JMJD3-deficient impair CD4 T cell trafficking in autoimmune disease models and adoptive immunotherapy models by targeting cytoskeleton genes

Histone H3K27 demethylase, JMJD3 plays a critical role in gene expression and T-cell differentiation. However, the role and mechanisms of JMJD3 in T cell trafficking remain poorly understood. Here we show that JMJD3 deficiency in CD4+ T cells resulted in T cell trafficking deficiency autoimmune dise...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2020-05, Vol.204 (1_Supplement), p.238-238.21
Main Authors: Fu, Chuntang, Xing, Changsheng, Yin, Bingnan, Chu, Junjun, Duan, Tianhao, Liu, Xin, Wang, Rongfu
Format: Article
Language:English
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Summary:Histone H3K27 demethylase, JMJD3 plays a critical role in gene expression and T-cell differentiation. However, the role and mechanisms of JMJD3 in T cell trafficking remain poorly understood. Here we show that JMJD3 deficiency in CD4+ T cells resulted in T cell trafficking deficiency autoimmune disease models and adoptive immunotherapy models. We identified PDLIM4 and S1P1 as significantly down-regulated target genes in JMJD3-deficient CD4+ T cells by gene profiling and ChIP-seq analyses. The further study showed that PDLIM4 regulate actin cytoskeleton, thus serving as a key regulator of T cell trafficking. These results demonstrate that manipulating JMJD3 expression can benefit autoimmune disease treatment and generate better T cell grafts for adoptive immunotherapy.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.204.Supp.238.21