Benchang Guo, PhD

Head, Laboratory of B Cell Signaling, The Feinstein Institute for Medical Research

Assistant Investigator, The Feinstein Institute for Medical Research

Phone: (516) 562-2573
Email: bguo@northwell.edu

About the Investigator

Benchang Guo, PhD, is the Head of the Laboratory of B Cell Signaling and an Assistant Investigator at the Feinstein Institute for Medical Research. He obtained his PhD from the Shanghai Institute of Cell Biology, Chinese Academy of Science (CAS), in 2001. During his PhD study, he cloned and analyzed function of hepatoma-related gene Adir.

His studies are focused on antigen-initiated B cell activation under the influence of T cells (T cell help). He dissected the mechanism by which T cell-derived cytokine IL-4 amplifies antigen-initiated B cell activation. His findings uncover a “real-time” dialogue between B cells and T cells in immunity. Dr. Guo joined the Feinstein Institute for Medical Research in 2006.

Research Focus

Optimal B cell activation is a prerequisite for an efficient immune response, which is initiated by antigen and enhanced by T cell help such as Tfh-derived cytokine IL-4. In the past several years, Dr. Guo’s team uncovered the mechanism by which IL-4 amplifies BCR-initiated B cell activation. They found that IL-4 up-regulates Igaa and Igb expression, which leads to elevated surface IgM expression. Therefore, immune response is amplified in germinal center microenvironment. IL-4 expression is associated with autoimmune disease and tumor. Their future work will focus on dissecting the roles of IL-4 in the regulation of lupus, autoimmune disease and lymphoma such as B-CLL.

Ostepontin (Opn) is a pro-inflammatory cytokine that is implicated in multiple diseases. Multiple cell types secrete Opn upon activation. Naïve B2 cells do not express Opn even after BCR stimulation. His group found for the first time that B2 cells acquire the ability to secrete Opn after encountering T cell help such as IL-4. Elevated Opn expression is closely associated with autoimmune diseases. They found that Opn over-expressing B2 cells are hyperresponsive to CpG stimulation. Furthermore, old Opn transgenic mice (Ig promoter) spontaneously secrete anti-dsDNA IgM and IgG antibodies. Thus, B2 cell-derived Opn has a potential role in the pathogenesis of autoimmune disease. Their future work will focus on elucidating the mechanism by which B cell-derived Opn influence the pathogenesis of autoimmune disease.

B1 cells are the major source for natural IgM antibody, which is critical for maintaining homeostasis and preventing microbial invasion. PD-L2+ B1 cells are enriched with autoreactive specificities and secrete autoreactive natural IgM antibody, which facilitates clearance of autoantigens. Thus, elucidation of molecular mechanisms that govern B1 cell development and function is another research interest in his laboratory.

Education

Anhui Normal University
Degree: BS
1994
Field of Study: Biology

Xiamen University
Degree: MS
1997
Field of Study: Microbiology

The Shanghai Institute of Cell Biology, Chinese Academy of Science (CAS)
Degree: PhD
2001
Field of Study: Cellular & Molecular Biology

Honors and Awards

1995 First class, Guang-hua Award, Xiamen University
2011 Faculty Research Award, the Feinstein Institute for Medical Research

Publications
  1. Rothstein, T.L. and B. Guo. “RasGRP1 is a key mediator for classical BCR signaling that shapes antigen-specific receptor repertoire in B1 cells.” In preparation.
  2. Guo B* and T.L. Rothstein. 2013. “IL-4 upregulates Iga and Igb protein, resulting in augmented IgM maturation and BCR-triggered B cell activation.” J. Immunol. 2013. 191:670-7. *Correspond author.
  3. Guo B* and T.L. Rothstein. 2013. “A novel Lyn-protein kinase Cδ/ε-protein kinase D axis is activated in B cells by signalosome-independent alternate pathway BCR signaling.” Eur J Immunol. 43:1643-50. *Corresponding author.
  4. Rothstein T.L., B. Guo. 2009. “Receptor crosstalk: reprogramming B cell receptor signaling to an alternate pathway results in expression and secretion of the autoimmunity-associated cytokine, osteopontin.” J Intern Med. 265:632-43.
  5. Guo B., J.R. Tumang, T.L. Rothstein. 2009. “B Cell Receptor Crosstalk: B Cells Express Osteopontin Through the Combined Action of the Alternate and Classical BCR signaling Pathways.” Mol Immunol. 46:587-91.
  6. Dye, J.R., A. Palvanov, B. Guo, and T.L. Rothstein. 2007. “B cell receptor crosstalk: Exposure to LPS induces an alternate pathway for BCR-induced ERK phosphorylation and NF-B activation.” J. Immunol. 179:229-235.

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