Makoto Inoue

makotoi@illinois.edu

Veterinary Medical Sciences Building
2001 S. Lincoln Ave
MC 002
Urbana, IL 61801

Lab Page
Publications

Makoto Inoue

Assistant Professor of Comparative Biosciences
Ph.D., Nagasaki University

Neuroimmunology in autoimmune, infectious, and neurodegenerative diseases

The long-term objective of our laboratory research is to elucidate the interaction between immune system and nervous system in autoimmune diseases, infectious diseases, and neurodegenerative diseases. For example, inflammation in the peripheral lymphoid organs by infections, or in the CNS by traumatic injury, could cause blood brain barrier damage, which may further result in immune cell infiltration into the CNS. Infiltrated immune cells may pathologically affect the nervous system, and vice versa. A recent study demonstrated that strong activation of innate immunity by acute pathogen infection alters T cell pathogenicity to induce neuronal damage in the CNS. Therefore, investigation of interactions between nervous system and immune system in individual situations is currently important to identify the mechanisms of autoimmune diseases, infectious diseases, and neurodegenerative diseases. The research goal of our lab is to lead the push towards the development of novel and effective therapeutic protocols for treating several diseases.

Research Areas

Representative Publications

Selected from 67 peer-reviewed papers

Inoue M, Chen PH, Siecinski S, Li QJ, Liu C, Steinman L, Gregory SG, Benner E, Shinohara ML. An interferon-?- resistant and inflammasome-independent subtype of EAE with neuronal damage. Nat. Neurosci. Nov 7. 2016

Inoue M, Arikawa T, Chen YH, Moriwaki Y, Price M, Brown M, Perfect JM, Shinohara M. T cells downregulate macrophage TNF production by IRAK1-mediated IL-10 expression and control innate hyperinflammation. Proc Natl Acad Sci U S A. 11:5295-300, 2014

Inoue M, Williams KL, Oliver T, Vandenabeele P, Rajan JV, Miao EA, Shinohara ML. Interferon-? therapy against EAE is effective only when development of the disease depends on the NLRP3 inflammasome. Sci. Signal. 5, ra38, 2012. (F1000)

Inoue M, Williams KL, Gunn MD, Shinohara ML. NLRP3 inflammasome induces chemotactic immune cell recruitment in the CNS in a mouse EAE model. Proc Natl Acad Sci U S A. 109:10480-5, 2012

Inoue M, Moriwaki Y, Arikawa T, Chen YH, Oh YJ, Oliver T, Shinohara ML. Cutting edge: Critical role of intracellular osteopontin in antifungal innate immune responses. J Immunol. 186:19-23, 2011

Inoue M, Ma L, Aoki J, Ueda H. Simultaneous stimulation of spinal neurokinin 1 and NMDA receptors produces lysophosphatidylcholine, which undergoes autotaxin-mediated conversion to lysophosphatidic acid, an initiator of neuropathic pain. J. Neurochemistry 107: 1556-65, 2008

Complete Publications List (PubMed)

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