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Peter Seiler

Researcher at Max Planck Society

Publications -  29
Citations -  4978

Peter Seiler is an academic researcher from Max Planck Society. The author has contributed to research in topics: Lymphocytic choriomeningitis & Virus. The author has an hindex of 23, co-authored 29 publications receiving 4827 citations. Previous affiliations of Peter Seiler include University of Zurich.

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Cytotoxicity mediated by T cells and natural killer cells is greatly impaired in perforin-deficient mice

TL;DR: Perforin-deficient mice have been generated by homologous recombination to determine whether the effects of CDS+ cytolytic T cells and natural killer cells are mediated by pore formation involving perform, and perforin is therefore a key effector molecule for T-cell- and natural Killer- cell-mediated cy tolysis.
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The roles of perforin- and Fas-dependent cytotoxicity in protection against cytopathic and noncytopathic viruses.

TL;DR: It is suggested that perforin‐dependent cytotoxicity mediated by T cells is crucial for protection against noncytopathic viruses, whereas infections with cytopATHic viruses are controlled by nonlytic T cell‐dependent soluble mediators such as cytokines and neutralizing antibodies.
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Reduced Incidence and Delayed Onset of Diabetes in Perforin-deficient Nonobese Diabetic Mice

TL;DR: Perforin-dependent cytotoxicity is a crucial effector mechanism for β cell elimination by cytotoxic T cells in autoimmune diabetes, however, in the absence of perforin chronic inflammation of the islets can lead to diabetogenic β cell loss by less efficient secondary effector mechanisms.
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Macrophages of the Splenic Marginal Zone Are Essential for Trapping of Blood-Borne Particulate Antigen but Dispensable for Induction of Specific T Cell Responses

TL;DR: To identify the cell populations responsible for Ag trapping in the marginal zone, mice were selectively depleted of marginal zone macrophage and marginal metallophilic macrophages, and in the absence of these cells, trapping of microspheres and Listeria monocytogenes organisms was lost, and early control of infection was impaired.