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Disease-protected major histocompatibility complex Ea-transgenic non- obese diabetic (NOD) mice show interleukin-4 production not seen in susceptible Ea-transgenic and non-transgenic NOD mice
Södertörns högskola, Avdelning Naturvetenskap. Karolinska Institute.
1998 (engelsk)Inngår i: Immunology, ISSN 0019-2805, E-ISSN 1365-2567, Vol. 95, nr 1, s. 1-7Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The non-obese diabetic (NOD) mouse is an animal model for insulin- dependent diabetes that has many similarities to the human disease. NOD mice transgenic for the Ea gene, allowing expression of the E molecule, are protected from diabetes and rarely develop insulitis. An Ea transgene mutated in the promoter region, (ΔY) lacks E expression on most B cells, thymic medullary epithelium and primary antigen-presenting cells, and confers no protection whatsoever. We have used these transgenic NOD mice, together with non-transgenic NOD mice, to study the correlation of E expression and production of interleukin-4 (IL-4) and interferon-γ (IFN-γ). We show that protected E-transgenic NOD mice have elevated levels of IL-4 compared with non-transgenic mice, both in the thymus and in the periphery. However, susceptible ΔY-transgenic mice have elevated thymic IL-4 levels, but express almost as little IL-4 as non-transgenic NOD mice in the periphery. This drop in peripheral IL-4 production seen in ΔY-transgenic mice thus correlates with the decreased E expression in the periphery of ΔY-transgenic NOD mice. In contrast, there were no differences in IFN-γ production between the three NOD lines. We suggest that Ea-transgenic NOD mice have E-selected regulatory T cells producing IL-4, which are subsequently activated by E-expressing primary antigen-presenting cells in the periphery. This activation would then be instrumental for the E-mediated protection from disease in NOD mice. Such a process would explain the total absence of protection in ΔY-transgenic NOD mice, despite their widespread E expression.

sted, utgiver, år, opplag, sider
1998. Vol. 95, nr 1, s. 1-7
Emneord [en]
cd4 antigen, cd8 antigen, gamma interferon, interleukin 4, major histocompatibility antigen class 2, messenger rna, animal cell, animal experiment, animal model, animal tissue, article, controlled study, disease predisposition, gene mutation, insulin dependent diabetes mellitus, insulitis, major histocompatibility complex, mouse, nonhuman, priority journal, promoter region, protection, t lymphocyte, transgenic mouse, Animals, Cells, Cultured, Diabetes Mellitus, Type 1, Enzyme-Linked Immunosorbent Assay, Gene Expression, Genetic Predisposition to Disease, Histocompatibility Antigens Class I, HLA Antigens, Interferon Type II, Interleukin-4, Mice, Mice, Inbred NOD, Mice, Transgenic, Reverse Transcriptase Polymerase Chain Reaction, RNA, Messenger, Spleen, T-Lymphocytes, Thymus Gland
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Identifikatorer
URN: urn:nbn:se:sh:diva-22931DOI: 10.1046/j.1365-2567.1998.00580.xISI: 000075792400001PubMedID: 9767450Scopus ID: 2-s2.0-0031661151OAI: oai:DiVA.org:sh-22931DiVA, id: diva2:710630
Tilgjengelig fra: 2014-04-07 Laget: 2014-03-28 Sist oppdatert: 2017-07-20bibliografisk kontrollert

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