Hammer, Christian

[["dc.bibliographiccitation.firstpage","738"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","American journal of human genetics"],["dc.bibliographiccitation.lastpage","743"],["dc.bibliographiccitation.volume","97"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","McLaren, P. J."],["dc.contributor.author","Bartha, István"],["dc.contributor.author","Michel, Angelika"],["dc.contributor.author","Klose, Beate"],["dc.contributor.author","Schmitt, Corinna"],["dc.contributor.author","Waterboer, Tim"],["dc.contributor.author","Pawlita, Michael"],["dc.contributor.author","Schulz, Thomas F."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Fellay, Jacques"],["dc.date.accessioned","2017-09-07T11:46:17Z"],["dc.date.available","2017-09-07T11:46:17Z"],["dc.date.issued","2015"],["dc.description.abstract","The magnitude of the human antibody response to viral antigens is highly variable. To explore the human genetic contribution to this variability, we performed genome-wide association studies of the immunoglobulin G response to 14 pathogenic viruses in 2,363 immunocompetent adults. Significant associations were observed in the major histocompatibility complex region on chromosome 6 for influenza A virus, Epstein-Barr virus, JC polyomavirus, and Merkel cell polyomavirus. Using local imputation and fine mapping, we identified specific amino acid residues in human leucocyte antigen (HLA) class II proteins as the most probable causal variants underlying these association signals. Common HLA-DRβ1 haplotypes showed virus-specific patterns of humoral-response regulation. We observed an overlap between variants affecting the humoral response to influenza A and EBV and variants previously associated with autoimmune diseases related to these viruses. The results of this study emphasize the central and pathogen-specific role of HLA class II variation in the modulation of humoral immune response to viral antigens in humans."],["dc.identifier.doi","10.1016/j.ajhg.2015.09.008"],["dc.identifier.gro","3150467"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12609"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7235"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","0002-9297"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Amino acid variation in HLA class II proteins is a major determinant of humoral response to common viruses"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1143"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","1149"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Tantra, Martesa"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Mohd Jofrry, Sue"],["dc.contributor.author","Gurvich, Artem"],["dc.contributor.author","Jensen, Niels"],["dc.contributor.author","Ostmeier, Katrin"],["dc.contributor.author","Lühder, F."],["dc.contributor.author","Probst, Christian"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Gillis, M."],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Assogna, F."],["dc.contributor.author","Spalletta, Gianfranco"],["dc.contributor.author","Stöcker, W."],["dc.contributor.author","Schulz, Thomas F."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:37Z"],["dc.date.available","2017-09-07T11:46:37Z"],["dc.date.issued","2014"],["dc.description.abstract","In 2007, a multifaceted syndrome, associated with anti-NMDA receptor autoantibodies (NMDAR-AB) of immunoglobulin-G isotype, has been described, which variably consists of psychosis, epilepsy, cognitive decline and extrapyramidal symptoms. Prevalence and significance of NMDAR-AB in complex neuropsychiatric disease versus health, however, have remained unclear. We tested sera of 2817 subjects (1325 healthy, 1081 schizophrenic, 263 Parkinson and 148 affective-disorder subjects) for presence of NMDAR-AB, conducted a genome-wide genetic association study, comparing AB carriers versus non-carriers, and assessed their influenza AB status. For mechanistic insight and documentation of AB functionality, in vivo experiments involving mice with deficient blood-brain barrier (ApoE(-/-)) and in vitro endocytosis assays in primary cortical neurons were performed. In 10.5% of subjects, NMDAR-AB (NR1 subunit) of any immunoglobulin isotype were detected, with no difference in seroprevalence, titer or in vitro functionality between patients and healthy controls. Administration of extracted human serum to mice influenced basal and MK-801-induced activity in the open field only in ApoE(-/-) mice injected with NMDAR-AB-positive serum but not in respective controls. Seropositive schizophrenic patients with a history of neurotrauma or birth complications, indicating an at least temporarily compromised blood-brain barrier, had more neurological abnormalities than seronegative patients with comparable history. A common genetic variant (rs524991, P=6.15E-08) as well as past influenza A (P=0.024) or B (P=0.006) infection were identified as predisposing factors for NMDAR-AB seropositivity. The >10% overall seroprevalence of NMDAR-AB of both healthy individuals and patients is unexpectedly high. Clinical significance, however, apparently depends on association with past or present perturbations of blood-brain barrier function."],["dc.identifier.doi","10.1038/mp.2013.110"],["dc.identifier.gro","3150565"],["dc.identifier.pmid","23999527"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7339"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Neuropsychiatric disease relevance of circulating anti-NMDA receptor autoantibodies depends on blood-brain barrier integrity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","144"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","151"],["dc.bibliographiccitation.volume","79"],["dc.contributor.author","Castillo-Gomez, Esther"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Steiner, Johann"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Hettling, Bilke"],["dc.contributor.author","Poggi, Giulia"],["dc.contributor.author","Ostehr, Kristin"],["dc.contributor.author","Uhr, Manfred"],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Matzke, Mike"],["dc.contributor.author","Schmidt, Ulrike"],["dc.contributor.author","Pfander, Viktoria"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Schulz, Thomas F."],["dc.contributor.author","Binder, Lutz"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Weber, Frank"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:35Z"],["dc.date.available","2017-09-07T11:46:35Z"],["dc.date.issued","2016"],["dc.description.abstract","Autoantibodies (AB) against N-methyl-D-aspartate receptor subunit NR1 (NMDAR1) are highly seroprevalent in health and disease. Symptomatic relevance may arise upon compromised blood–brain barrier (BBB). However, it remained unknown whether circulating NMDAR1 AB appear in the cerebrospinal fluid (CSF). Of n = 271 subjects with CSF–serum pairs, 26 were NMDAR1 AB seropositive, but only 1 was CSF positive. Contrariwise, tetanus AB (non–brain-binding) were present in serum and CSF of all subjects, with CSF levels higher upon BBB dysfunction. Translational mouse experiments proved the hypothesis that the brain acts as an ‘immunoprecipitator’; simultaneous injection of NMDAR1 AB and the non–brain-binding green fluorescent protein AB resulted in high detectability of the former in brain and the latter in CSF."],["dc.identifier.doi","10.1002/ana.24545"],["dc.identifier.gro","3150536"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7309"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0364-5134"],["dc.title","The brain as immunoprecipitator of serum autoantibodies against N-Methyl-D-aspartate receptor subunit NR1"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","26"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Medicine"],["dc.bibliographiccitation.lastpage","37"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Wanitchakool, Podchanart"],["dc.contributor.author","Sirianant, Lalida"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Monnheimer, Mathieu"],["dc.contributor.author","Faria, Diana"],["dc.contributor.author","Ousingsawat, Jiraporn"],["dc.contributor.author","Schramek, Natalie"],["dc.contributor.author","Schmitt, Corinna"],["dc.contributor.author","Margos, Gabriele"],["dc.contributor.author","Michel, Angelika"],["dc.contributor.author","Kraiczy, Peter"],["dc.contributor.author","Pawlita, Michael"],["dc.contributor.author","Schreiber, Rainer"],["dc.contributor.author","Schulz, Thomas F."],["dc.contributor.author","Fingerle, Volker"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Kunzelmann, Karl"],["dc.date.accessioned","2017-09-07T11:46:14Z"],["dc.date.available","2017-09-07T11:46:14Z"],["dc.date.issued","2015"],["dc.description.abstract","In a first genome-wide association study (GWAS) approach to anti-Borrelia seropositivity, we identified two significant single nucleotide polymorphisms (SNPs) (rs17850869, P = 4.17E-09; rs41289586, P = 7.18E-08). Both markers, located on chromosomes 16 and 3, respectively, are within or close to genes previously connected to spinocerebellar ataxia. The risk SNP rs41289586 represents a missense variant (R263H) of anoctamin 10 (ANO10), a member of a protein family encoding Cl(-) channels and phospholipid scramblases. ANO10 augments volume-regulated Cl(-) currents (IHypo) in Xenopus oocytes, HEK293 cells, lymphocytes and macrophages and controls volume regulation by enhancing regulatory volume decrease (RVD). ANO10 supports migration of macrophages and phagocytosis of spirochetes. The R263H variant is inhibitory on IHypo, RVD and intracellular Ca(2+) signals, which may delay spirochete clearance, thereby sensitizing adaptive immunity. Our data demonstrate for the first time that ANO10 has a central role in innate immune defense against Borrelia infection."],["dc.identifier.doi","10.2119/molmed.2014.00219"],["dc.identifier.gro","3150465"],["dc.identifier.pmid","25730773"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7233"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","A coding variant of ANO10, affecting volume regulation of macrophages, is associated with Borrelia seropositivity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]