May 9, 2019

Front Row:  Michael Crawford, Sterling Ortega, Shailesh Shahi and Pranav Renavikar
Back Row:  Ashley Brate, Sushmita Sinha, Nitin Karandikar, Ashutosh Mangalam, Alex Boyden and Samantha Freedman

Alex Boyden, who won a podium presentation and travel award, will be presenting his research “CNS-specific autoregulatory CD8 T cells rely on IFNγ signaling for optimal suppression of pathogenic CD4 T cell responses during inhibition of demyelinating disease.” Alex’s work builds upon his discovery that CNS-specific CD8 T cells utilize different regulatory mechanisms at different stages of demyelinating disease, and suggests an IFNγ-cytotoxicity immunosuppression axis, which may have implications for future immunotherapy design.

Ashley Brate, who also won a podium presentation and travel award, will be presenting her research evaluating the therapeutic potential of autoregulatory CD8 T cells in suppressing relapsing-remitting autoimmune demyelinating disease, a disease course most commonly experienced among MS patients.

Michael Crawford will present his project titled “CD4+ T-helper 17 (Th17) signature cytokine, IL-17, mediates CD4 resistance to immune suppression.”  Dr. Crawford and his associates demonstrate that a subsection of human Th17 cells are resistant to immunosuppression by regulatory T cells.  For autoimmune illnesses that present with a proinflammatory Th17 phenotype, such as Multiple Sclerosis, Psoriasis and Inflammatory Bowel Disease, these findings could have far reaching implications into the mechanisms and pathogenesis of human Th17 driven disease processes.

Samantha Freedman (Mangalam Lab), another recipient of a travel award and podium presentation, will present her talk and poster titled “Linking diet, gut microbiota and autoimmunity: A phytoestrogen diet alters the gut microbiota and influences Experimental Autoimmune Encephalomyelitis (EAE).” Samantha and colleagues show that a phytoestrogen diet alters the gut microbiota of mice and protects against central nervous system autoimmunity. This study may provide insights into preventative and therapeutic strategies for MS patients. 

Sterling Ortega was awarded an early career faculty travel grant and will present a poster titled “Adaptive immune cell activation in acute pediatric traumatic brain injury.” Dr. Ortega and colleagues show an early adaptive immune cell response in pediatric patients following head trauma. This study may help explain why these patients suffer long-term neuro-cognitive deficits.

Pranav Renavikar will present his research finding related to cytokine driven differentiation of human CD8 T-cells into distinct lineages, which bear a differential ability to suppress CD4 immune responses. These findings will have implications in CD8 T-cell based immune regulation of autoimmune diseases like Multiple Sclerosis.

Shailesh Shahi (Mangalam Lab) won a podium presentation and travel award for presenting findings entitled “IL-17A control CNS Inflammatory disease by regulating Treg cells through modulation of gut microbiota in HLA Class-II transgenic mice model of multiple sclerosis (MS).” Dr. Shahi and colleagues have revealed that IL17A regulate disease in HLA class-II transgenic mice model of MS by inducing CD4⁺CD25⁺FoxP3⁺ Treg cells. Additionally, the study showed that IL17A deficient mice had altered gut microbiota with increases in Treg promoting bacteria (Lactobacillus and Clostridia). The overall findings suggest that there is a bidirectional link between the gut microbiota and IL-17A and the inverse relationship between IL-17A and Tregs might determine the susceptibility vs. protection from disease in an animal model of MS.

Sushmita Sinha was awarded an early career faculty travel grant and will present a poster entitled “An autoimmune disease risk SNP, rs2281808, in SIRPG is associated with reduced expression of SIRPγ and heightened effector state in human CD8 T-cells.” Sinha and colleagues have identified an as yet unknown role for SIRPγ in human T-cells. The studies will have a broad impact given SIRPγ’s association with multiple autoimmune diseases and may enlighten our understanding of targetable pathways in autoimmunity.