Lymphocyte transfusions prevent diabetes in the Bio-Breeding/Worcester rat.

Rossini, A A; Faustman, Denise L.; Woda, Bruce A.; Like, A A; Szymanski, Irma O.; Mordes, John P.

doi:10.1172/jci111416

Cited by 87 publications

(38 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Diabetes in BBDR rats can also be induced by depletion of ART2 ϩ Tregs (2), whereas T1D in BBDP rats is prevented by adoptive transfer of a population of CD4 ϩ ART2 ϩ cells (3)(4)(5). These data suggest that a population of Tregs is capable of preventing diabetes in BB rats and resides within a population of CD4 ϩ ART2 ϩ T cells.…”

Section: Nbred Biobreeding (Bb)mentioning

confidence: 99%

A Regulatory CD4+ T Cell Subset in the BB Rat Model of Autoimmune Diabetes Expresses Neither CD25 Nor Foxp3

Hillebrands

Whalen

Visser

et al. 2006

The Journal of Immunology

View full text Add to dashboard Cite

Biobreeding (BB) rats model type 1 autoimmune diabetes (T1D). BB diabetes-prone (BBDP) rats develop T1D spontaneously. BB diabetes-resistant (BBDR) rats develop T1D after immunological perturbations that include regulatory T cell (Treg) depletion plus administration of low doses of a TLR ligand, polyinosinic-polycytidylic acid. Using both models, we analyzed CD4+CD25+ and CD4+CD45RC− candidate rat Treg populations. In BBDR and control Wistar Furth rats, CD25+ T cells comprised 5–8% of CD4+ T cells. In vitro, rat CD4+CD25+ T cells were hyporesponsive and suppressed T cell proliferation in the absence of TGF-β and IL-10, suggesting that they are natural Tregs. In contrast, CD4+CD45RC− T cells proliferated in vitro in response to mitogen and were not suppressive. Adoptive transfer of purified CD4+CD25+ BBDR T cells to prediabetic BBDP rats prevented diabetes in 80% of recipients. Surprisingly, CD4+CD45RC−CD25− T cells were equally protective. Quantitative studies in an adoptive cotransfer model confirmed the protective capability of both cell populations, but the latter was less potent on a per cell basis. The disease-suppressing CD4+CD45RC−CD25− population expressed PD-1 but not Foxp3, which was confined to CD4+CD25+ cells. We conclude that CD4+CD25+ cells in the BBDR rat act in vitro and in vivo as natural Tregs. In addition, another population that is CD4+CD45RC−CD25− also participates in the regulation of autoimmune diabetes.

show abstract

Section: Nbred Biobreeding (Bb)mentioning

confidence: 99%

A Regulatory CD4+ T Cell Subset in the BB Rat Model of Autoimmune Diabetes Expresses Neither CD25 Nor Foxp3

Hillebrands

Whalen

Visser

et al. 2006

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…I mmunotherapeutic trials for various substances useful in' treating type I diabetes have been carried out in animals 1 - 3 and humans 47 BB rats had been protected from hyperglycemia by antilymphocyte serum (ALS), 1 by transfusion of normal T cells, 8 and by cyclosporin A. 2 The nonobese diabetic (NOD) mouse, derived from the CTS subline of an ICR strain, is an animal model of type I diabetes characterized by insulitis 9 and a perturbed immune system.…”

mentioning

confidence: 99%

Streptococcal Preparation (OK-432) Inhibits Development of Type I Diabetes in NOD Mice

et al. 1986

View full text Add to dashboard Cite

SUMMARYOK-432 (a streptococcal preparation) has been widely used for cancer immunotherapy in Japan. It is the most potent immunomodulator in activating both macrophages and killer T cells and in increasing interleukin 2 production. Two K.E. (Klinische Einheit, clinical unit) of OK-432 were given intraperitoneally to each of 17 female nonobese diabetic (NOD) mice every week from 4-24 wk of age. NOD mice as well as BB rats spontaneously develop type I diabetes. During administration of OK-432, the development of diabetes was inhibited in 17 of 17 mice over the 24-wk observation period, whereas 14 of 17 female NOD mice given physiological saline had developed diabetes by 24 wk of age. At the onset of diabetes, nonfasting blood glucose was 511 ± 8 2 mg/dl. Histologic examination showed that in the OK-432-treated NOD mice, 98% of total islets were intact or mildly infiltrated with mononuclear cells, whereas in saline-treated NOD mice, 79% of total islets exhibited severe insulitis. In OK-432-treated NOD mice, both the number of the mononuclear spleen cells and their natural killer cell activity was significantly increased. DIABETES 1986; 32:496-99. 10^12 Ultrastructural examinations of female NOD mice show infiltration of macrophages and lymphocytes into the islets and reduction of islet size. 13 As reported previously,

show abstract

“…It is interesting to note that transfusions ofcertain cells protect against diabetes, (12) while a soluble factor obtained from the same cells can induce and accelerate the onset of the disease. One may speculate that viable transfused lymphocytes specifically enhance suppressor cell activity, perhaps by establishing a chimera.…”

Section: Discussionmentioning

confidence: 99%

Diabetes in the Bio-Breeding/Worcester rat. Induction and acceleration by spleen cell-conditioned media.

Handler¹,

Mordes²,

Seals³

et al. 1985

J. Clin. Invest.

Self Cite

View full text Add to dashboard Cite

Lymphocyte transfusions prevent diabetes in the Bio-Breeding/Worcester rat.

Cited by 87 publications

References 23 publications

A Regulatory CD4+ T Cell Subset in the BB Rat Model of Autoimmune Diabetes Expresses Neither CD25 Nor Foxp3

A Regulatory CD4+ T Cell Subset in the BB Rat Model of Autoimmune Diabetes Expresses Neither CD25 Nor Foxp3

Streptococcal Preparation (OK-432) Inhibits Development of Type I Diabetes in NOD Mice

Diabetes in the Bio-Breeding/Worcester rat. Induction and acceleration by spleen cell-conditioned media.

Contact Info

Product

Resources

About