Islet expression of interferon-α precedes diabetes in both the BB rat and streptozotocin-treated mice

Huang, Xiaojian; Hultgren, Bruce; Dybdal, Noël; Stewart, Timothy A.

doi:10.1016/1074-7613(94)90089-2

Cited by 79 publications

(59 citation statements)

References 59 publications

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“…Thus, their data suggest that enhanced HLA class I expression by islet cells is an early pathogenic event (preceding HLA class II expression by islet ,iicelts) [3]and this is associated with expression of IFN-(t by the ji cells [21 ]. Furthermore, in the BB rat model of type I diabetes, islet expression of IFN-a precedes lymphocytic infiltration and diabetes [22].…”

Section: Discussionmentioning

confidence: 99%

Enhanced expression of MHC class I molecules on cultured human thyroid follicular cells infected with reovirus through induction of type 1 interferons

Atta

Irving

Powell

et al. 1995

Clinical and Experimental Immunology

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SUMMARYCertain viruses are known to modulate the cellular expression of MHC molecules. We have investigated whether reovirus types I or 3 can alter the normal MHC molecule expression on cultured human thyroid follicular cells (TFC). Primary TFC cultures were established from eight human thyroid donors and MHC class I and II expression was assessed by indirect immunofluorescence microscopy. Both types ot" reovirus enhanced MHC class 1 expression on TFC from all thyroid donors. Class II MHC prolein was strongly induced by type 1 reovirus on TFC from one donor, while weak induction of expression, by either reo-l or reo-3 virus, was noted on the TFC of five other donors. Studies on the mechanism(s) of MHC class I hyperexpression showed that mouse MoAb against the type 3 reovirus haemagglutinin {anti-HA3) reduced the ability ofthe virus to induce hyperexpression of class I MHC molecules on TFC. However, supernatant harvested from type 3 reovirus-infected TFC cultures maintained its ability to enhance class I expression after incubation with anti-HA3. Moreover, adding rabbit anti-sera lo interferon-alpha (IFN-a) or IFN-/? inhibited the increased class 1 MHC expression on TFC by both types of reovirus. These data suggest that reoviruses (types I and 3) can enhance MHC class I on cultured TFC. The mechanism of MHC class I enhancement is most probably through the release of IFN-cv and lFN-/y.

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Section: Discussionmentioning

confidence: 99%

Enhanced expression of MHC class I molecules on cultured human thyroid follicular cells infected with reovirus through induction of type 1 interferons

Atta

Irving

Powell

et al. 1995

Clinical and Experimental Immunology

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“…These mice were treated with multiple low doses of streptozotocin (STZ). This treatment induces insulitis (35), the extent of which depends on genetic background, the expression of cytokines in islets (36), and β cell death by apoptosis (37). Furthermore, STZ treatment induces β cell production of reactive oxygen intermediates and nitric oxide (38), which are involved in β cell destruction (39,40).…”

Section: Introductionmentioning

confidence: 99%

β cell expression of IGF-I leads to recovery from type 1 diabetes

George¹,

Ayuso²,

Casellas³

et al. 2002

J. Clin. Invest.

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Patients with type 1 diabetes are identified after the onset of the disease, when β cell destruction is almost complete. β cell regeneration from islet cell precursors might reverse this disease, but factors that can induce β cell neogenesis and replication and prevent a new round of autoimmune destruction remain to be identified. Here we show that expression of IGF-I in β cells of transgenic mice (in both C57BL/6-SJL and CD-1 genetic backgrounds) counteracts cytotoxicity and insulitis after treatment with multiple low doses of streptozotocin (STZ). STZ-treated nontransgenic mice developed high hyperglycemia and hypoinsulinemia, lost body weight, and died. In contrast, STZtreated C57BL/6-SJL transgenic mice showed mild hyperglycemia for about 1 month, after which they normalized glycemia and survived. After STZ treatment, all CD-1 mice developed high hyperglycemia, hypoinsulinemia, polydipsia, and polyphagia. However, STZ-treated CD-1 transgenic mice gradually normalized all metabolic parameters and survived. β cell mass increased in parallel as a result of neogenesis and β cell replication. Thus, our results indicate that local expression of IGF-I in β cells regenerates pancreatic islets and counteracts type 1 diabetes, suggesting that IGF-I gene transfer to the pancreas might be a suitable therapy for this disease.

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“…*Occasionally, very few scattered mononuclear cells could be found in rare islets of 2ϫ STZ-treated transgene-positive and transgene-negative recipients. We graded as "ϩ," although it is much milder than the "ϩ" score by Huang et al (28). ) and human MHC class II (DQ) on splenocytes was upregulated by STZ treatment, particularly MHC class I (Fig.…”

Section: Generationmentioning

confidence: 99%

Induction of insulitis by glutamic acid decarboxylase peptide-specific and HLA-DQ8-restricted CD4(+) T cells from human DQ transgenic mice.

Wong²,

Burkly³

et al. 1998

J. Clin. Invest.

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Islet expression of interferon-α precedes diabetes in both the BB rat and streptozotocin-treated mice

Cited by 79 publications

References 59 publications

Enhanced expression of MHC class I molecules on cultured human thyroid follicular cells infected with reovirus through induction of type 1 interferons

Enhanced expression of MHC class I molecules on cultured human thyroid follicular cells infected with reovirus through induction of type 1 interferons

β cell expression of IGF-I leads to recovery from type 1 diabetes

Induction of insulitis by glutamic acid decarboxylase peptide-specific and HLA-DQ8-restricted CD4(+) T cells from human DQ transgenic mice.

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