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The role of macrophages in T cell-mediated autoimmune diabetes in nonobese diabetic mice.

DC Field Value Language
dc.contributor.authorJun, HS-
dc.contributor.authorYoon, CS-
dc.contributor.authorZbytnuik, L-
dc.contributor.authorvan Rooijen, N-
dc.contributor.authorYoon, JW-
dc.date.accessioned2011-09-19T05:37:41Z-
dc.date.available2011-09-19T05:37:41Z-
dc.date.issued1999-
dc.identifier.issn0022-1007-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/4223-
dc.description.abstractWe have shown previously that the inactivation of macrophages in nonobese diabetic (NOD) mice results in the prevention of diabetes; however, the mechanisms involved remain unknown. In this study, we found that T cells in a macrophage-depleted environment lost their ability to differentiate into beta cell-cytotoxic T cells, resulting in the prevention of autoimmune diabetes, but these T cells regained their beta cell-cytotoxic potential when returned to a macrophage-containing environment. To learn why T cells in a macrophage-depleted environment lose their ability to kill beta cells, we examined the islet antigen-specific immune response and T cell activation in macrophage-depleted NOD mice. There was a shift in the immune balance, a decrease in the T helper cell type 1 (Th1) immune response, and an increase in the Th2 immune response, due to the reduced expression of the macrophage-derived cytokine IL-12. As well, there was a deficit in T cell activation, evidenced by significant decreases in the expression of Fas ligand and perforin. The administration of IL-12 substantially reversed the prevention of diabetes in NOD mice conferred by macrophage depletion. We conclude that macrophages play an essential role in the development and activation of beta cell-cytotoxic T cells that cause beta cell destruction, resulting in autoimmune diabetes in NOD mice.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHAutoimmunity-
dc.subject.MESHCell Differentiation-
dc.subject.MESHClodronic Acid-
dc.subject.MESHCytotoxicity, Immunologic-
dc.subject.MESHDiabetes Mellitus-
dc.subject.MESHFas Ligand Protein-
dc.subject.MESHFemale-
dc.subject.MESHInterleukin-12-
dc.subject.MESHIslets of Langerhans-
dc.subject.MESHMacrophages-
dc.subject.MESHMembrane Glycoproteins-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred NOD-
dc.subject.MESHPancreas-
dc.subject.MESHPerforin-
dc.subject.MESHPore Forming Cytotoxic Proteins-
dc.subject.MESHSpleen-
dc.subject.MESHT-Lymphocytes-
dc.subject.MESHTissue Transplantation-
dc.titleThe role of macrophages in T cell-mediated autoimmune diabetes in nonobese diabetic mice.-
dc.typeArticle-
dc.identifier.pmid9892617-
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192977/-
dc.contributor.affiliatedAuthor윤, 지원-
dc.type.localJournal Papers-
dc.citation.titleThe Journal of experimental medicine-
dc.citation.volume189-
dc.citation.number2-
dc.citation.date1999-
dc.citation.startPage347-
dc.citation.endPage358-
dc.identifier.bibliographicCitationThe Journal of experimental medicine, 189(2). : 347-358, 1999-
dc.identifier.eissn1540-9538-
dc.relation.journalidJ000221007-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Endocrinology & Metabolism
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