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Proteoglycan isolated from Phellinus linteus inhibits tumor growth through mechanisms leading to an activation of CD11c + CD8 + DC and type I helper T cell‐dominant immune state
Author(s) -
Kim Gi-Young,
Oh Won-Kyo,
Shin Byung-Cheul,
Shin Yong-Il,
Park Young-Chul,
Ahn Soon-Cheol,
Lee Jae-Dong,
Bae Yoe-Sik,
Kwak Jong-Young,
Park Yeong-Min
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.09.047
Subject(s) - cd86 , cd8 , cytokine , microbiology and biotechnology , cytotoxic t cell , chemistry , biology , immune system , cd80 , t cell , antigen presenting cell , immunology , in vitro , cd40 , biochemistry
Dendritic cells (DC) are known to not only induce the activation of T cells, but are also associated with the polarization of T cells. This study investigated whether or not proteoglycan (PG) isolated from Phellinus linteus induces the phenotypic and functional maturation of CD11c + DC in vitro and in vivo. PG was found to induce the phenotypic and functional maturation of bone marrow‐derived DC via Toll‐like receptors (TLR) 2 and 4 in vitro. Administration of PG in vivo strongly inhibited the MCA‐102 tumor growth and increase in vivo. The ratio of CD8 + DC to CD8 − DC increased, and PG enhanced IL‐12 and IFN‐γ production, and expression of surface molecules including major histocompatibility complexes (MHC) classes I, MHC II, CD80, and CD86 in MCA‐102‐challenged mice. PG also caused a marked increase in the production of Th (helper T cells)‐1 cytokine (IFN‐γ) and a decrease in the production of Th‐2 cytokine (IL‐4) by splenic cells and inguinal lymph node cells in MCA‐102 tumor‐bearing mice. Furthermore, PG stimulated the proliferation of CD4 + and CD8 + T cells. In addition, a combination of PG and tumor lysate‐pulsed DC inhibited completely the growth of MCA‐102 cells in tumor‐bearing mice. These results indicate that the administration of PG inhibited the tumor growth through a mechanism leading to a Th‐1 dominant immune state and the activation of CD11c + CD8 + DC.