AbstractThe induction of autoimmunity by viruses has been hypothesized to occur by a number of mechanisms. Coxsackievirus B4 (CB4) induces hyperglycemia in SJL mice resembling diabetes in humans. While virus is effectively cleared within 2 weeks, hyperglycemia does not appear until about 8–12 weeks postinfection at a time when replicative virus is no longer detectable. In SJL mice, reinfection with CB4 enhanced the development of hyperglycemia. As predicted, the immune system responded more rapidly to the second infection and virus was cleared more swiftly. However, while infiltrating T cells were found within the pancreas, depletion of the CD4 T cell population prior to secondary infection or use of CD8 knock-out mice had no effect on the ...
AbstractCoxsackieviral infections have been linked etiologically to multiple diseases. The serotype ...
Type 1 diabetes (T1D) is an autoimmune disease caused by loss of pancreatic β cells via apoptosis wh...
This is the final version of the article. Available from eLife Sciences Publications via the DOI in ...
AbstractThe induction of autoimmunity by viruses has been hypothesized to occur by a number of mecha...
The induction of autoimmunity by viruses has been attributed to numerous mechanisms. In mice, coxsac...
Coxsackievirus infections have been proposed as an environmental trigger for the development of T-ce...
Coxsackievirus infections have been proposed as an environmental trigger for the development of T-ce...
Background: Viral infections are thought to play a role in the development of autoimmune diseases li...
AbstractWe evaluated the role of the costimulatory molecule B7-1 in overcoming peripheral ignorance ...
Type I diabetes is a multi-factorial disease resulting from the destruction of beta cells in the is...
To study self reactivity, a transgenic mouse model has been established in which the lymphocytic cho...
Type 1 diabetes (T1D) is characterized by the destruction of the insulin-producing β-cells of pancre...
International audienceThe evidence for an association between coxsackievirus B (CVB) infection, panc...
Type 1 diabetes (T1D) is characterized by the destruction of the insulin-producing beta-cells of pan...
Diabetes mellitus (DM) and its complications are now increasing in human and animals. There are two ...
AbstractCoxsackieviral infections have been linked etiologically to multiple diseases. The serotype ...
Type 1 diabetes (T1D) is an autoimmune disease caused by loss of pancreatic β cells via apoptosis wh...
This is the final version of the article. Available from eLife Sciences Publications via the DOI in ...
AbstractThe induction of autoimmunity by viruses has been hypothesized to occur by a number of mecha...
The induction of autoimmunity by viruses has been attributed to numerous mechanisms. In mice, coxsac...
Coxsackievirus infections have been proposed as an environmental trigger for the development of T-ce...
Coxsackievirus infections have been proposed as an environmental trigger for the development of T-ce...
Background: Viral infections are thought to play a role in the development of autoimmune diseases li...
AbstractWe evaluated the role of the costimulatory molecule B7-1 in overcoming peripheral ignorance ...
Type I diabetes is a multi-factorial disease resulting from the destruction of beta cells in the is...
To study self reactivity, a transgenic mouse model has been established in which the lymphocytic cho...
Type 1 diabetes (T1D) is characterized by the destruction of the insulin-producing β-cells of pancre...
International audienceThe evidence for an association between coxsackievirus B (CVB) infection, panc...
Type 1 diabetes (T1D) is characterized by the destruction of the insulin-producing beta-cells of pan...
Diabetes mellitus (DM) and its complications are now increasing in human and animals. There are two ...
AbstractCoxsackieviral infections have been linked etiologically to multiple diseases. The serotype ...
Type 1 diabetes (T1D) is an autoimmune disease caused by loss of pancreatic β cells via apoptosis wh...
This is the final version of the article. Available from eLife Sciences Publications via the DOI in ...