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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 513542, 11 pages
Research Article

Reishi Protein LZ-8 Induces FOXP3+ Treg Expansion via a CD45-Dependent Signaling Pathway and Alleviates Acute Intestinal Inflammation in Mice

1Department of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, No. 155, Section 2, Li-Nong Street, Taipei 11221, Taiwan
2The Genomics Research Center, Academia Sinica, Taipei 11574, Taiwan
3Program in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei 11574, Taiwan
4Center for Biotechnology, National Taiwan University, No. 1, Section 4, Roosevelt Road, Taipei 10673, Taiwan
5Department of Horticulture, National Taiwan University, No. 1, Section 4, Roosevelt Road, Taipei 10673, Taiwan
6Fordham University, New York, NY 10458, USA

Received 9 January 2013; Revised 18 April 2013; Accepted 27 April 2013

Academic Editor: Ruixin Zhang

Copyright © 2013 Hsien-Yeh Hsu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


LZ-8, an immunomodulatory protein isolated from Ganoderma lucidum (also known as Ling-Zhi or Reishi), has been shown to promote cell proliferation and IL-2 production in T cells. In this study, we show that LZ-8 induces the expansion of both murine and human CD4+ T cells into FOXP3+ regulatory T (Treg) cells. LZ-8 treatment was found to stimulate a 4-fold and a 10-fold expansion in the Treg populations of murine and human primary CD4+ T cells, respectively. In addition, the expression of CTLA-4 and IL-10 was induced in LZ-8-treated CD4+ T cells. Using neutralizing antibodies and gene-deficient T-cell lines, we also found that LZ-8 promotes Treg expansion through a CD45-mediated signaling pathway and that the CD18-dependent induction of IL-2 was involved in Treg formation and IL-10 production. The suppressive activity of LZ-8 was confirmed using a murine model of DSS-induced colitis; the disease was alleviated by the adoptive transfer of LZ-8-treated CD4+ T cells. In conclusion, a new regulatory function for LZ-8 was identified, and the molecular mechanisms underlying this function were elucidated.