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Hartmut Wekerle

Researcher at Max Planck Society

Publications -  288
Citations -  28375

Hartmut Wekerle is an academic researcher from Max Planck Society. The author has contributed to research in topics: T cell & Antigen. The author has an hindex of 91, co-authored 282 publications receiving 26862 citations. Previous affiliations of Hartmut Wekerle include Weizmann Institute of Science & Austrian Academy of Sciences.

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Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination

TL;DR: It is shown that the commensal gut flora—in the absence of pathogenic agents—is essential in triggering immune processes, leading to a relapsing–remitting autoimmune disease driven by myelin-specific CD4+ T cells.
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The rapid isolation of clonable antigen‐specific T lymphocyte lines capable of mediating autoimmune encephalomyelitis

TL;DR: These lines were found to recognize foreign or self antigens in association with accessory cells of syngeneic major histocompatibility complex genotype and it is possible to study biological function as well as antigen specificity using T cell lines.
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Cellular immune reactivity within the CNS

TL;DR: Using autoaggressive rat T lymphocyte lines specific for defined protein components of peripheral or central myelin to study lymphocyte migration and antigen recognition within the nervous system suggests that the nervoussystem is constantly patrolled by low numbers of activated T cells.
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Astrocytes present myelin basic protein to encephalitogenic T-cell lines.

TL;DR: It is shown that rat astrocytes are able to present antigen to T lymphocytes in a specific manner which is restricted by the major histocompatibility complex (MHC) and that they can in particular activate myelin basic protein (BP)-specific, encephalitogenic T-cell lines.
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Effector T cell interactions with meningeal vascular structures in nascent autoimmune CNS lesions

TL;DR: Using intravital two-photon imaging in a Lewis rat model of experimental autoimmune encephalomyelitis, this work presents in real-time the interactive processes between effector T cells and cerebral structures from their first arrival to manifest autoimmune disease.