Antigen-presenting cells in adoptively transferred and spontaneous autoimmune diabetes - PubMed (original) (raw)
Antigen-presenting cells in adoptively transferred and spontaneous autoimmune diabetes
D Lo et al. Eur J Immunol. 1993 Jul.
Abstract
Histological techniques were used to identify antigen-presenting cells (APC) in adoptively transferred diabetes in NOD mice and Ins-HA transgenic mice, and in spontaneously diabetic NOD mice. In adoptively transferred disease, CD4+ T cells and F4/80+ macrophages dominated early infiltrates. By contrast, in spontaneously developing diabetes in NOD mice, lymphocytic infiltrates appeared to be well organized around a network of VCAM-1+ NLDC-145+ ICAM-1+ dendritic cells. Thus, the primary APC spontaneous autoimmune disease appears to be the strongly stimulatory dendritic cell rather than the normally resident macrophage. Next, we used chimeric animals to demonstrate that insulitis and diabetes could occur even when responding T cells were unable to recognize islet-specific antigen directly on beta cells. Altogether, the results demonstrate that immune-mediated damage does not require direct contact between CD4+ T cells and beta cells. Moreover, despite the induction of ICAM-1, VCAM-1, and class II on vascular endothelium near islet infiltrates, these experiments show that recruitment of lymphocytes occurs even when antigen presentation is not possible on vascular endothelium.
Similar articles
- Presentation of beta-cell antigens to CD4+ and CD8+ T cells of non-obese diabetic mice.
Shimizu J, Kanagawa O, Unanue ER. Shimizu J, et al. J Immunol. 1993 Aug 1;151(3):1723-30. J Immunol. 1993. PMID: 8101546 - Differences in adhesion markers, activation markers, and TcR in islet infiltrating vs. peripheral lymphocytes in the NOD mouse.
Goldrath AW, Barber L, Chen KE, Alters SE. Goldrath AW, et al. J Autoimmun. 1995 Apr;8(2):209-20. doi: 10.1006/jaut.1995.0016. J Autoimmun. 1995. PMID: 7612149 - I-Ag7-mediated antigen presentation by B lymphocytes is critical in overcoming a checkpoint in T cell tolerance to islet beta cells of nonobese diabetic mice.
Noorchashm H, Lieu YK, Noorchashm N, Rostami SY, Greeley SA, Schlachterman A, Song HK, Noto LE, Jevnikar AM, Barker CF, Naji A. Noorchashm H, et al. J Immunol. 1999 Jul 15;163(2):743-50. J Immunol. 1999. PMID: 10395666 - Contribution of T cells to the development of autoimmune diabetes in the NOD mouse model.
Toyoda H, Formby B. Toyoda H, et al. Bioessays. 1998 Sep;20(9):750-7. doi: 10.1002/(SICI)1521-1878(199809)20:9<750::AID-BIES8>3.0.CO;2-K. Bioessays. 1998. PMID: 9819564 Review. - Molecular pathology of type 1 diabetes.
Campbell IL, Harrison LC. Campbell IL, et al. Mol Biol Med. 1990 Aug;7(4):299-309. Mol Biol Med. 1990. PMID: 2233244 Review.
Cited by
- Cyclooxygenase-independent inhibition of dendritic cell maturation by aspirin.
Matasic R, Dietz AB, Vuk-Pavlovic S. Matasic R, et al. Immunology. 2000 Sep;101(1):53-60. doi: 10.1046/j.1365-2567.2000.00065.x. Immunology. 2000. PMID: 11012753 Free PMC article. - The strategy of T cell antigen-presenting cell encounter in antigen-draining lymph nodes revealed by imaging of initial T cell activation.
Bajénoff M, Granjeaud S, Guerder S. Bajénoff M, et al. J Exp Med. 2003 Sep 1;198(5):715-24. doi: 10.1084/jem.20030167. J Exp Med. 2003. PMID: 12953093 Free PMC article. - Virus-induced immunosuppression: immune system-mediated destruction of virus-infected dendritic cells results in generalized immune suppression.
Borrow P, Evans CF, Oldstone MB. Borrow P, et al. J Virol. 1995 Feb;69(2):1059-70. doi: 10.1128/JVI.69.2.1059-1070.1995. J Virol. 1995. PMID: 7815484 Free PMC article. - Manipulating the type 1 vs type 2 balance in type 1 diabetes.
Christen U, von Herrath MG. Christen U, et al. Immunol Res. 2004;30(3):309-25. doi: 10.1385/IR:30:3:309. Immunol Res. 2004. PMID: 15531772 Review. - Polyinosinic:polycytidylic acid is a potent activator of endothelial cells.
Doukas J, Cutler AH, Mordes JP. Doukas J, et al. Am J Pathol. 1994 Jul;145(1):137-47. Am J Pathol. 1994. PMID: 7518192 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical
Research Materials
Miscellaneous