Joseph Reynolds, PhD

Assistant Professor
Room 2.351
Phone: 847-578-8332
Fax: 847-578-3349
joseph.reynolds@rosalindfranklin.edu
Biography

Joseph Reynolds graduated from the University of Louisville School of Medicine in 2007 with a Ph.D. in Microbiology and Immunology.  Working in the laboratory of Dr. Jill Suttles, he studied the effect of fatty acid-binding proteins (FABPs) in the regulation of inflammation and disease.  Their findings demonstrated that deletion of certain FABPs in macrophages and dendritic cells reduced inflammatory potential and protected against the development of autoimmune inflammation.

In 2008 Joseph joined the laboratory of Dr. Chen Dong in the Department of Immunology at the University of Texas MD Anderson Cancer Center to study the regulation and function of interleukin-17 (IL-17) and related IL-17 family cytokines.  Their primary discoveries were that IL-17 production by T lymphocytes could be regulated by innate signaling pathways, namely Toll-like receptors (TLR).  Moreover, direct TLR signaling in T lymphocytes positively regulated the development of IL-17-dependent inflammation.  Another project dealt with examining the function of an additional IL-17 family cytokine, IL-17C.  Their laboratory found that IL-17C signaling was important for IL-17 production from T cells.  Furthermore, they demonstrated that IL-17C was important for intestinal epithelial cell function and that IL-17C is protective against the development of acute colitis.  

In July 2013 Joseph joined the Department of Microbiology and Immunology in the Chicago Medical School at the Rosalind Franklin University of Medicine and Science as an Assistant Professor.

Research Interests

The overall goal of the laboratory is to further our understanding of mechanisms governing inflammatory responses and mucosal immunity.  Our research is currently focused on the role of the IL-17 family of cytokines in the promotion of inflammation and disease.  Research projects ongoing in the lab include:

The regulation of IL-17 production by T lymphocytes.  Our previous work has shown that both CD4+ T helper 17 (Th17) and gamma/delta T cells can respond to exogenous and endogenous TLR signals by producing IL-17.  The characterization of such innate-like pathways involved in the regulation of adaptive immune responses will further our understanding of the development and progression of inflammatory disease.  Moreover, we are interested in identifying how host-derived “danger” signals, such as endogenous TLR ligands, directly modulate T lymphocyte function in a disease setting.

IL-17C signaling in intestinal epithelial cells.  We are currently studying the roles of IL-17C in regulating colon epithelial cell function.  This project is based off of our previous finding that IL-17C is protective against the development of chemically-induced colitis.  Our studies now are focused on investigating the mechanisms responsible for these observations.

Additional IL-17 cytokines.  The IL-17 family consists of a group of 6 cytokines with varying degrees of homology (IL-17A-F).  Our laboratory is interested in examining the regulation and function of the more poorly described members of this cytokine family.

 

Publications

Smith AR, and Reynolds JM.  The contribution of myeloid-derived suppression to inflammatory disease.  2014.  Journal of Leukocyte Biology 2014, 96: 361-364

Lim H, Kim YU, Sun H, Reynolds JM, Hanabuchi S, Teng B, and Chung Y.  Proatherogenic conditions promote autoimmune Th17 responses in vivo.  Immunity 2014, 40(1): 153-165

hung Y, Yamazaki T, Kim B, Zhang Y, Reynolds JM, Martinez GJ, Chang SH, Lim H, Birkenbach M, and Dong C.  2013.  Epstein Barr Virus-Induced 3 (EBI3) together with IL-12 negatively regulates T helper 17-mediated immunity to Listeria monocytogenes infection.  PLoS Pathogens 2013, 9(9): e1003628

Reynolds JM, Dong C. Toll-like receptor regulation of effector T lymphocyte function. Trends in Immunology 2013, 34(10):511-9.

Reynolds JM, Martinez GJ, Nallaparaju KC, Chang SH, Wang YH, Dong C. Cutting edge: regulation of intestinal inflammation and barrier function by IL-17C. Journal of Immunology 2012, 189(9): 4226-4230.

Zhong B, Liu X, Wang X, Chang SH, Liu X, Wang A, Reynolds JM, Dong C. Negative regulation of IL-17-mediated signaling and inflammation by the ubiquitin-specific protease USP25. Nature Immunology 2012, 13(11): 1110-1117.

Reynolds JM, Martinez GJ, Chung Y, Dong C. Toll-like receptor 4 signaling in T cells promotes autoimmune inflammation. Proceedings of the National Academy of Sciences of the United States of America 2012, 109(32): 13064-13069.

Chang SH*, Reynolds JM*, Pappu BP, Chen G, Martinez GJ, Dong C. Interleukin-17C promotes Th17 cell responses and autoimmune disease via interleukin-17 receptor E. Immunity 2011, 35(4): 611-621.

*Co-first author/equal contribution*

Chung Y, Tanaka S, Chu F, Nurieva RI, Martinez GJ, Rawal S, Wang YH, Lim H, Reynolds JM, Zhou XH, Fan HM, Liu ZM, Neelapu SS, Dong C. Follicular regulatory T cells expressing Foxp3 and Bcl-6 suppress germinal center reactions. Nature Medicine 2011, 17(8): 983-988.

Reynolds JM, Angkasekwinai P, Dong C. IL-17 family member cytokines: regulation and function in innate immunity. Cytokine & Growth Factor Reviews 2010, 21(6): 413-423.

Martinez GJ, Zhang Z, Reynolds JM, Tanaka S, Chung Y, Liu T, Robertson E, Lin X, Feng XH, Dong C. Smad2 positively regulates the generation of Th17 cells. The Journal of Biological Chemistry 2010, 285(38): 29039-29043.

Nurieva RI, Zheng S, Jin W, Chung Y, Zhang Y, Martinez GJ, Reynolds JM, Wang SL, Lin X, Sun SC, Lozano G, Dong C. The E3 ubiquitin ligase GRAIL regulates T cell tolerance and regulatory T cell function by mediating T cell receptor-CD3 degradation. Immunity 2010, 32(5): 670-680.

Reynolds JM, Pappu BP, Peng J, Martinez GJ, Zhang Y, Chung Y, Ma L, Yang XO, Nurieva RI, Tian Q, Dong C. Toll-like receptor 2 signaling in CD4(+) T lymphocytes promotes T helper 17 responses and regulates the pathogenesis of autoimmune disease. Immunity 2010, 32(5): 692-702.

Martinez GJ, Zhang Z, Chung Y, Reynolds JM, Lin X, Jetten AM, Feng XH, Dong C. Smad3 differentially regulates the induction of regulatory and inflammatory T cell differentiation. The Journal of Biological Chemistry 2009, 284(51): 35283-35286

Zhang Y, Reynolds JM, Chang SH, Martin-Orozco N, Chung Y, Nurieva RI, Dong C. MKP-1 is necessary for T cell activation and function. The Journal of Biological Chemistry 2009, 284(45): 30815-30824.

Hertzel AV, Hellberg K, Reynolds JM, Kruse AC, Juhlmann BE, Smith AJ, Sanders MA, Ohlendorf DH, Suttles J, Bernlohr DA. Identification and characterization of a small molecule inhibitor of Fatty Acid binding proteins. Journal of Medicinal Chemistry 2009, 52(19): 6024-6031.

Li B, Reynolds JM, Stout RD, Bernlohr DA, Suttles J. Regulation of Th17 differentiation by epidermal fatty acid-binding protein. Journal of Immunology 2009, 182(12): 7625-7633.

Reynolds JM, Liu Q, Brittingham KC, Liu Y, Gruenthal M, Gorgun CZ, Hotamisligil GS, Stout RD, Suttles J. Deficiency of fatty acid-binding proteins in mice confers protection from development of experimental autoimmune encephalomyelitis. Journal of Immunology 2007, 179(1): 313-321. 

Makowski L, Brittingham KC, Reynolds JM, Suttles J, Hotamisligil GS. The fatty acid-binding protein, aP2, coordinates macrophage cholesterol trafficking and inflammatory activity. Macrophage expression of aP2 impacts peroxisome proliferator-activated receptor gamma and IkappaB kinase activities. The Journal of Biological Chemistry 2005, 280(13): 12888-12895.            

Updated: 11.19.2014

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