@phdthesis{Hemprich2022,
  author    = {Hemprich, Antonia},
  title     = {Detektion von Autoantik{\"o}rpern gegen Cortactin und Agrin im Serum von Patient*innen mit Myasthenia gravis},
  doi       = {10.25972/OPUS-28692},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-286920},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2022},
  abstract  = {Myasthenia gravis ist eine Autoimmunerkrankung, die durch St{\"o}rung der Erregungs{\"u}bertragung an der neuromuskul{\"a}ren Endplatte zu einer Schw{\"a}che der Muskulatur f{\"u}hrt. In dieser Arbeit wird die Rolle von Cortactin und Agrin als potentielle neue Antigene von Autoantik{\"o}rpern bei Myasthenia gravis untersucht. Die detektierten Antik{\"o}rper werden charakterisiert und die klinischen Merkmale der Patient*innen ausgewertet.},
  subject      = {Myasthenia gravis},
  language  = {de}
}
@article{GschmackMonoranuMaroufetal.2022,
  author    = {Gschmack, Eva and Monoranu, Camelia-Maria and Marouf, Hecham and Meyer, Sarah and Lessel, Lena and Idris, Raja and Berg, Daniela and Maetzler, Walter and Steigerwald, Frank and Volkmann, Jens and Gerlach, Manfred and Riederer, Peter and Koutsilieri, Eleni and Scheller, Carsten},
  title     = {Plasma autoantibodies to glial fibrillary acidic protein (GFAP) react with brain areas according to Braak staging of Parkinson's disease},
  series = {Journal of Neural Transmission},
  volume    = {129},
  journal   = {Journal of Neural Transmission},
  number    = {5-6},
  doi       = {10.1007/s00702-022-02495-4},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-325161},
  pages     = {545-555},
  year      = {2022},
  abstract  = {Idiopathic Parkinson's disease (PD) is characterized by a progredient degeneration of the brain, starting at deep subcortical areas such as the dorsal motor nucleus of the glossopharyngeal and vagal nerves (DM) (stage 1), followed by the coeruleus-subcoeruleus complex; (stage 2), the substantia nigra (SN) (stage 3), the anteromedial temporal mesocortex (MC) (stage 4), high-order sensory association areas and prefrontal fields (HC) (stage 5) and finally first-order sensory association areas, premotor areas, as well as primary sensory and motor field (FC) (stage 6). Autoimmunity might play a role in PD pathogenesis. Here we analyzed whether anti-brain autoantibodies differentially recognize different human brain areas and identified autoantigens that correlate with the above-described dissemination of PD pathology in the brain. Brain tissue was obtained from deceased individuals with no history of neurological or psychiatric disease and no neuropathological abnormalities. Tissue homogenates from different brain regions (DM, SN, MC, HC, FC) were subjected to SDS-PAGE and Western blot. Blots were incubated with plasma samples from 30 PD patients and 30 control subjects and stained with anti-IgG antibodies to detect anti-brain autoantibodies. Signals were quantified. Prominent autoantigens were identified by 2D-gel-coupled mass spectrometry sequencing. Anti-brain autoantibodies are frequent and occur both in healthy controls and individuals with PD. Glial fibrillary acidic protein (GFAP) was identified as a prominent autoantigen recognized in all plasma samples. GFAP immunoreactivity was highest in DM areas and lowest in FC areas with no significant differences in anti-GFAP autoantibody titers between healthy controls and individuals with PD. The anti-GFAP autoimmunoreactivity of different brain areas correlates with the dissemination of histopathological neurodegeneration in PD. We hypothesize that GFAP autoantibodies are physiological but might be involved as a cofactor in PD pathogenesis secondary to a leakage of the blood-brain barrier.},
  language  = {en}
}
@article{WildeLiebLeichtetal.2021,
  author    = {Wilde, Anne-Christin Beatrice and Lieb, Charlotte and Leicht, Elise and Greverath, Lena Maria and Steinhagen, Lara Marleen and Wald de Chamorro, Nina and Petersen, J{\"o}rg and Hofmann, Wolf Peter and Hinrichsen, Holger and Heyne, Renate and Berg, Thomas and Naumann, Uwe and Schwenzer, Jeannette and Vermehren, Johannes and Geier, Andreas and Tacke, Frank and M{\"u}ller, Tobias},
  title     = {Real-world clinical management of patients with primary biliary cholangitis — a retrospective multicenter study from Germany},
  series = {Journal of Clinical Medicine},
  volume    = {10},
  journal   = {Journal of Clinical Medicine},
  number    = {5},
  issn      = {2077-0383},
  doi       = {10.3390/jcm10051061},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-234003},
  year      = {2021},
  abstract  = {Background: Clinical practice guidelines for patients with primary biliary cholangitis (PBC) have been recently revised and implemented for well-established response criteria to standard first-line ursodeoxycholic acid (UDCA) therapy at 12 months after treatment initiation for the early identification of high-risk patients with inadequate treatment responses who may require treatment modification. However, there are only very limited data concerning the real-world clinical management of patients with PBC in Germany. Objective: The aim of this retrospective multicenter study was to evaluate response rates to standard first-line UDCA therapy and subsequent Second-line treatment regimens in a large cohort of well-characterized patients with PBC from 10 independent hepatological referral centers in Germany prior to the introduction of obeticholic acid as a licensed second-line treatment option. Methods: Diagnostic confirmation of PBC, standard first-line UDCA treatment regimens and response rates at 12 months according to Paris-I, Paris-II, and Barcelona criteria, the follow-up cut-off alkaline phosphatase (ALP) ≤ 1.67 × upper limit of normal (ULN) and the normalization of bilirubin (bilirubin ≤ 1 × ULN) were retrospectively examined between June 1986 and March 2017. The management and hitherto applied second-line treatment regimens in patients with an inadequate response to UDCA and subsequent response rates at 12 months were also evaluated. Results: Overall, 480 PBC patients were included in this study. The median UDCA dosage was 13.2 mg UDCA/kg bodyweight (BW)/d. Adequate UDCA treatment response rates according to Paris-I, Paris-II, and Barcelona criteria were observed in 91, 71.3, and 61.3\% of patients, respectively. In 83.8\% of patients, ALP ≤ 1.67 × ULN were achieved. A total of 116 patients (24.2\%) showed an inadequate response to UDCA according to at least one criterion. The diverse second-line treatment regimens applied led to significantly higher response rates according to Paris-II (35 vs. 60\%, p = 0.005), Barcelona (13 vs. 34\%, p = 0.0005), ALP ≤ 1.67 × ULN and bilirubin ≤ 1 × ULN (52.1 vs. 75\%, p = 0.002). The addition of bezafibrates appeared to induce the strongest beneficial effect in this cohort (Paris II: 24 vs. 74\%, p = 0.004; Barcelona: 50 vs. 84\%, p = 0.046; ALP < 1.67 × ULN and bilirubin ≤ 1 × ULN: 33 vs. 86\%, p = 0.001). Conclusion: Our large retrospective multicenter study confirms high response rates following UDCA first-line standard treatment in patients with PBC and highlights the need for close monitoring and early treatment modification in high-risk patients with an insufficient response to UDCA since early treatment modification significantly increases subsequent response rates of these patients.},
  language  = {en}
}
@article{DoghmanBouguerraFinettiDurandetal.2020,
  author    = {Doghman-Bouguerra, Mabrouka and Finetti, Pascal and Durand, Nelly and Parise, Ivy Zort{\´e}a S. and Sbiera, Silviu and Cantini, Giulia and Canu, Letizia and Hescot, S{\´e}gol{\`e}ne and Figueiredo, Mirna M. O. and Komechen, Heloisa and Sbiera, Iuliu and Nesi, Gabriella and Paci, Angelo and Al Ghuzlan, Abir and Birnbaum, Daniel and Baudin, Eric and Luconi, Michaela and Fassnacht, Martin and Figueiredo, Bonald C. and Bertucci, Fran{\c{c}}ois and Lalli, Enzo},
  title     = {Cancer-testis antigen FATE1 expression in adrenocortical tumors is associated with a pervasive autoimmune response and is a marker of malignancy in adult, but not children, ACC},
  series = {Cancers},
  volume    = {12},
  journal   = {Cancers},
  number    = {3},
  issn      = {2072-6694},
  doi       = {10.3390/cancers12030689},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-203211},
  year      = {2020},
  abstract  = {The SF-1 transcription factor target gene FATE1 encodes a cancer-testis antigen that has an important role in regulating apoptosis and response to chemotherapy in adrenocortical carcinoma (ACC) cells. Autoantibodies directed against FATE1 were previously detected in patients with hepatocellular carcinoma. In this study, we investigated the prevalence of circulating anti-FATE1 antibodies in pediatric and adult patients with adrenocortical tumors using three different methods (immunofluorescence, ELISA and Western blot). Our results show that a pervasive anti-FATE1 immune response is present in those patients. Furthermore, FATE1 expression is a robust prognostic indicator in adult patients with ACC and is associated with increased steroidogenic and decreased immune response gene expression. These data can open perspectives for novel strategies in ACC immunotherapy.},
  language  = {en}
}
@article{AppeltshauserBrunderHeiniusetal.2020,
  author    = {Appeltshauser, Luise and Brunder, Anna-Michelle and Heinius, Annika and K{\"o}rtv{\´e}lyessy, Peter and Wandinger, Klaus-Peter and Junker, Ralf and Villmann, Carmen and Sommer, Claudia and Leypoldt, Frank and Doppler, Kathrin},
  title     = {Antiparanodal antibodies and IgG subclasses in acute autoimmune neuropathy},
  series = {Neurology: Neuroimmunology \& Neuroinflammation},
  volume    = {7},
  journal   = {Neurology: Neuroimmunology \& Neuroinflammation},
  number    = {5},
  doi       = {10.1212/NXI.0000000000000817},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-230079},
  year      = {2020},
  abstract  = {Objective To determine whether IgG subclasses of antiparanodal autoantibodies are related to disease course and treatment response in acute- to subacute-onset neuropathies, we retrospectively screened 161 baseline serum/CSF samples and 66 follow-up serum/CSF samples. Methods We used ELISA and immunofluorescence assays to detect antiparanodal IgG and their subclasses and titers in serum/CSF of patients with Guillain-Barre syndrome (GBS), recurrent GBS (R-GBS), Miller-Fisher syndrome, and acute- to subacute-onset chronic inflammatory demyelinating polyradiculoneuropathy (A-CIDP). We evaluated clinical data retrospectively. Results We detected antiparanodal autoantibodies with a prevalence of 4.3\% (7/161), more often in A-CIDP (4/23, 17.4\%) compared with GBS (3/114, 2.6\%). Longitudinal subclass analysis in the patients with GBS revealed IgG2/3 autoantibodies against Caspr-1 and against anti-contactin-1/Caspr-1, which disappeared at remission. At disease onset, patients with A-CIDP had IgG2/3 anti-Caspr-1 and anti-contactin-1/Caspr-1 or IgG4 anti-contactin-1 antibodies, IgG3 being associated with good response to IV immunoglobulins (IVIg). In the chronic phase of disease, IgG subclass of one patient with A-CIDP switched from IgG3 to IgG4. Conclusion Our data (1) confirm and extend previous observations that antiparanodal IgG2/3 but not IgG4 antibodies can occur in acute-onset neuropathies manifesting as monophasic GBS, (2) suggest association of IgG3 to a favorable response to IVIg, and (3) lend support to the hypothesis that in some patients, an IgG subclass switch from IgG3 to IgG4 may be the correlate of a secondary progressive or relapsing course following a GBS-like onset.},
  language  = {en}
}
@article{ReckeKonitzerLemckeetal.2018,
  author    = {Recke, Andreas and Konitzer, Sarah and Lemcke, Susanne and Freitag, Miriam and Sommer, Nele Maxi and Abdelhady, Mohammad and Amoli, Mahsa M. and Benoit, Sandrine and El-Chennawy, Farha and Eldarouti, Mohammad and Eming, R{\"u}diger and Gl{\"a}ser, Regine and G{\"u}nther, Claudia and Hadaschik, Eva and Homey, Bernhard and Lieb, Wolfgang and Peitsch, Wiebke K. and Pf{\"o}hler, Claudia and Robati, Reza M. and Saeedi, Marjan and S{\´a}rdy, Mikl{\´o}s and Sticherling, Michael and Uzun, Soner and Worm, Margitta and Zillikens, Detlef and Ibrahim, Saleh and Vidarsson, Gestur and Schmidt, Enno},
  title     = {The p.Arg435His Variation of IgG3 With High Affinity to FcRn Is Associated With Susceptibility for Pemphigus Vulgaris-Analysis of Four Different Ethnic Cohorts},
  series = {frontiers in Immunology},
  volume    = {9},
  journal   = {frontiers in Immunology},
  doi       = {10.3389/fimmu.2018.01788},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-225073},
  pages     = {1788, 1-8},
  year      = {2018},
  abstract  = {IgG3 is the IgG subclass with the strongest effector functions among all four IgG subclasses and the highest degree of allelic variability among all constant immunoglobulin genes. Due to its genetic position, IgG3 is often the first isotype an antibody switches to before IgG1 or IgG4. Compared with the other IgG subclasses, it has a reduced half-life which is probably connected to a decreased affinity to the neonatal Fc receptor (FcRn). However, a few allelic variants harbor an amino acid replacement of His435 to Arg that reverts the half-life of the resulting IgG3 to the same level as the other IgG subclasses. Because of its functional impact, we hypothesized that the p.Arg435His variation could be associated with susceptibility to autoantibody-mediated diseases like pemphigus vulgaris (PV) and bullous pemphigoid (BP). Using a set of samples from German, Turkish, Egyptian, and Iranian patients and controls, we were able to demonstrate a genetic association of the p.Arg435His variation with PV risk, but not with BP risk. Our results suggest a hitherto unknown role for the function of IgG3 in the pathogenesis of PV.},
  subject      = {Diagnose},
  language  = {en}
}
@phdthesis{Ruschil2014,
  author    = {Ruschil, Christoph},
  title     = {Der Einfluss von Autoantik{\"o}rpern gegen Aquaporin 4 bei der Pathogenese der Neuromyelitis optica},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-105787},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2014},
  abstract  = {Neuromyelitis optica (NMO) ist eine schwerwiegende Autoimmunerkrankung des zentralen Nervensystems, deren pathogene Ursache in Zusammenhang mit Autoantik{\"o}rpern gegen Aquaporin 4 (AQP4) steht. In einem intrathekalen Passiv-Transfermodell der Ratte wurden die Auswirkungen von NMO-Immunglobulin (IgG) aus Plasmapheresematerial und rekombinanten Antik{\"o}rpern gegen AQP4 sowie der Effekt von additiver Applikation von humanem Komplement untersucht. NMO-IgG, rekombinante Antik{\"o}rper und modifizierte Antik{\"o}rper ohne F{\"a}higkeit zur Aktivierung der Komplementkaskade waren bei repetitiver Applikation in der Lage, auch ohne additives humanes Komplement NMO-{\"a}hnliche progrediente motorische Symptome zu induzieren. Durch Ko-Injektion von humanem Komplement konnte keine signifikante Exazerbation der Pathologie bewirkt werden. MRT-Studien zeigten lokale Schrankenst{\"o}rungen am Ort der h{\"o}chsten Antik{\"o}rperkonzentration. In histologischen Aufarbeitungen von R{\"u}ckenmarksschnitten zeigten sich lokale Deposition an humanem IgG, ein dazu korrelierender Verlust an AQP4 sowie eine dar{\"u}ber hinausgehende Reduktion des Glutamattransporters EAAT2, w{\"a}hrend GFAP-reaktive Astrozyten tendenziell hypertroph und vermehrt waren. Auch bei additiver Applikation von humanem Komplement wiesen die L{\"a}sionsareale im Gegensatz zu histopathologischen Befunden bei NMO-Patienten und anderen Tiermodellen nur eine geringe Ablagerung von aktivem Komplement und wenig Infiltration durch ED1-positive Makrophagen auf. Da in einem Kontrollexperiment mit intrazerebraler intraparenchymaler Applikation von NMO-IgG die beschriebene additive Zytotoxizit{\"a}t von humanem Komplement reproduziert werden konnte, erscheint die Verwendbarkeit des intrathkalen Modells zur Evaluation der Wirkung von humanem Komplement bei Autoimmunerkrankungen mit intraspinalen Zielepitopen nicht geeignet. Die Ergebnisse lassen sich als Komplement-unabh{\"a}ngige intrinsische Wirkungen von Antik{\"o}rpern gegen AQP4 deuten, die in einer Reduktion der Oberfl{\"a}chenexpresseion von AQP4 und EAAT2 resultieren und zu einer progredienten Myelopathie f{\"u}hren. Neben der bekannten Antik{\"o}rper-induzierten Komplement-abh{\"a}ngigen Zytotoxizit{\"a}t k{\"o}nnten diese Effekte einen bislang nicht beschriebenen zus{\"a}tzlichen Pathomechanismus bei der NMO darstellen.},
  subject      = {Autoantik{\"o}rper},
  language  = {de}
}
@phdthesis{Gruenewald2012,
  author    = {Gr{\"u}newald, Benedikt},
  title     = {Autoantik{\"o}rper-vermittelte St{\"o}rungen der synaptischen {\"U}bertragung im ZNS},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-73283},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2012},
  abstract  = {Die Anzahl neurologischer Erkrankungen bei denen Autoantik{\"o}rper gegen zentralnerv{\"o}se An-tigene bekannt sind, hat in den letzten Jahren deutlich zugenommen. Allerdings gibt es nur f{\"u}r wenige dieser Erkrankungen hinreichende experimentelle Belege f{\"u}r eine pathogene Wir-kung der Autoantik{\"o}rper. Zwei dieser Erkrankungen wurden im Rahmen dieser Arbeit n{\"a}her untersucht: die Juvenile Neuronale Zeroid-Lipofuszinose (JNCL) mit Autoantik{\"o}rpern gegen die 65 kD Isoform der Glutamatdecarboxylase und das Stiff Person Syndrom (SPS) mit Auto-antik{\"o}rpern gegen Amphiphysin. Die ph{\"a}notypische Charakterisierung der cln3 knockout-Maus, einem Mausmodell f{\"u}r die JNCL, zeigte eine progressive Verschlechterung der motorischen und koordinativen F{\"a}-higkeiten, eingeschr{\"a}nktes reizbedingtes Lernen und gesteigertes angst{\"a}hnliches Verhalten. Diese Symptome {\"a}hneln denen der humanen Erkrankung. Elektrophysiologisch konnte eine Antik{\"o}rper-induzierte zerebell{\"a}re Dysfunktion identifiziert werden, die einer verminderten lokalen GABAergen Hemmung zugeordnet wird. Eine Reduktion der Antik{\"o}perproduktion im Tiermodell durch eine Depletion der Plasmazellen durch den Proteseinhibitor Bortezomib hatte einen positiven Effekt auf die Krankheitsentwicklung. Im zweiten experimentellen Teil der Arbeit wurde der Einfluss von Autoantik{\"o}rpern gegen Amphiphysin von Patienten mit SPS auf die synaptische Transmission untersucht. Es zeigte sich hierbei in Patch-Clamp Experimenten eine St{\"o}rung der GABAergen {\"U}bertragung v.a. bei hochfrequenter Stimulation, was im Einklang mit dem vermuteten Antik{\"o}rper-induzierten Endozytosedefekt steht. Passiver Transfer von humanen Autoantik{\"o}rpern gegen Amphiphysin induzierte angst-{\"a}hnliches Verhalten in Ratten, einem weiteren Kernsymptom des SPS. Aktive Immunisierung gegen Amphiphysin und anschließende {\"O}ffnung der Blut-Hirn-Schranke in M{\"a}usen f{\"u}hrte zu einer subklinischen Ver{\"a}nderung der Reflexverarbeitung von Ia Afferenzen auf Motoneurone im R{\"u}ckenmark der M{\"a}use. Insgesamt konnten in zwei Erkrankungen des ZNS autoimmune Mechanismen identifi-ziert werden, die zu einer Antik{\"o}rper-induzierten Fehlregulation der zentralen synaptischen Transmission f{\"u}hren. Diese Ergebnisse k{\"o}nnen wegweisend sein auch f{\"u}r die Erforschung der Pathophysiologie anderer Antik{\"o}rper-assoziierte Erkrankungen des ZNS.},
  subject      = {Glutamat-Decarboxylase},
  language  = {de}
}
@article{GeisWeishauptGruenewaldetal.2011,
  author    = {Geis, Christian and Weishaupt, Andreas and Gr{\"u}newald, Benedikt and Wultsch, Thomas and Reif, Andreas and Gerlach, Manfred and Dirkx, Ron and Solimena, Michele and Toyka, Klaus V and Folli, Franco and Perani, Daniela and Heckmann, Manfred and Sommer, Claudia},
  title     = {Human Stiff-Person Syndrome IgG Induces Anxious Behavior in Rats},
  series = {Plos One},
  volume    = {6},
  journal   = {Plos One},
  number    = {2},
  doi       = {10.1371/journal.pone.0016775},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-140506},
  pages     = {e16775},
  year      = {2011},
  abstract  = {Background: Anxiety is a heterogeneous behavioral domain playing a role in a variety of neuropsychiatric diseases. While anxiety is the cardinal symptom in disorders such as panic disorder, co-morbid anxious behavior can occur in a variety of diseases. Stiff person syndrome (SPS) is a CNS disorder characterized by increased muscle tone and prominent agoraphobia and anxiety. Most patients have high-titer antibodies against glutamate decarboxylase (GAD) 65. The pathogenic role of these autoantibodies is unclear. Methodology/Principal Findings: We re-investigated a 53 year old woman with SPS and profound anxiety for GABA-A receptor binding in the amygdala with (11) C-flumazenil PET scan and studied the potential pathogenic role of purified IgG from her plasma filtrates containing high-titer antibodies against GAD 65. We passively transferred the IgG fraction intrathecally into rats and analyzed the effects using behavioral and in vivo electrophysiological methods. In cell culture, we measured the effect of patient IgG on GABA release from hippocampal neurons. Repetitive intrathecal application of purified patient IgG in rats resulted in an anxious phenotype resembling the core symptoms of the patient. Patient IgG selectively bound to rat amygdala, hippocampus, and frontal cortical areas. In cultured rat hippocampal neurons, patient IgG inhibited GABA release. In line with these experimental results, the GABA-A receptor binding potential was reduced in the patient's amygdala/hippocampus complex. No motor abnormalities were found in recipient rats. Conclusion/Significance: The observations in rats after passive transfer lead us to propose that anxiety-like behavior can be induced in rats by passive transfer of IgG from a SPS patient positive for anti-GAD 65 antibodies. Anxiety, in this case, thus may be an antibody-mediated phenomenon with consecutive disturbance of GABAergic signaling in the amygdala region.},
  language  = {en}
}
@phdthesis{Stock2009,
  author    = {Stock, Michael},
  title     = {Untersuchungen zu immunologischen Pathomechanismen bei der Entstehung chronischer Schmerzsyndrome},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-37533},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2009},
  abstract  = {Im Rahmen der vorliegenden Arbeit wurden anhand eines Tiermodells zun{\"a}chst Hinweise f{\"u}r die pathogene Relevanz von Serumfaktoren f{\"u}r die Entstehung von chronischen Schmerzsyndromen und assoziierten Symptomen gesucht. Es zeigten sich bei Versuchsm{\"a}usen nach intraperitonealer Injektion von Serum eines Patienten mit komplexem regionalem Schmerzsyndrom (CRPS) im Vergleich zu Kontrolltieren, denen Serum von gesunden Blutspendern injiziert wurde, Ver{\"a}nderungen des Spezies-spezifischen, explorativen Verhaltensmusters, welche erste Hinweise auf schmerzassoziiertes Verhalten liefern. Aufgrund dieser Befunde und der Hypothese der Pr{\"a}senz einer humoralen Autoimmunreaktion bei der Entstehung chronischer Schmerzsyndrome wurde die Seropr{\"a}valenz f{\"u}r Antik{\"o}rper gegen eine Vielzahl potentieller Autoantigene bei Patienten mit CRPS oder Fibromyalgiesyndrom im Vergleich zu gesunden Kontrollprobanden mittels immunhistochemischer F{\"a}rbungen gegen murines Gewebe untersucht, wobei kein f{\"u}r die beschriebenen Schmerzerkrankungen pathognomonischer Autoantik{\"o}rper identifiziert werden konnte. Die vorliegende Arbeit erf{\"u}llte ihren Zweck als Pilotprojekt, indem sie wichtige Daten lieferte, die f{\"u}r weitere Untersuchungen wegweisend sind. Dies bezieht sich im Besondern auf notwendige {\"A}nderungen bei den In-vitro-Methoden zur Detektion von Autoantik{\"o}rpern. Zudem m{\"u}ssen die In-vivo-Experimente unter Einbeziehung sensorischer Verhaltenstests wiederholt und durch Fraktionierung der injizierten Serumproben erweitert werden, um gegebenenfalls Autoantik{\"o}rper als Pathogene der Erkrankungen identifizieren zu k{\"o}nnen. Die in der vorliegenden Arbeit beschriebenen Erkenntnisse bieten einen Einblick in m{\"o}gliche pathophysiologische Mechanismen bei der Entstehung von chronischen, idiopathischen Schmerzzust{\"a}nden und k{\"o}nnten als Basis f{\"u}r neue {\"U}berlegungen {\"u}ber den Einsatz immunmodulierender Therapiestrategien bei derartigen Syndromen dienen.},
  subject      = {Fibromyalgie},
  language  = {de}
}