Skip to main content

Mari L. Shinohara

Associate Professor of Immunology
Campus Mail: 338JONES Building, 207 Researc, Box 3010 Dumc, Dept of Immunology, Durham, NC 27710
Phone: (919) 613-6977
Email: mari.shinohara@duke.edu

Shinohara Lab Website

Immune responses against pathogens are essential for host protection, but excessive and uncontrolled immune reactions can lead to autoimmunity. How does our immune system keep the balance fine-tuned? This is a central question being asked in my laboratory.

The immune system needs to detect pathogens quickly and effectively. This is performed by the innate immune system, which includes cells such as macrophages and dendritic cells (DCs). Pathogens are recognized by pattern recognition receptors (PRRs) and may be cleared in the innate immune system. However, when pathogens cannot be eliminated by innate immunity, the adaptive immune system participates by exploiting the ability of T cells and B cells. The two immune systems work together not only to clear pathogens effectively but also to avoid collateral damages by our own immune responses. 

In my lab, we use mouse models for infectious and autoimmune diseases to understand the cellular and molecular mechanisms of; pathogen recognition by PRRs in macrophages and DCs, initiation of inflammatory responses in the innate immune system, and the impact of innate immune inflammation on the development and regulation of T cell-mediated adaptive immune responses. 

Several projects are ongoing in the lab. They are to study (1) the roles of PRR in EAE (an animal model of multiple sclerosis), (2) the interplay between immune cells and CNS (central nervous system)-resident cells during EAE and fungal infection, (3) protective and pathogenic mechanisms of immune cells in the lung during fungal infection and inflammation, and (4) the roles of a protein termed osteopontin (OPN), as both secreted (sOPN) and intracellular (iOPN) isoforms, in regulation of immune responses . Although we are very active in EAE to study autoimmunity, other mouse models, such as graft-versus-host disease (GvHD) is ongoing. Cell types we study are mainly DCs, macrophagesneutrophils, and T cells

Selected Publications

Shinohara, Mari L., Marianne Jansson, Eun Sook Hwang, Miriam B. F. Werneck, Laurie H. Glimcher, and Harvey Cantor. “T-bet-dependent expression of osteopontin contributes to T cell polarization.” Proc Natl Acad Sci U S A 102, no. 47 (November 22, 2005): 17101–6. https://doi.org/10.1073/pnas.0508666102.

Full Text

Shinohara, Mari L., Alejandro Correa, Deborah Bell-Pedersen, Jay C. Dunlap, and Jennifer J. Loros. “Neurospora clock-controlled gene 9 (ccg-9) encodes trehalose synthase: circadian regulation of stress responses and development.” Eukaryot Cell 1, no. 1 (February 2002): 33–43. https://doi.org/10.1128/ec.1.1.33-43.2002.

Full Text

Shinohara, M. L., K. F. LoBuglio, and S. O. Rogers. “Comparison of ribosomal DNA ITS regions among geographic isolates of Cenococcum geophilum.” Curr Genet 35, no. 5 (June 1999): 527–35. https://doi.org/10.1007/s002940050449.

Full Text

Shinohara, M. L., J. J. Loros, and J. C. Dunlap. “Glyceraldehyde-3-phosphate dehydrogenase is regulated on a daily basis by the circadian clock.” J Biol Chem 273, no. 1 (January 2, 1998): 446–52. https://doi.org/10.1074/jbc.273.1.446.

Full Text

Pages