Type 1 diabetes: virus infection or autoimmune disease?

  title={Type 1 diabetes: virus infection or autoimmune disease?},
  author={DeLisa Fairweather and Noel R. Rose},
  journal={Nature Immunology},
What does Coxsackie virus have to do with diabetes? Evidence is emerging that insulin-producing β cells are highly susceptible to acute infection by Coxsackie virus if their production of interferon is inhibited, resulting in diabetes. 
Mechanisms of lymphatic system‐specific viral replication and its potential role in autoimmune disease
In this review, the mechanisms that contribute to enforced viral replication are summarized and anti‐viral immune activation and, counterintuitively, accelerates virus control are summarized.
This work summarizes current knowledge on virus-induced diabetes together with evidence from experimental models, susceptibility genes in mice, candidate diabetogenic viruses and susceptible genes in humans, and Perspectives on the identification of diabetic viruses are presented.
Women and Autoimmune Diseases
Recent evidence indicates that sex hormones may exacerbate autoimmune diseases, particularly in women, by increasing the adjuvant effect of infections.
Tunicamycin Inhibits Diabetes
It is found that a single dose of tunicamycin reduced the activation and pancreatic infiltration of CD8+ T cells and delayed the incidence of virus-induced diabetes and improved survival rates.
Mast Cells and Innate Cytokines are Associated with Susceptibility to Autoimmune Heart Disease Following Coxsackievirus B3 Infection
Comparing the early cytokine response of mice susceptible or resistant to the development of autoimmune heart disease following viral infection found that susceptible BALB/c mice produced elevated levels of TNF-α, IL-1β, and IL-4 within hours of Coxsackievirus B3 (CB3) infection.
β-cell regeneration to treat Type 1 diabetes mellitus
The most important studies related to probable precursor cells implied in the process of regeneration, and the results of various immunomodulatory regimens aiming at blocking autoimmunity against pancreatic β-cells and at promoting β-cell preservation are summarized.
Viruses as adjuvants for autoimmunity: evidence from Coxsackievirus‐induced myocarditis
Many similarities are described in the pathogenesis of Coxsackievirus and the adjuvant‐induced model of myocarditis including upregulation of particular TLRs and cytokines soon after inoculation.


Diabetes induced by Coxsackie virus: Initiation by bystander damage and not molecular mimicry
Results show that diabetes induced by Coxsackie virus infection is a direct result of local infection leading to inflammation, tissue damage, and the release of sequestered islet antigen resulting in the re-stimulation of resting autoreactive T cells, further indicating that the is let antigen sensitization is an indirect consequence of the viral infection.
Type 1 diabetes
The increase in knowledge of basic immunology has allowed the initiation of large-scale clinical efforts to prevent diabetes in humans and animal models.
Diabetes mellitus due to viruses — some recent developments
It is clear that there are many viruses with the potential to induce diabetes, and a viral involvement in the pathogenesis of diabetes has been established in some instances.
Pancreatic expression of interferon-γ protects mice from lethal coxsackievirus B3 infection and subsequent myocarditis
The benefit of reducing the level of viremia early during infection is emphasized, thereby reducing the incidence of virus-mediated heart damage and autoimmunity.
Autoimmunity provoked by infection: how good is the case for T cell epitope mimicry?
For decades there have been tantalizing associations between infectious agents and autoimmunity, but many of the associations appear less than convincing and, even for those that seem to be on solid footing, there is no real understanding of the underlying mechanism(s).
Noncytolytic control of viral infections by the innate and adaptive immune response.
The contribution of noncytolytic mechanisms to the control of viral infections with a particular emphasis on the role of cytokines is described, by modulating the induction, amplification, recruitment, and effector functions of the immune response.
Molecular mimicry: a critical look at exemplary instances in human diseases
No clear examples of a human disease caused by molecular mimicry are found, but the concept that antigenic determinants of microorganisms resemble antigeniceterminants of the host is frequently cited as a plausible mechanism to account for the association of infection and autoimmune disease.
Induction of Bystander T Cell Proliferation by Viruses and Type I Interferon in Vivo
In mice, IFN I [poly(I:C)]-stimulated CD8+ cells survived for prolonged periods in vivo and displayed the same phenotype as did long-lived antigen-specific CD8-specific cells, and production ofIFN I may play an important role in the generation and maintenance of specific memory.