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Frequency of IDDM

60%-80% in non-VAF housing; >80% in VAF housing

30% with poly(IC) or KRV alone; >90% with anti-RT6 MAb plus poly(IC); >90% with anti-RT6 MAb plus KRV

Time of onset of IDDM

55-110 days of age (mean 80 days)

14-21 days after treatment begins

Immunocompetence

Lymphopenic, deficient in RT6+ and CD8+ T cells; indolent graft rejection; defective T cell response to mitogen

Normal T cell phenotype; immunocompetent

Adoptive transfer of IDDM

Spleen and lymph node cells, requires mitogen activation

Spleen and lymph node cells do not require mitogen activation; thymocytes require treatment of all recipients with anti-aRT6.1 MAb and VAF-housed recipients with poly(IC)

Diabetogenic effector cells

CD4+ RT6.1- and CD8+ RT6.1-

CD4+ RT6.1- and CD8+ RT6.1-

Associated autoimmunity Thyroiditis

Procedures that induce IDDM also induce thyroiditis

"Based on Crisa et al. (1991) and Rossini et al. (1995).

Abbreviations: DP, diabetes prone; DR, diabetes resistant; IDDM, insulin-dependent diabetes mellitus; KRV, Kilham rat virus; MAb, monoclonal antibody; NA, not applicable; poly(IC), polyinosinic/polycytidylic acid; VAF, viral antigen free.

"Based on Crisa et al. (1991) and Rossini et al. (1995).

Abbreviations: DP, diabetes prone; DR, diabetes resistant; IDDM, insulin-dependent diabetes mellitus; KRV, Kilham rat virus; MAb, monoclonal antibody; NA, not applicable; poly(IC), polyinosinic/polycytidylic acid; VAF, viral antigen free.

vated in vitro with concanavalin A prior to transfer (McKeever et al., 1990). The ineffectiveness of fresh DP-BB spleen cells in the adoptive transfer model is most likely due to the short life span of peripheral T cells in these animals. In contrast, IDDM transfer by DR-BB rat spleen cells, lymph node cells, or thymocytes does not require in vitro T cell activation.

The use of animal models to study the pathogenesis of human IDDM provides numerous benefits, but certain caveats apply (Rossini et al., 1995). It is not certain how accurately BB rats or nonobese diabetic (NOD) mice reflect the pathogenesis of human IDDM. BB rats and NOD mice differ in that many treatment modalities that prevent diabetes in NOD mice do not prevent disease in BB rats. The efficacy of these modalities in preventing human IDDM is unknown.

Critical Parameters and Troubleshooting

Inbreeding in the various dispersed colonies of BB rats worldwide has resulted in genetic polymorphisms and significant differences in autoimmune characteristics among rats from the different colonies. For example, the diabetes-resistant BB-DR/Ed rat is lymphopenic, yet none of the animals develop IDDM (Joseph et al., 1993). For studies not intended to address idiosyncratic or strain-specific characteristics, the authors recommend use of BB/Wor rats from the NIH-sponsored colony in Worcester,

Animal Models for Autoimmune and

Inflammatory Disease

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