scispace - formally typeset
S

Stefan Meuer

Researcher at Heidelberg University

Publications -  238
Citations -  13277

Stefan Meuer is an academic researcher from Heidelberg University. The author has contributed to research in topics: T cell & Antigen. The author has an hindex of 58, co-authored 233 publications receiving 12977 citations. Previous affiliations of Stefan Meuer include German Cancer Research Center & University of Oxford.

Papers
More filters
Journal ArticleDOI

An alternative pathway of T-cell activation: A functional role for the 50 kd T11 sheep erythrocyte receptor protein

TL;DR: Given that T11 is the earliest T-lineage surface glycoprotein to appear in thymic ontogeny and is thus expressed before T3-Ti, the former may be involved in clonal expansion and/or differentiation during early development.
Journal ArticleDOI

Clonotypic structures involved in antigen-specific human T cell function. Relationship to the T3 molecular complex.

TL;DR: The development of monoclonal antibodies to such polymorphic T cell surface structures should provide important probes to further define the surface receptor for antigen.
Journal ArticleDOI

Clonal analysis of human cytotoxic T lymphocytes: T4+ and T8+ effector T cells recognize products of different major histocompatibility complex regions.

TL;DR: The results indicate that T4+ and T8+ T lymphocytes have receptors for different classes of MHC antigens and suggest cytotoxic T 4+ subpopulations might be important in human transplantation and autoimmune disorders.
Journal ArticleDOI

Antigen recognition by human T lymphocytes is linked to surface expression of the T3 molecular complex.

TL;DR: Evidence is provided for a direct linkage between antigen recognition by T lymphocytes and surface expression of the T3 molecular complex, which inhibits cytotoxic T lymphocyte effector function by T4 and T8 clones as well as antigen-specific T cell recognition.
Journal ArticleDOI

Triggering of the T3-Ti antigen-receptor complex results in clonal T-cell proliferation through an interleukin 2-dependent autocrine pathway

TL;DR: The findings demonstrate that antigen-induced proliferation is mediated through an autocrine pathway involving endogenous IL-2 production, release, and subsequent binding to IL-3-Ti receptor cross-linking.