Suppression of insulitis in non-obese diabetic (NOD) mice by oral insulin administration is associated with selective expression of interleukin-4 and -10, transforming growth factor-beta, and prostaglandin-E.
about
Mechanism of oral tolerance induction to therapeutic proteinsType I (insulin-dependent) diabetes is a Th1- and Th2-mediated autoimmune diseaseThe nature of the active suppression of responses associated with experimental autoimmune myasthenia gravis by a dual altered peptide ligand administered by different routesEfferocytosis promotes suppressive effects on dendritic cells through prostaglandin E2 production in the context of autoimmunity.Impact of intranasal insulin on insulin antibody affinity and isotypes in young children with HLA-conferred susceptibility to type 1 diabetes.Autoimmune diabetes: ongoing development of immunological intervention strategies targeted directly against autoreactive T cellsUse of autoantigen-loaded phosphatidylserine-liposomes to arrest autoimmunity in type 1 diabetesEfficacy of Setarud (IMOD™), a novel electromagnetically-treated multi-herbal compound, in mouse immunogenic type-1 diabetesCostimulatory function and expression of CD40 ligand, CD80, and CD86 in vascularized murine cardiac allograft rejection.Changes in microRNA expression contribute to pancreatic β-cell dysfunction in prediabetic NOD miceExpression of a ricin toxin B subunit: insulin fusion protein in edible plant tissues.Interferon-alpha initiates type 1 diabetes in nonobese diabetic mice.Antigen-specific effector CD4 T lymphocytes school lamina propria dendritic cells to transfer innate tolerance.Oral insulin treatment suppresses virus-induced antigen-specific destruction of beta cells and prevents autoimmune diabetes in transgenic mice.Oral tolerization to adenoviral antigens permits long-term gene expression using recombinant adenoviral vectors.Metabolically inactive insulin analog prevents type I diabetes in prediabetic NOD miceLocal expression of immunoregulatory IL-12p40 gene prolonged syngeneic islet graft survival in diabetic NOD mice.Characterization of T cell phenotype and function in a double transgenic (collagen-specific TCR/HLA-DR1) humanized model of arthritis.Oral gene application using chitosan-DNA nanoparticles induces transferable tolerance.Association of the gene expression variation of tumor necrosis factor-α and expressions changes of dopamine receptor genes in progression of diabetic severe foot ulcers.Intestinal type 1 regulatory T cells migrate to periphery to suppress diabetogenic T cells and prevent diabetes development.The pathogenicity of islet-infiltrating lymphocytes in the non-obese diabetic (NOD) mouse.Inhalation of glutamic acid decarboxylase 65-derived peptides can protect against recurrent autoimmune but not alloimmune responses in the non-obese diabetic mouse.Induction of specific transplantation immunity by oral immunization with allogeneic cells.
P2860
Q26866369-9129207E-A7F9-46E0-AB10-FAA4F6C507F2Q33606814-44ACE40B-7A7E-4872-A0ED-2FDC9BD79CCEQ33947964-D0222720-4597-490A-BEA7-F80A1F23094FQ34730167-206FB7E3-5915-4817-8179-FE531B24390CQ35043241-DBB4132B-3728-4762-9290-043BDA6109D0Q35612613-2D41D603-E2C6-416B-B8D0-96E2834CE47BQ35651667-6360CA47-3DF4-4D94-A032-B17AB0062F1DQ35817695-5093DC3D-94D3-4025-A41E-FBC58195C061Q35939463-26F6BA5A-CB74-4C7C-AF3B-7F67F3B45457Q36047577-03BB1CEB-B3D7-40B8-882B-8A70E75ECFABQ36591189-70131826-098C-47A4-9A71-52C277B49364Q36858608-85320445-58DD-4A8E-A455-B7B4C5EC2925Q36920276-29070404-27C1-43D4-A338-00527C92F368Q37359669-E43021F9-F84E-4CAB-9D2F-46E9E79C5569Q37364744-C321FD7C-475D-4221-8429-826F13D192F4Q37372373-41D1DD96-616A-4B4C-BB38-34420A3F2D96Q37387946-F4F3B52F-E347-45E0-9155-7EFA203F48A4Q37690636-A60A5B39-9FAF-402B-886D-32343B6BC2CBQ41426532-0915083C-63B7-4177-8FF3-339E2C3CA66DQ47155984-5DB9D5E4-7CE5-4091-BED4-991C1A3E809DQ48000827-533A2D9B-0ED5-4B43-ABA5-2FAF26208F2FQ50535751-8CA427A8-6C65-473F-B720-1A526B9E69FCQ51756787-43A1CD27-E16C-4783-AEC7-F347DEEF2923Q53706683-0242341B-6E69-4829-9372-9F3185F4CA5A
P2860
Suppression of insulitis in non-obese diabetic (NOD) mice by oral insulin administration is associated with selective expression of interleukin-4 and -10, transforming growth factor-beta, and prostaglandin-E.
description
1995 nî lūn-bûn
@nan
1995年の論文
@ja
1995年論文
@yue
1995年論文
@zh-hant
1995年論文
@zh-hk
1995年論文
@zh-mo
1995年論文
@zh-tw
1995年论文
@wuu
1995年论文
@zh
1995年论文
@zh-cn
name
Suppression of insulitis in no ...... tor-beta, and prostaglandin-E.
@ast
Suppression of insulitis in no ...... tor-beta, and prostaglandin-E.
@en
type
label
Suppression of insulitis in no ...... tor-beta, and prostaglandin-E.
@ast
Suppression of insulitis in no ...... tor-beta, and prostaglandin-E.
@en
prefLabel
Suppression of insulitis in no ...... tor-beta, and prostaglandin-E.
@ast
Suppression of insulitis in no ...... tor-beta, and prostaglandin-E.
@en
P2093
P2860
P1476
Suppression of insulitis in no ...... tor-beta, and prostaglandin-E.
@en
P2093
P2860
P304
P407
P577
1995-11-01T00:00:00Z