ROG 在輔助T細胞分化及免疫所扮演的角色
Date Issued
2004
Date
2004
Author(s)
繆希椿
DOI
922321B002023
Abstract
Upon encountering antigen, naïve CD4 + precursor helper T (Th) cells
differentiate into mature effector Th1 and Th2 cells. Th1 responses are important in
defense of intracellular pathogens and responsible for mounting organ–specific
autoreactive immune responses. Th2 responses are known to be critical in
anti-helminthic and anti-inflammatory reactions.
Repressor of GATA (ROG), a transcriptional repressor, is a direct target gene of
NF-AT and a putative negative regulator of T cell activation. GATA-3, a T
cell-specific transcription factor, is essential for the development of the Th2 cell
lineage. In addition, overexpression of ROG suppressed the activity of GATA-3,
suggesting a role of ROG in the differentiation and function of Th cells. ROG is
mediated a negative feedback mechanism of T cell activation by NF-AT (Nuclear
Factor of Activated T cells). Overexpression of ROG attenuates the TCR signaling in
vivo. ROG-deficient T cells are hypersensitive to anti-CD3 stimulation and produce
more IL-2 due to enhanced NF-kB activity. However, ROG-deficient Th cells are
capable of differentiating into Th1 and Th2 cells and ROG-deficient mice have no
defect in mounting appropriate Th immune responses in vivo.
In this research plan, I further studied the function of ROG in two related
areas:(1) the role of ROG-interacting proteins in the immune system, and (2) the
transcriptional regulation of ROG. In conclusion, we have cloned ROG-interacting
partners from spleen cDNA library by using the yeast-two-hybrid system. We are
analyzing the function of them in the immune response aggressively. Furthermore, the
cytokines IL4, but not interferon-gamma (IFN摯瑬敳獩 ), has the role in controlling the
expression of ROG in the naïve CD4 + T cells. The IL4 inhibits the expression of ROG
transcripts through STAT6 signaling.
Subjects
T helper cells
Publisher
臺北市：國立臺灣大學醫學院免疫學研究所
Type
journal article
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