Th1/Th17 polarization and acquisition of an arthritogenic phenotype in arthritis-susceptible BALB/c, but not in MHC-matched, arthritis-resistant DBA/2 mice.
Th1/Th17 polarization and acquisition of an arthritogenic phenotype in arthritis-susceptible BALB/c, but not in MHC-matched, arthritis-resistant DBA/2 mice.
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TH1/TH17在受关节炎敏感的BALB/C中的关节炎表型的极化和获取,但在MHC匹配的,具有关节炎的DBA/2小鼠中却不是。
DOI:
10.1093/intimm/dxp018
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发表时间:
2009-05
影响因子:
4.4
通讯作者:
Glant TT
中科院分区:
文献类型:
--
作者:
Boldizsar F;Tarjanyi O;Nemeth P;Mikecz K;Glant TT
Proteoglycan (PG) aggrecan-induced arthritis (PGIA) is a murine model of rheumatoid arthritis (RA). Although BALB/c and DBA/2 mice share the same MHC (H-2d) haplotype, the BALB/c strain is susceptible to PGIA, while DBA/2 mice are resistant. Therefore, these two inbred mouse strains provide an opportunity to study arthritis susceptibility factors excluding the effects of MHC-associated genetic components. The goal of this study was to monitor changes in the cellular composition and activation state following intra-peritoneal (i.p.) immunization to induce PGIA; additionally, we sought to identify new susceptibility factors by comparing PG-induced immune responses in BALB/c and DBA/2 mice. Upon i.p. PG injection, resident naive B1 cells are replaced by both T cells and conventional B cells in the peritoneum of BALB/c mice. These peritoneal T cells produce IFNγ and IL-17, cytokines shown to be important in RA and corresponding arthritis models. Moreover, peritoneal cells can adoptively transfer PGIA to SCID mice, demonstrating their arthritogenic properties. Our results indicate that repeatedly injected antigen leads to the recruitment and activation of immune cells in the peritoneum; these cells then trigger the effector phase of the disease. The migration and activation of Th1/Th17 cells in the peritoneal cavity in response to PG immunization, which did not occur in the arthritis-resistant DBA/2 strain, may be critical factors of arthritis susceptibility in BALB/c mice.
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影响因子:
4.4
作者:
Doodes, Paul D.;Cao, Yanxia;Hamel, Keith M.;Wang, Yumei;Farkas, Balint;Iwakura, Yoichiro;Finnegan, Alison
通讯作者:
Finnegan, Alison
影响因子:
--
作者:
Berlo, Suzanne E.;Guichelaar, Teun;Glant, Tibor T.
通讯作者:
Glant, Tibor T.
影响因子:
5.5
作者:
Klinguer-Hamour, C;Libon, C;Beck, A
通讯作者:
Beck, A
影响因子:
--
作者:
Hanyecz, A;Berlo, SE;Glant, TT
通讯作者:
Glant, TT
影响因子:
4.3
作者:
GRUN, JL;MAURER, PH
通讯作者:
MAURER, PH