B7-1 is a co-stimulatory molecule that signals T-cells that recognize antigen to proliferate and differentiate into effector T-cells. The same cell must present antigen and express co-stimulatory molecules, such as B7-1, to activate naive T-cells. Thus, tissues that do not express co-stimulatory molecules would not be expected to induce immune responses, while expression of a co-stimulator on tissue cells may convert them into effective antigen-presenting cells and induce autoimmunity. To test this, transgenic mice have been generated that express B7-1 on the β-cells of the pancreatic islets of Langerhans. On a B6 genetic background, B7-1 expression on β-cells does not predispose to diabetes. B6 mice are resistant to diabetes. However, when B7-1 is expressed on the β-cells of B6 mice backcrossed once to the genetically susceptible NOD strain, the onset of diabetes is accelerated and the autoimmune attack intensified. This illustrates that B7-1 is a very potent co-stimulatory molecule in vivo and that its presence on the surface of tissue cells can potentiate the autoimmune process.
Expression of the Co-stimulator Molecule B7–1 in Pancreatic β-Cells Accelerates Diabetes in the NOD Mouse
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Susan Wong, Sylvie Guerder, Irene Visintin, Eva-Pia Reich, Karl E Swenson, Richard A Flavell, Charles A Janeway; Expression of the Co-stimulator Molecule B7–1 in Pancreatic β-Cells Accelerates Diabetes in the NOD Mouse. Diabetes 1 March 1995; 44 (3): 326–329. https://doi.org/10.2337/diab.44.3.326
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