Cell
Diabetes and tolerance in transgenic mice expressing class II MHC molecules in pancreatic beta cells
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Rheumatoid Rescue of Misfolded Cellular Proteins by MHC Class II Molecules: A New Hypothesis for Autoimmune Diseases
2016, Advances in ImmunologyCitation Excerpt :However, autoantibodies against these misfolded proteins are not produced in steady state; immune cells are exposed constitutively to these complexes, a process that appears to have induced tolerance. Indeed, transgenic mice expressing MHC class II molecules on pancreatic β cells did not exhibit β cell autoimmunity (Lo et al., 1988; Sarvetnick, Liggitt, Pitts, Hansen, & Stewart, 1988). Because MHC class II expression is not inducible in these transgenic mice, even if certain β cell-specific misfolded proteins are presented on MHC class II molecules, the proteins associated with MHC class II molecules are always presented to immune cells and may not be recognized as “neo-self”-antigens.
Lymphotoxin-alpha contributes to lymphangiogenesis
2010, BloodCitation Excerpt :Mice deficient in LTα lack all lymph nodes and Peyer patches,19 whereas those deficient in LTβ retain some cervical, sacral, and mesenteric lymph nodes.22 Transgenic expression of mouse LTα under the control of the rat insulin promoter II (RIP) leads to its expression in the β cells of the islets of Langerhans in the pancreas as expected, and in the skin23 and proximal convoluted tubules of the kidney23,24 as this promoter is somewhat “leaky.” These mice develop accumulations of T and B cells, dendritic cells, follicular dendritic cells, and macrophages that are organized into TLOs that resemble lymph nodes in cellular composition and compartmentalization, the presence of high endothelial venules (HEVs) and lymphoid chemokine expression,18,25 due to signaling through TNFR1.26
Peripheral CD8<sup>+</sup> T Cell Tolerance to Self-Proteins Is Regulated Proximally at the T Cell Receptor
2008, ImmunityCitation Excerpt :Immune-mediated destruction of normal tissues is limited by deletion of autoreactive lymphocytes during development. However, some self-reactive T cells evade thymic deletion (Danke et al., 2004; Huseby et al., 2001; Lo et al., 1988; Morahan et al., 1989; Ohlen et al., 2002; Steinman, 2001), making peripheral tolerance induction essential to prevent autoimmunity. Unfortunately, CD8+ T cell tolerance to self-antigens can interfere with generation of effective T cell responses to tumors because many potentially targetable tumor-associated antigens are aberrantly expressed self-proteins (Pardoll, 2003).
Tolerance and Autoimmunity: T Cells
2006, The Autoimmune Diseases, Fourth EditionDeath effectors of β-cell apoptosis in type 1 diabetes
2004, Molecular Genetics and MetabolismInduction of GVHD-like skin disease by passively transferred CD8 <sup>+</sup> T-cell receptor transgenic T cells into keratin 14-ovalbumin transgenic mice
2004, Journal of Investigative DermatologyCitation Excerpt :Tg mouse models have been used as tools to investigate the mechanisms involved in peripheral tolerance. Early studies using tissue-specific expression of allogenic MHC class I (Miller et al, 1990;Schonrich et al, 1991) and class II (Lo et al, 1988;Sarvetnick et al, 1988;Bohme et al, 1989;Lo et al, 1989;Miller et al, 1990) molecules demonstrated functional peripheral tolerance in vivo. Mice expressing model self-antigens such as lymphocytic choriomeningitis virus (LCMV) nucleoprotein, LCMV glycoprotein (Oldstone et al, 1991;Lo et al, 1992;Ohashi et al, 1993;Morgan et al, 1999) or influenza virus hemagglutinin (Roman et al, 1990) under the control of an insulin promoter did not exhibit autoimmunity, unless they were infected with the respective virus.