dc.contributor.author |
Green, E. Allison |
dc.contributor.author |
Wong, F. Susan |
dc.contributor.author |
Eshima, Koji |
dc.contributor.author |
Mora Giral, Concepció |
dc.contributor.author |
Flavell, Richard A. |
dc.date |
2015-07-09T10:31:35Z |
dc.date |
2015-07-09T10:31:35Z |
dc.date |
2000 |
dc.identifier |
0022-1007 |
dc.identifier |
http://hdl.handle.net/10459.1/48455 |
dc.identifier.uri |
http://hdl.handle.net/10459.1/48455 |
dc.description |
Neonatal islet-specific expression of tumor necrosis factor (TNF)-α in nonobese diabetic mice promotes diabetes by provoking islet-infiltrating antigen-presenting cells to present islet peptides to autoreactive T cells. Here we show that TNF-α promotes autoaggression of both effector CD4+ and CD8+ T cells. Whereas CD8+ T cells are critical for diabetes progression, CD4+ T cells play a lesser role. TNF-α–mediated diabetes development was not dependent on CD154–CD40 signals or activated CD4+ T cells. Instead, it appears that TNF-α can promote cross-presentation of islet antigen to CD8+ T cells using a unique CD40–CD154-independent pathway. These data provide new insights into the mechanisms by which inflammatory stimuli can bypass CD154–CD40 immune regulatory signals and cause activation of autoreactive T cells. |
dc.language |
eng |
dc.publisher |
Rockefeller University Press |
dc.relation |
Reproducció del document publicat a http://jem.rupress.org/content/191/2/225.full.pdf+html |
dc.relation |
The Journal of experimental medicine, 2000, vol. 191, núm. 2, p. 225-238 |
dc.rights |
cc-by-nc-sa, (c) Green et al., 2000 |
dc.rights |
http://creativecommons.org/licenses/by-nc-sa/3.0/es/ |
dc.rights |
info:eu-repo/semantics/openAccess |
dc.subject |
CD154 |
dc.subject |
Diabetes |
dc.subject |
NOD mice |
dc.subject |
CD8+ cells |
dc.title |
Neonatal tumor necrosis factor alpha promotes diabetes in nonobese diabetic mice by CD154-independent antigen presentation to CD8(+) T cells |
dc.type |
article |
dc.type |
publishedVersion |