Mike Recher

TL;DR: The circumstances under which CD8+ T cells specific for pancreatic beta-islet antigens induce disease in mice expressing lymphocytic choriomeningitis virus as a transgene under the control of the rat insulin promoter are investigated to identify the 'inflammatory status' of the target organ as a separate and limiting factor determining the development of autoimmune disease.

TL;DR: Serotonin treatment of infected mice delayed entry of activated CD8+ T cells into the liver, delayed virus control and aggravated immunopathological hepatitis, suggesting vasoactive serotonin supports virus persistence in the liver and aggravates virus-induced immunopathology.

TL;DR: Hypergammaglobulinemia may arise when specific helper T cells recognize B cells that have processed viral antigens irrespective of the B cell receptor specificity, and this nonspecific B cell activation may contribute to antibody-mediated autoimmunity.

TL;DR: It is demonstrated that highly activated liver-specific effector CD8+ T cells alone were not sufficient to trigger immune destruction of the liver in mice, and only additional innate immune signals orchestrated by TLR3 provoked liver damage.

TL;DR: Evidence is provided that, paradoxically, because of polyclonal B cell activation, virus-specific T cell help impairs the induction of neutralizing antibody responses.