Overview

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Interested in working with us?

We have a limited number of positions for students both at the undergrad and graduate levels. Please email Dr. Carrithers (mcar1@uic.edu)

Laboratory of Michael Carrithers, M.D., Ph.D.

Program in Neuroimmunology and Neurological Infections

The Carrithers laboratory focuses on basic innate immune signaling mechanisms, immune-mediated repair, and molecular determinants of treatment response to biological therapies.

Innate Immunity

Poly I:C, a synthetic mimic of dsRNA, activates the intracellular SCN5A channel that is expressed in human macrophages. From Jones et al., 2014

We have identified a novel mechanism of pattern recognition mediated by intracellular voltage-gated sodium channels. In human macrophages, one of these channels recognizes dsRNA and initiates anti-viral signaling.  A genetically related channel in the yellow fever mosquito is activated by viral ssRNA and regulates insect innate immune pathways.  These pathways are also relevant to immune-mediated repair in autoimmune conditions such as multiple sclerosis.

Pharmacogenomics of Multiple Sclerosis Treatments

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Reduced EVA expression leads to an enhanced humoral response and lack of response to treatments similar to natalizumab. From Wright et al. 2013

We discovered a gene that is required for response to anti-alpha4integrin treatment in a mouse model of multiple sclerosis.  The product of this gene, epithelial V-like antigen (EVA), limits the extent of B and T lymphocyte activation and migration following immunization and other inflammatory stimuli. The goal of this work is to develop individualized treatment approaches for patients with multiple sclerosis and related disorders.

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