuropathologica communications, E-ISSN 2051-5960, Vol. 8, no 1, article id 49Article in journal (Refereed) Published
Abstract [en]

Most cases of neuromyelitis optica spectrum disorders (NMOSD) harbor pathogenic autoantibodies against the water channel aquaporin 4 (AQP4). Binding of these antibodies to AQP4 on astrocytes initiates damage to these cells, which culminates in the formation of large tissue destructive lesions in the central nervous system (CNS). Consequently, untreated patients may become permanently blind or paralyzed. Studies on the induction and breakage of tolerance to AQP4 could be of great benefit for NMOSD patients. So far, however, all attempts to create suitable animal models by active sensitization have failed. We addressed this challenge and identified peptides, which mimic the conformational AQP4 epitopes recognized by pathogenic antibodies of NMOSD patients. Here we show that these mimotopes can induce the production of AQP4-reactive antibodies in Lewis rats. Hence, our results provide a conceptual framework for the formation of such antibodies in NMOSD patients, and aid to improve immunization strategies for the creation of animal models suitable for tolerance studies in this devastating disease.

Place, publisher, year, edition, pages
BMC, 2020
Keywords
Neuromyelitis optica spectrum disorders; Antibodies; Mimotopes; Aquaporin 4; Infections; Animal model
National Category
Neurosciences
Identifiers
urn:nbn:se:liu:diva-173523 (URN)10.1186/s40478-020-00920-x (DOI)000615216800003 ()32293546 (PubMedID)
Note

Funding Agencies|Else Kroner-Fresenius-Stiftung [2013_A283]; Austrian Science FundAustrian Science Fund (FWF) [P28476-B30, P32699B]; Austrian Ministery of Science, Research and Economy (BIGWIG-MS); Ministry of Education, Culture, Sports, Science and Technology of JapanMinistry of Education, Culture, Sports, Science and Technology, Japan (MEXT)

Available from: 2021-02-21 Created: 2021-02-21 Last updated: 2021-03-30
Frodlund, M., Wetterö, J., Dahle, C., Dahlström, Ö., Skogh, T., Ronnelid, J. & Sjöwall, C. (2020). Longitudinal anti-nuclear antibody (ANA) seroconversion in systemic lupus erythematosus: a prospective study of Swedish cases with recent-onset disease. Clinical and Experimental Immunology, 199(3), 245-254
Open this publication in new window or tab >>Longitudinal anti-nuclear antibody (ANA) seroconversion in systemic lupus erythematosus: a prospective study of Swedish cases with recent-onset disease
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2020 (English)In: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. 199, no 3, p. 245-254Article in journal (Refereed) Published
Abstract [en]

Serum immunoglobulin (Ig)G anti-nuclear antibodies (ANA) detected by indirect immunofluorescence (IF) microscopy remains a hallmark of systemic lupus erythematosus (SLE). Whether or not IF-ANA status varies over time is controversial. We therefore designed a prospective study with longitudinal follow-up of patients with recent-onset SLE. The study population consisted of 54 recently diagnosed SLE cases, all meeting the 1982 American College of Rheumatology (ACR) and/or the 2012 Systemic Lupus International Collaborating Clinics (SLICC) criteria. Clinical follow-up data, including disease activity, organ damage and sera, were collected from clinical onset of SLE and onwards, in most cases yearly (0-96 months). IF-ANA was analysed on human epithelial cells-2 (HEp-2) cells and categorized regarding staining patterns. Using an addressable laser bead assay (FIDIS (TM) Connective profile), we measured IgG-ANA fine specificities against Ro52/SSA, Ro60/SSA, Sjogrens syndrome type B antigen (La/SSB), Smith antigen (Sm), Smith antigen/ribonucleoprotein (Sm/RNP), U1 RNP (U1RNP), dsDNA, ribosomal-P protein and histone. At baseline, all patients were judged ANA-positive at an abnormal titre corresponding to the 95th percentile of healthy blood donors, but seven of 54 patients (13%) lost ANA-positivity over time. Homogeneous (AC-1; 46%) and speckled (AC-4 or 5; 31%) were the most frequently observed patterns at inclusion, whereas 7% switched pattern at least once during follow-up. Established associations between ANA fine specificities and clinical data were confirmed. Levels of anti-Sm/RNP, but not of anti-dsDNA, correlated with clinical disease activity [modified SLE disease activity 2000 (mSLEDAI-2K)]. Our data indicate that a considerable proportion of Swedish patients with SLE lose ANA-positivity over time, whereas consistent staining patterns were frequent. The clinical and mechanistic relevance of ANA seroconversion remains uncertain. Further prospective evaluations in larger SLE populations with more diverse ethnicities are warranted.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2020
Keywords
autoantibodies; autoimmunity; complement; human; systemic lupus erythematosus
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:liu:diva-164196 (URN)10.1111/cei.13402 (DOI)000513952100007 ()31778219 (PubMedID)2-s2.0-85076720021 (Scopus ID)
Note

Funding Agencies|the Swedish Society of Medicine; Swedish Society of Medicine; the County Council of Ostergotland; Swedish Rheumatism Association; the Swedish Rheumatism Association; the King Gustaf V and Queen Victorias Freemasons foundation; the King Gustaf Vs 80-year Anniversary foundation

Available from: 2020-03-11 Created: 2020-03-11 Last updated: 2025-02-11Bibliographically approved
Nilsson, I., Palmer, J., Apostolou, E., Gottfries, C.-G., Rizwan, M., Dahle, C. & Rosén, A. (2020). Metabolic Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Not Due to Anti-mitochondrial Antibodies. Frontiers in Medicine, 7, Article ID 108.
Open this publication in new window or tab >>Metabolic Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Not Due to Anti-mitochondrial Antibodies
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2020 (English)In: Frontiers in Medicine, E-ISSN 2296-858X, Vol. 7, article id 108Article in journal (Refereed) Published
Abstract [en]

Metabolic profiling studies have recently indicated dysfunctional mitochondria in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This includes an impaired function of pyruvate dehydrogenase complex (PDC), possibly driven by serum factor(s), which leads to inadequate adenosine triphosphate generation and excessive lactate accumulation. A reminiscent energy blockade is likely to occur in primary biliary cholangitis (PBC), caused by anti-PDC autoantibodies, as recently proposed. PBC is associated with fatigue and post-exertional malaise, also signifying ME/CFS. We herein have investigated whether ME/CFS patients have autoreactive antibodies that could interfere with mitochondrial function. We found that only 1 of 161 examined ME/CFS patients was positive for anti-PDC, while all PBC patients (15/15) presented significant IgM, IgG, and IgA anti-PDC reactivity, as previously shown. None of fibromyalgia patients (0/14), multiple sclerosis patients (0/29), and healthy blood donors (0/44) controls showed reactivities. Anti-mitochondrial autoantibodies (inner and outer membrane) were negative in ME/CFS cohort. Anti-cardiolipin antibody levels in patients did not differ significantly from healthy blood donors. In conclusion, the impaired mitochondrial/metabolic dysfunction, observed in ME/CFS, cannot be explained by presence of circulating autoantibodies against the tested mitochondrial epitopes.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2020
Keywords
myalgic encephalomyelitis; chronic fatigue syndrome; anti-pyruvate dehydrogenase complex antibodies; PDC; anti-mitochondrial autoantibodies; AMA
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-165479 (URN)10.3389/fmed.2020.00108 (DOI)000526870400001 ()32296708 (PubMedID)2-s2.0-85083316140 (Scopus ID)
Note

Funding Agencies|Swedish ME Association; Solve ME/CFS; Swedish Cancer Association; Open Medicine Foundation (OMF)

Available from: 2020-05-05 Created: 2020-05-05 Last updated: 2025-02-18Bibliographically approved
Enocsson, H., Wirestam, L., Dahle, C., Padyukov, L., Jonsen, A., Urowitz, M. B., . . . Sjöwall, C. (2020). Soluble urokinase plasminogen activator receptor (suPAR) levels predict damage accrual in patients with recent-onset systemic lupus erythematosus. Journal of Autoimmunity, 106, Article ID 102340.
Open this publication in new window or tab >>Soluble urokinase plasminogen activator receptor (suPAR) levels predict damage accrual in patients with recent-onset systemic lupus erythematosus
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2020 (English)In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 106, article id 102340Article in journal (Refereed) Published
Abstract [en]

Objective

The soluble urokinase plasminogen activator receptor (suPAR) has potential as a prognosis and severity biomarker in several inflammatory and infectious diseases. In a previous cross-sectional study, suPAR levels were shown to reflect damage accrual in cases of systemic lupus erythematosus (SLE). Herein, we evaluated suPAR as a predictor of future organ damage in recent-onset SLE.

Methods

Included were 344 patients from the Systemic Lupus International Collaborating Clinics (SLICC) Inception Cohort who met the 1997 American College of Rheumatology classification criteria with 5-years of follow-up data available. Baseline sera from patients and age- and sex-matched controls were assayed for suPAR. Organ damage was assessed annually using the SLICC/ACR damage index (SDI).

Results

The levels of suPAR were higher in patients who accrued damage, particularly those with SDI≥2 at 5 years (N = 32, 46.8% increase, p = 0.004), as compared to patients without damage. Logistic regression analysis revealed a significant impact of suPAR on SDI outcome (SDI≥2; OR = 1.14; 95% CI 1.03–1.26), also after adjustment for confounding factors. In an optimized logistic regression to predict damage, suPAR persisted as a predictor, together with baseline disease activity (SLEDAI-2K), age, and non-Caucasian ethnicity (model AUC = 0.77). Dissecting SDI into organ systems revealed higher suPAR levels in patients who developed musculoskeletal damage (SDI≥1; p = 0.007).

Conclusion

Prognostic biomarkers identify patients who are at risk of acquiring early damage and therefore need careful observation and targeted treatment strategies. Overall, suPAR constitutes an interesting biomarker for patient stratification and for identifying SLE patients who are at risk of acquiring organ damage during the first 5 years of disease.

Place, publisher, year, edition, pages
Elsevier, 2020
Keywords
Biomarker; SLE; Organ damage; Prognosis; Outcome
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-163458 (URN)10.1016/j.jaut.2019.102340 (DOI)000508747000012 ()31629628 (PubMedID)2-s2.0-85073722485 (Scopus ID)
Note

Funding Agencies|Swedish Rheumatism Association; Region Ostergotland (ALF Grants); King Gustaf Vs 80-year Anniversary Foundation; King Gustaf V and Queen Victorias Freemasons Foundation; Versus ArthritisVersus Arthritis; NIHR Manchester Biomedical Research CentreNational Institute for Health Research (NIHR); NIHR/Welcome Trust Manchester Clinical Research Facility; Lupus UK; Sandwell and West Birmingham Hospitals NHS Trust; National Institute for Health Research (NIHR)/Wellcome Trust Birmingham Clinical Research Facility; NIHUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [8UL1TR000150]; National Research Foundation of KoreaNational Research Foundation of Korea [NRF-2017M3A9B4050335]

Available from: 2020-02-17 Created: 2020-02-17 Last updated: 2025-02-18Bibliographically approved
Theodorsson, E., Löwbeer, C., Ridefelt, P., Carlson, M., Dahle, C. & Simonsson, P. (2018). Digestionsorganens sjukdomar (10ed.). In: Laurells klinisk kemi i praktisk medicin: (pp. 465-516). Lund: Studentlitteratur AB
Open this publication in new window or tab >>Digestionsorganens sjukdomar
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2018 (Swedish)In: Laurells klinisk kemi i praktisk medicin, Lund: Studentlitteratur AB, 2018, 10, p. 465-516Chapter in book (Other academic)
Place, publisher, year, edition, pages
Lund: Studentlitteratur AB, 2018 Edition: 10
National Category
Clinical Laboratory Medicine
Identifiers
urn:nbn:se:liu:diva-154593 (URN)9789144119748 (ISBN)
Available from: 2019-02-21 Created: 2019-02-21 Last updated: 2019-02-21
Oji, S., Nicolussi, E.-M., Kaufmann, N., Zeka, B., Schanda, K., Fujihara, K., . . . Bradl, M. (2016). Experimental Neuromyelitis Optica Induces a Type I Interferon Signature in the Spinal Cord. PLOS ONE, 11(3), e0151244
Open this publication in new window or tab >>Experimental Neuromyelitis Optica Induces a Type I Interferon Signature in the Spinal Cord
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2016 (English)In: PLOS ONE, E-ISSN 1932-6203, Vol. 11, no 3, p. e0151244-Article in journal (Refereed) Published
Abstract [en]

Neuromyelitis optica (NMO) is an acute inflammatory disease of the central nervous system (CNS) which predominantly affects spinal cord and optic nerves. Most patients harbor pathogenic autoantibodies, the so-called NMO-IgGs, which are directed against the water channel aquaporin 4 (AQP4) on astrocytes. When these antibodies gain access to the CNS, they mediate astrocyte destruction by complement-dependent and by antibody-dependent cellular cytotoxicity. In contrast to multiple sclerosis (MS) patients who benefit from therapies involving type I interferons (I-IFN), NMO patients typically do not profit from such treatments. How is I-IFN involved in NMO pathogenesis? To address this question, we made gene expression profiles of spinal cords from Lewis rat models of experimental neuromyelitis optica (ENMO) and experimental autoimmune encephalomyelitis (EAE). We found an upregulation of I-IFN signature genes in EAE spinal cords, and a further upregulation of these genes in ENMO. To learn whether the local I-IFN signature is harmful or beneficial, we induced ENMO by transfer of CNS antigen-specific T cells and NMO-IgG, and treated the animals with I-IFN at the very onset of clinical symptoms, when the blood-brain barrier was open. With this treatment regimen, we could amplify possible effects of the I-IFN induced genes on the transmigration of infiltrating cells through the blood brain barrier, and on lesion formation and expansion, but could avoid effects of I-IFN on the differentiation of pathogenic T and B cells in the lymph nodes. We observed that I-IFN treated ENMO rats had spinal cord lesions with fewer T cells, macrophages/activated microglia and activated neutrophils, and less astrocyte damage than their vehicle treated counterparts, suggesting beneficial effects of I-IFN.

Place, publisher, year, edition, pages
PUBLIC LIBRARY SCIENCE, 2016
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-127436 (URN)10.1371/journal.pone.0151244 (DOI)000372582800051 ()26990978 (PubMedID)
Note

Funding Agencies|Austrian Science Fund [P25240-B24]; Austrian Ministry of Science, Research and Economy (BIGWIG-MS); Ministry of Education, Culture, Sports, Science and Technology of Japan; Alumni Association of Saitama Medical University

Available from: 2016-05-01 Created: 2016-04-26 Last updated: 2021-06-14
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