Thomas G. Blanchard, PhD, JD

University of Massachusetts, B.S., Biology, 1985

University of Massachusetts, Ph.D., Immunology, 1991

Case Western Reserve University, J.D., 2002

Dr. Blanchard is an immunologist with a longstanding interest in the interaction of commensal and pathogenic bacteria with the mucosa of the gastrointestinal tract. He is a leading expert in the study of the host response to Helicobacter pylori (H. pylori) infections of the stomach.  H. pylori colonizes the surface of the stomach in over half the world’s population and induces histologic inflammation in all infected individuals. Although most individuals remain asymptomatic, over 15% develop gastric diseases including peptic ulcer disease, gastric adenocarcinoma, gastric MALT lymphoma, and atrophic gastritis. Dr. Blanchard’s laboratory has contributed to our understanding of why the host immune response fails to eradicate H. pylori including investigations into the role of IL-10, Treg cells, and the dendritic cell response in limiting the host response. He has also made seminal contributions to the study of vaccine development for H. pylori infection and identifying how a vaccine-induced immune response differs from the host response to infection. Some of these contributions include 1) demonstrating that antibodies are not required for protective immunity, 2) demonstrating that anti-H. pylori immunity in the stomach can be induced through systemic as well as mucosal vaccinations, 3) eliciting protective immunity by vaccinating neonates, 4) establishing a crucial role for neutrophils in the protective immune response, and 5) demonstrating the importance of Th17 cells in the protective immune response and the ability of the host to compensate with Th1 immunity when the Th17 response is compromised.

 Dr. Blanchard also studies mechanisms of anti-cancer cell therapies with an emphasis on colon cancer cells. He has recently explored the molecular events induced by the plant compound andrographolide (AGP), previously demonstrated to induce cell cycle arrest and apoptosis in many types of cancer cells. His work has illustrated that AGP induces ER stress leading to the unfolded protein response in which IRE-1 promotes XBP-1 mRNA splicing and upregulation of CHOP leading to apoptosis. More recent results show that AGP induces the expression of two tumor suppressor genes PTEN and RASSF1A. Expression of these genes is typically limited in colon cancer cells. AGP induced expression of RASSF1A appears to contribute to cell cycle arrest which can ultimately also lead to apoptosis. Efforts are ongoing to outline AGP activity in further detail in the interest of improving its efficacy, identify targets for other anti-cancer agents, and advance the use of AGP to the clinic.  

Immunology, mucosal immunology, lymphocytes, Helicobacter pylori, microbiota, inflammation, vaccines, epithelium, cancer, tumor suppressor genes, three dimensional epithelial organoids.

DeLyria, E.S., R.W. Redline, and T.G. Blanchard. (2009) Protective immunity against Helicobacter pylori in mice is neutrophil-dependent and associated with local IL-17. Gastroenterology 136:247-256. PMCID: PMC4960660.

Blanchard, T.G., S.J. Czinn, P. Correa, T. Nakazawa, M. Keelan, L. Morningstar, I. Santana-Cruz, A. Maroo, C. McCracken, K. Shefchek, S. Daugherty, Y. Song, C.M. Fraser, and W.F. Fricke. (2013) Genome Sequences of 65 Helicobacter pylori Strains Isolated from Asymptomatic Individuals and Patients with Gastric Cancer, Peptic Ulcer Disease, or Gastritis. Pathogens and Disease 68(2):39-43. PMCID: PMC3780442.

Shiu, J., S.J. Czinn, K. Kobayashi, Y. Sun, and T.G. Blanchard. (2013) IRAK-M expression limits dendritic cell activation and proinflamamtory cytokine production in response to Helicobacter pylori. PLoS ONE Jun 11;8(6):e66914. doi: 10.1371/journal.pone.0066914. PMCID: PMC3679069.

Shiu J., M.B. Piazuelo, H. Ding, S.J. Czinn, M.L. Drakes, A. Banerjee, N. Basappa, K.S. Kobayashi, W.F. Fricke, and T.G. Blanchard. (2015) Gastric LTi cells promote lymphoid follicle formation but are limited by IRAK-M and do not alter microbial growth. Mucosal Immunology Sep;8(5):1047-59. doi: 10.1038/mi.2014.132. Epub 2015 Jan 21. PMCID: PMC4510039.

Banerjee, A., H. Ahmed, P. Yang, S.J. Czinn, and T.G. Blanchard. (2016) Endoplasmic reticulum stress and IRE-1 signaling cause apoptosis in colon cancer cells in response to andrographolide treatment. Oncotarget May 5. doi: 10.18632/oncotarget.9180. [Epub ahead of print] PMCID: PMC5173070.