D******9
发帖数: 2665 | | S*****s
发帖数: 242 | 2 很多啊，什么EAE,CIA et al，都是Th1。
【在 D******9 的大作中提到】
: 谢谢
| s****9
发帖数: 932 | 3 I would recommend colitis model. Both Fiona's one (needs adaptive transfer)
and DSS treated model (no transfer requirement) are fine.
For EAE, CIA, Th17 cells mediated disease pathogenesis as well. IFNgKO mice
have exacerbated EAE and CIA, whereas IFNgKO or TbetKO mice do not develop
colitis.
【在 S*****s 的大作中提到】
: 很多啊，什么EAE,CIA et al，都是Th1。
| b********i
发帖数: 73 | 4 Communicable ulcerative colitis induced by T-bet deficiency in the innate
immune system.
Garrett WS, Lord GM, Punit S, Lugo-Villarino G, Mazmanian SK, Ito S,
Glickman JN, Glimcher LH.
blabla..... T-bet deficiency in the innate immune system results in
spontaneous and communicable ulcerative colitis in the absence of adaptive
immunity and increased susceptibility to colitis in immunologically intact
hosts. T-bet controls the response of the mucosal immune system to
commensal bacteria by regulating TNF-alpha production in colonic dendritic
cells, critical for colonic epithelial barrier maintenance. Loss of T-bet
influences bacterial populations to become colitogenic, and this colitis is
communicable to genetically intact hosts. These findings reveal a novel
function for T-bet as a peacekeeper of host-commensal relationships and
provide new perspectives on the pathophysiology of IBD.
by the way, for Th1 immunity, infection with low CFU listeria is a good one.
transfer)
mice
develop
【在 s****9 的大作中提到】
: I would recommend colitis model. Both Fiona's one (needs adaptive transfer)
: and DSS treated model (no transfer requirement) are fine.
: For EAE, CIA, Th17 cells mediated disease pathogenesis as well. IFNgKO mice
: have exacerbated EAE and CIA, whereas IFNgKO or TbetKO mice do not develop
: colitis.
| D******9
发帖数: 2665 | |
|
