CPB 697 RESEARCH SEMINAR
Hyung Wook Lim, M.S.
Graduate Student in Biochemistry & Molecular Biology
Department of Comparative Pathobiology
“Suppression Of Humoral Immune Responses By FOXP3+ T Cells
And Regulation Of Chemokine Receptor Expression In
FOXP3+ T Cells”
Thursday, March 8, 2007
VPTH 112
3:30 p.m.
Abstract:
FOXP3 is a member of fork-head/winged-helix family of transcription factors
expressed in the nucleus of regulatory T cells (FOXP3+ T cells).
FOXP3+ T cells play a
central role in regulation of humoral immune responses and prevention of
autoimmunity by suppressing proliferation,
activation, and function of immune cells.
It has been known that
chemokine receptors play an important role in guiding cell migration during
immune responses/homeostasis in our body.
However, it has been
unclear how FOXP3+ T cells migrate to follicles (B cell area of
secondary lymphoid tissue), whether they suppress B cell immune responses, and
how chemokine receptors expression is regulated in FOXP3+ T cells.
We found that upon activation, they acquire migration capacity toward B
cell area of secondary lymphoid tissue by up-regulating expression of B cell
zone chemokine receptor CXCR5. In the follicle, FOXP3+ T cells
efficiently suppress not only T cells and T cell driven B cell immune
responses, but also they can directly suppress B cell and B cell immune
responses.
We also found that
chemokine receptors are differentially expressed on the surface of FOXP3+ T cells depending on the stage of differentiation
and activation. FOXP3+ T cells
are divided into naïve and memory types based upon CD45RA and CD45RO
expression. Naïve FOXP3+ T cells mainly express secondary lymphoid
tissue homing receptors, while memory FOXP3+ T cells express
non-lymphoid tissue and lymphoid tissue homing receptors. Upon activation and
differentiation, naïve FOXP3+ T cells change their chemokine
receptor expression pattern from naïve to memory type.
Our result showed that potential mechanism of FOXP3+ T cells in follicles of secondary lymphoid tissue and the regulation of trafficking receptors in FOXP3+ T cells in human body.