Effect of Bacillus Calmette-Guerin vaccination on new-onset type 1 diabetes. A randomized clinical study.

Allen, Holley; Klingensmith, G J; Jensen, Paul N.; Simões, Eric A F; Hayward, A; Chase, H. Peter

doi:10.2337/diacare.22.10.1703

Cited by 110 publications

(66 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Immunological features. The LEW.1WR1 rat is not lymphopenic; total spleen cell counts (ϫ10 6 ) were 504 Ϯ 80 in LEW.1WR1 rats (n ϭ 3) compared with 300 Ϯ 58 in BBDR rats (n ϭ 3). Table 2 shows the comparative phenotypic profiles of LEW.1WR1, BBDR, and LEW rats at 35-42 days of age.…”

Section: Lew1wr1 Rats and Autoimmune Diabetesmentioning

confidence: 95%

LEW.1WR1 Rats Develop Autoimmune Diabetes Spontaneously and in Response to Environmental Perturbation

et al. 2005

View full text Add to dashboard Cite

We describe a new rat model of autoimmune diabetes that arose in a major histocompatibility complex congenic LEW rat. Spontaneous diabetes in LEW.1WR1 rats (RT1 u/u/a ) occurs with a cumulative frequency of ϳ2% at a median age of 59 days. The disease is characterized by hyperglycemia, glycosuria, ketonuria, and polyuria. Both sexes are affected, and islets of acutely diabetic rats are devoid of ␤-cells, whereas ␣-and ␦-cell populations are spared. The peripheral lymphoid phenotype is normal, including the fraction of ART2 ؉ regulatory T-cells. We tested the hypothesis that the expression of diabetes would be increased by immunological perturbation of innate or adaptive immunity. Treatment of young rats with depleting anti-ART2.1 monoclonal antibody increased the frequency of diabetes to 50%. Treatment with the toll-like receptor 3 ligand polyinosinic:polycytidylic acid increased the frequency of diabetes to 100%. All diabetic rats exhibited end-stage islets. The LEW.1WR1 rat is also susceptible to collagen-induced arthritis but is free of spontaneous thyroiditis. The LEW.1WR1 rat provides a new model for studying autoimmune diabetes and arthritis in an animal with a genetic predisposition to both disorders that can be amplified by environmental perturbation. Diabetes 54: 2727-2733, 2005

show abstract

Section: Lew1wr1 Rats and Autoimmune Diabetesmentioning

confidence: 95%

LEW.1WR1 Rats Develop Autoimmune Diabetes Spontaneously and in Response to Environmental Perturbation

et al. 2005

View full text Add to dashboard Cite

show abstract

“…However, subsequent studies found that early administration of bacille Calmette-Guerin vaccine did not prevent type 1 diabetes. 76,77 Also, the analytical methods used in the Finnish study of Hib vaccine were incorrect, and there were no significant differences in the incidence of type 1 diabetes in Hib-vaccinated infants 10 years later. 78 In addition, 21 421 children who received the Hib conjugate vaccine between 1988 and 1990 in the United States were followed for 10 years and the risk of type 1 diabetes was 0.78 when compared with a group of 22 557 children who did not receive the vaccine.…”

Section: Clinical Studies Evaluating the Relationship Between Vaccinementioning

confidence: 99%

Addressing Parents’ Concerns: Do Vaccines Cause Allergic or Autoimmune Diseases?

Offit

Hackett

2003

Pediatrics

View full text Add to dashboard Cite

ABSTRACT. Anecdotal case reports and uncontrolled observational studies in the medical literature claim that vaccines cause chronic diseases such as asthma, multiple sclerosis, chronic arthritis, and diabetes. Several biological mechanisms have been proposed to explain how vaccines might cause allergic or autoimmune diseases. For example, allergic diseases might be caused by prevention of early childhood infections (the "hygiene hypothesis"), causing a prolongation of immunoglobulin E-promoting T-helper cell type 2-type responses. However, vaccines do not prevent most common childhood infections, and large well-controlled epidemiologic studies do not support the hypothesis that vaccines cause allergies. Autoimmune diseases might occur after immunization because proteins on microbial pathogens are similar to human proteins ("molecular mimicry") and could induce immune responses that damage human cells. However, wild-type viruses and bacteria are much better adapted to growth in humans than vaccines and much more likely to stimulate potentially damaging selfreactive lymphocytes. Consistent with critical differences between natural infection and immunization, well-controlled epidemiologic studies do not support the hypothesis that vaccines cause autoimmunity.Flaws in proposed biological mechanisms that explain how vaccines might cause chronic diseases are consistent with the findings of many well-controlled large epidemiologic studies that fail to show a causal relationship.

show abstract

“…Both goals are not easy to achieve using the techniques currently available for patients. Numerous immunological methods have been employed to inhibit autoimmune responses to beta cells in human or animal models of type 1 diabetes [17][18][19][20][21][22][23][24][25][26][27]. However, immunological methods alone were largely unsuccessful in the treatment of clinically overt type 1 diabetes, probably because of the already significantly compromised beta cell mass.…”

Section: Discussionmentioning

confidence: 99%

Treatment of autoimmune diabetes in NOD mice by Toll-like receptor 2 tolerance in conjunction with dipeptidyl peptidase 4 inhibition

Kim

Lee

et al. 2012

Diabetologia

View full text Add to dashboard Cite

Aims/hypothesis We have shown that chronic administration of the Toll-like receptor 2 (TLR2) agonist Pam3CSK 4 prevents diabetes in NOD mice by inducing TLR2 tolerance of dendritic cells (DCs). We have also reported that a novel dipeptidyl peptidase 4 (DPP4) inhibitor, DA-1229, could increase beta cell mass. Here we investigated whether a combination of DPP4 inhibition, with beneficial effects on beta cell mass, and TLR2 tolerisation, protecting beta cells from autoimmune destruction, could treat a model of established type 1 diabetes. Methods Diabetic NOD mice were treated with 100 μg Pam3CSK 4 , administered three times a week for 3 weeks, in combination with feeding with chow containing 0.3% DA-1229. Beta cell mass and proliferation were studied by immunohistochemistry. DC tolerance was assessed by studying diabetogenic CD4 + T cell priming after adoptive transfer and expression of costimulatory molecules on DCs by flow cytometry. Results

show abstract

Effect of Bacillus Calmette-Guerin vaccination on new-onset type 1 diabetes. A randomized clinical study.

Abstract: Vaccination with BCG at the time of onset of type 1 diabetes does not increase the remission rate or preserve beta-cell function.

Cited by 110 publications

References 0 publications

LEW.1WR1 Rats Develop Autoimmune Diabetes Spontaneously and in Response to Environmental Perturbation

LEW.1WR1 Rats Develop Autoimmune Diabetes Spontaneously and in Response to Environmental Perturbation

Addressing Parents’ Concerns: Do Vaccines Cause Allergic or Autoimmune Diseases?

Treatment of autoimmune diabetes in NOD mice by Toll-like receptor 2 tolerance in conjunction with dipeptidyl peptidase 4 inhibition

Contact Info

Product

Resources

About