Abstract
Immune context is an essential determinant of the host response to potential autoantigens. The clustering of the autoantigens targeted in systemic lupus erythematosus within surface blebs of apoptotic cells generates high concentrations of autoantigen within discrete subcellular packages. We demonstrate here that when apoptosis is induced by Sindbis virus infection, viral antigens and autoantigens cocluster exclusively in small surface blebs of apoptotic cells. The surface of these blebs is rich in viral glycoproteins, and virions can be seen blebbing from their surface. We propose that these blebs of mixed foreign and self-origin define a novel immune context that may challenge self-tolerance.
Highlights
Immune context is an essential determinant of the host response to potential autoantigens
Optosis is a morphologically and biochemically distinct form of cell death that occurs in many different cell types in response to a diverse range of stimuli [1, 2]
The previous demonstration that complexes of self- and viral antigens are able to break tolerance to self has suggested that viral infection might act as an initiating stimulus in autoimmunity, but the site and context in which significant concentrations of these complexes may be encountered in vivo has not been identified [7]
Summary
Immune context is an essential determinant of the host response to potential autoantigens. We demonstrate here that when apoptosis is induced by Sindbis virus infection, viral antigens and autoantigens cocluster exclusively in small surface blebs of apoptotic cells. The surface of these blebs is rich in viral glycoproteins, and virions can be seen blebbing from their surface. We propose that these blebs of mixed foreign and self-origin define a novel immune context that may challenge self-tolerance
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