Thomas Merlin
Max Planck Society
11 Papers
263 Citations
Thomas Merlin is an academic researcher from Max Planck Society. The author has contributed to research in topics: Gram-negative bacteria & Propionibacterium acnes. The author has an hindex of 9, co-authored 11 publications.
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Papers
Cutting Edge: A Murine, IL-12-Independent Pathway of IFN-γ Induction by Gram-Negative Bacteria Based on STAT4 Activation by Type I IFN and IL-18 Signaling
Marina A. Freudenberg,Thomas Merlin,Christoph Kalis,Yolande Chvatchko,Hella Stübig,Chris Galanos +5 more
TL;DR: It is shown that IFN-αβ alone induces tyrosine phosphorylation of STAT4 in murine splenocytes of different mouse strains, and in contradiction to current dogma, this pathway participates in the induction of IFn-γ by Gram-negative bacteria.
Bacterial Induction of Beta Interferon in Mice Is a Function of the Lipopolysaccharide Component
Andreas Sing,Thomas Merlin,Hans-Peter Knopf,Peter J. Nielsen,Harald Loppnow,Chris Galanos,Marina A. Freudenberg +6 more
TL;DR: It is suggested strongly that LPS is the only bacterial component capable of inducing IFN-β in significant amounts that are readily detectable under the conditions used in this study.
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A point mutation in the IL-12R beta 2 gene underlies the IL-12 unresponsiveness of Lps-defective C57BL/10ScCr mice.
Alexander Poltorak,Thomas Merlin,Peter J. Nielsen,O. Sandra,Irina Smirnova,Ingo Schupp,Thomas Boehm,Chris Galanos,Marina A. Freudenberg +8 more
TL;DR: It is shown here that this second defect of Cr mice is due to a mutation in a single gene located on mouse chromosome 6, in close proximity to the Igκ locus, which is IL-12Rβ2, responsible for their defective IFN-γ response to microorganisms.
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Role of lipopolysaccharide susceptibility in the innate immune response to Salmonella typhimurium infection: LPS, a primary target for recognition of Gram-negative bacteria
Marina A. Freudenberg,Thomas Merlin,Marina Gumenscheimer,Christoph Kalis,Regine Landmann,Chris Galanos +5 more
TL;DR: This review deals with the factors affecting LPS susceptibility and with the role of the latter in the course and outcome of Salmonella typhimurium infection.
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Inherited IL-12 unresponsiveness contributes to the high LPS resistance of the Lps(d) C57BL/10ScCr mouse.
TL;DR: A second genetic defect unrelated to the Lps/tlr4 mutation that underlies the IL-12 unresponsiveness and contributes to theLPS resistance and impaired innate immune response in this strain of mice is found.