A general interest of the lab is the role that infection plays in setting the stage for chronic immune mediated inflammatory diseases. Recently we have begun to investigate the human host immune response to infection with Borrelia burgdorferi the causative agent of Lyme disease. To date there is little information available as to how various cellular immune elements are mobilized following B. burgdorferi infection. We hypothesize that the varying outcomes (cure vs. long term symptoms) that follow infection with B. burgdorferi are the result of differences in the host immune response to the infection. We are addressing this issue by following a cohort of patients from onset of presentation with symptoms of infection through the course of disease. This effort will attempt to identify cellular and/or molecular immune biomarkers that associate with effectiveness of bacterial clearance and/or disease pathophysiology and employs genomic, proteomic and complex immune phenotyping approaches.
A second area of interest is the identification of immune targets in psoriatic arthritis and ankylosing spondylitis. We are utilizing samples from a well-characterized patient cohort to identify novel autoantigens. Our approach is to utilize state of the art proteomic and phage display based systems.
Lastly we are interested in the role of cellular elements of the immune response in controlling infection with gram-negative bacterial pathogens such as Salmonella typhimurium. This interest is driven not only because these bacteria cause significant acute disease but also due to the etiological link between infection with Salmonella and related species with the development of chronic autoimmune disease. We utilize a mouse model and have recently focused our attention on the role of the intestinal mucosal immune compartment in controlling oral infection. This effort has identified a new unrecognized subset of T cells residing within the epithelial barrier that expands following infection. Current efforts are focused on understanding the recognition properties and effector function of this T cell subset and determining if an analogous population exists in the human mucosa.
Lab Website: Soloski Lab
Bayview Flow Cytometry
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Soloski MJ, and Holowxzak JA. Characterization of supercoiled nucleoprotein complexes released from detergent treated vaccinia virions. J. Virol. (1981) 37:770-783.
Soloski MJ, Uhr JW, Flaherty L and Vitetta ES. Qa-2, H-2K, and H-2D alloantigens evolved from a common primordial gene. J. Exp. Med (1981) 153:1080-1093.
Soloski MJ, JJ, Uhr JW and Vitetta ES. Primary structural studies of the Qa-2 alloantigen: Implication for the evolution of the major histocpatibility complex. Nature (1982) 296:759-761.
Soloski MJ, Vernachio J, Einhorn G. and Lattimore A. Qa Gene Expression: Biosynthesis and Secretion of Qa-2 Molecules in Activated T Cells. Proc. Nat’l Acad. Sci. USA (1986) 83:2949-2953.
Stroynowski I, Soloski MJ, Hood L, and Low M. A Single Histocompatibility Qa-2 Antigen: Anchoring of the Product by a Phospholipid Tail. Cell. (1987) 50:759-768.
Soloski MJ, Hood L and Stroynowski I. Q- Region Class I Gene Expression: Identification of a Second Qa-Region Gene Encoding a Qa-2 polypeptide. Proc. Nat’l Acad. Sci. (1988) 85:3100-3104.
Imani F, and Soloski MJ. Heat shock proteins can regulate expression of the T1a region encoded class lb molecule, Qa1. Proc. Natl. Acad. Sci. (USA), (1991) 88:10475-10479.
Aldrich C, DeCloux A, Woods A, Cotter R, Soloski MJ and Forman J. Identification of a Tap dependent Leader Peptide Recognized by Alloreactive T Cells for a Class lb Antigen, (1994) Cell 79:649-658.
DeCloux A, Woods A, Cotter R, Soloski MJ and Forman J. Dominance of a single peptide bound to the class lb molecule Qa-1b. J. Immunol (1997) 158:2183-2191
Lo W-F, Woods AS, DeCloux A, Cotter R J, Metcalf ES and Soloski MJ. Molecular Mimicry Mediated by MHC Class lb Molecules Following Infection with Gram-Negative Pathogens. Nature Medicine (2000) 6:215- 218.
Davies A, Ramirez S, Liang B, Aldrich C, Lemonnier F, Jiang H, Cotter R and Soloski MJ. A Peptide from Heat Shock Protein 60 is the Dominant Peptide bound to Qa-1 in the absence of the MHC Class la Leader Sequence Peptide Qdm. J. Immunol. (2003) 170:5027-5033.
Wooden SL, Kalb SR, Cotter RJ, Soloski M.J. Cutting Edge: HLA-E Binds a Peptide Derived from the ATP-Binding Cassette Transporter Multidrug Resistance-Associated Protein 7 and Inhibits NK Cell-Mediated Lysis. J Immunol. (2005) 175:1383-7.
Eshoo, M.W., Crowder, C. C., Rebman, A. W., Rounds, M. A., Matthews, H.E., Picuri, J.M., Soloski, M. J., Ecker, D. J. Schutzer, S. E. and Aucott, J.A. (2012) Direct Molecular Detection and Genotyping of Borrelia burgdorferi from Whole Blood of Patients with Early Lyme Disease. PLoS ONE 7(5): e36825. doi:10.1371/journal.pone.0036825
Soloski, M. J., Crowder, L. A., Lahey, L. J., Wagner, C. A., Robinson, W. H., Aucott, J. N. (2014) Serum Inflammatory Mediators as Markers of Human Lyme Disease Activity. PLOSOne 6;9(4):e93243. doi: 10.1371/journal.pone.0093243.