Genetically driven target tissue overexpression of CD40: a novel mechanism in autoimmune disease.
Genetically driven target tissue overexpression of CD40: a novel mechanism in autoimmune disease.
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DOI:
10.4049/jimmunol.1200311
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发表时间:
2012-09-15
期刊:
影响因子:
--
通讯作者:
Tomer Y
中科院分区:
文献类型:
--
作者:
Huber AK;Finkelman FD;Li CW;Concepcion E;Smith E;Jacobson E;Latif R;Keddache M;Zhang W;Tomer Y
The CD40 gene, an important immune regulatory gene, is also expressed and functional on non-myeloid derived cells, many of which are targets for tissue specific autoimmune diseases, including beta cells in type 1 diabetes, intestinal epithelial cells in Crohn’s disease, and thyroid follicular cells in Graves’ disease (GD). Whether target tissue CD40 expression plays a role in autoimmune disease etiology has yet to be determined. Here we show, that target-tissue over-expression of CD40 plays a key role in the etiology of autoimmunity. Using a murine model of GD, we demonstrated that thyroidal CD40 over-expression augmented the production of thyroid specific antibodies, resulting in more severe experimental autoimmune Graves’ disease (EAGD), whereas deletion of thyroidal CD40 suppressed disease. Using transcriptome and immune-pathway analyses we showed that in both EAGD mouse thyroids and human primary thyrocytes, CD40 mediates this effect by activating downstream cytokines and chemokines, most notably IL-6. To translate these findings into therapy, we blocked IL-6 during EAGD induction in the setting of thyroidal CD40 over-expression, and showed decreased levels of TSHR stimulating antibodies and frequency of disease. We conclude that target tissue over-expression of CD40 plays a key role in the etiology of organ specific autoimmune disease.
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影响因子:
--
作者:
Min, DJ;Cho, ML;Kim, HY
通讯作者:
Kim, HY
影响因子:
4.8
作者:
Chen, CR;Pichurin, P;Rapoport, B
通讯作者:
Rapoport, B
影响因子:
11.2
作者:
Knauf, JA;Ma, XL;Fagin, JA
通讯作者:
Fagin, JA
DOI:
10.1006/clin.1997.4391
发表时间:
1997-08-01
期刊:
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY
影响因子:
--
作者:
Faure, GC;BensoussanLejzerowicz, D;Leclere, J
通讯作者:
Leclere, J
影响因子:
5
作者:
Jacobson, E. M.;Huber, A. K.;Tomer, Y.
通讯作者:
Tomer, Y.