Prof. Dr. Christine Gerber erforscht die frühe christliche Literatur, insbesondere die Paulusbriefe, aus kulturhistorischer und geschlechtertheoretischer Perspektive. Sie untersucht, wie antike Texte Fragen von Geschlecht, Sexualität, Männlichkeit und sozialen Rollen verhandeln und welche Narrative (etwa Dank- und Passionserzählungen) für Resilienz und Sinngebung relevant sind. Ihre Arbeiten verbinden Textinterpretation mit kulturwissenschaftlichen Ansätzen und richten sich auf die Rekonstruktion von Lebenswelten und Diskursen in der griechisch-römischen Antike und frühen Christenheit. Für Institutionen, Archive und Museen bietet sich ein Anknüpfungspunkt in der Vermittlung antiker Kulturgeschichte und Geschlechterforschung; ihre Methoden sind für die geisteswissenschaftliche Grundlagenforschung relevant.
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Prof. Dr. Christine Gerber
HU-FIS-Profil ↗Förderer: DFG Forschungsgruppe Zeitraum: 03/2024 - 02/2028 Projektleitung: Prof. Dr. Christine Gerber
Förderer: DFG Sachbeihilfe Zeitraum: 04/2025 - 03/2028 Projektleitung: Prof. Dr. Christine Gerber
Förderer: Alexander von Humboldt-Stiftung: Forschungskostenzuschuss Zeitraum: 04/2026 - 07/2026 Projektleitung: Prof. Dr. Christine Gerber
Biblische Zeitschrift · DOI
With his Epistles, the Apostle Paul not only gave theological instruction but also cultivated individual relationships with the communities he was addressing. This study examines how the Epistles set up and secure Paul’s continuing importance for the churches if it has not already been established through his Apostolate. This is achieved above all by means of metaphors. The study focuses on the parent-child metaphors (1 Thess. 2; 1 Cor. 4; Gal. 4) with which Paul seeks to bind his “children” to himself in a special way.
PLoS ONE · DOI
HYPOTHESIS: T cells modulate the antiviral and inflammatory responses of airway epithelial cells to human rhinoviruses (HRV). METHODS: Differentiated primary human nasal epithelial cells (HNEC) grown on collagen-coated filters were exposed apically to HRV14 for 6 h, washed thoroughly and co-cultured with anti-CD3/CD28 activated T cells added in the basolateral compartment for 40 h. RESULTS: HRV14 did not induce IFNγ, NOS2, CXCL8 and IL-6 in HNEC, but enhanced expression of the T cell attractant CXCL10. On the other hand, HNEC co-cultured with activated T cells produced CXCL10 at a level several orders of magnitude higher than that induced by HRV14. Albeit to a much lower degree, activated T cells also induced CXCL8, IL-6 and NOS2. Anti-IFNγ antibodies and TNF soluble receptor completely blocked CXCL10 upregulation. Furthermore, a significant correlation was observed between epithelial CXCL10 mRNA expression and the amounts of IFNγ and TNF secreted by T cells. Likewise, increasing numbers of T cells to a constant number of HNEC in co-cultures resulted in increasing epithelial CXCL10 production, attaining a plateau at high IFNγ and TNF levels. Hence, HNEC activation by T cells is induced mainly by IFNγ and/or TNF. Activated T cells also markedly inhibited viral replication in HNEC, partially through activation of the nitric oxide pathway. CONCLUSION: Cross-talk between T cells and HNEC results in activation of the latter and increases their contribution to airway inflammation and virus clearance.