Sherry Smith Phd Email & Phone Number

Dallas, Tx

Adjunct InstructorDept. Medical Laboratory Sciences, Public Health, and Nutrition ScienceTarleton State UniversityA Member of the Texas A&M University System

Dallas/Fort Worth Area

Dallas/Fort Worth Area

Granbury, Tx

Fort Worth, Tx

Teaching Anatomy & Physiology I and II (Lecture and Labs)

Senior Scientist- Lead scientist examining the role of complement and inflammation in age-related macular degeneration (AMD) • Responsible for assay development and proof of concept research related to the complement project.• Developed in vitro and ex vivo assays to test complement activation across multiple species (mouse, rat, NHP).• Developed cell-, protein-, and serum/plasma- based in vitro assays to detect complement activation and inhibition.• Generated a specialized colony of complement deficient mice to use in models of wet and dry AMD.• Developed the first SPF barrier labs and animal holding rooms at Alcon. Responsible for barrier room SOPs and training.• Created novel immuno/biochemical, and flow cytometric assays of complement activation, inflammation, blood-retina-barrier integrity, and cell viability for the photo-oxidative injury model in rodents and NHPs.• Demonstrated that early complement molecules in the alternative pathway are important for retina neuroprotection.• Characterization of complement and complement receptors/inhibitors on various cells within the eye by flow cytometry.• Worked across many groups in a collaborative approach to support discovery research.• Supervised/Directed and developed technicians and animal care staff.• Provided scientific input and support to discovery research and preclinical development.• Provided extensive knowledge in immunology, complement biology, and disease areas related to complement biology.• Managed external research collaborations and CROs. Completed written monthly reports, technical documents, scientific manuscripts, and presented data at lab and professional meetings.

Birmingham, Alabama Area

Postdoctoral Fellow, Professor Scott Barnum, Department of Microbiology, Examined the differential expression of beta2-integrins, trafficking, and cytokine production by gamma delta and alpha beta T cells in experimental autoimmune encephalomyelitis (EAE).• Used multiparameter flow cytometric analysis to compare beta2-integrin expression, kinetics of CNS trafficking, and cytokine production among gamma delta and alpha beta T cells over the acute course of disease. • Observed that beta2-integrin expression on gamma delta T cells was dramatically different from alpha beta T cells in all tissues examined throughout the disease course.• Demonstrated that alpha betaT cells infiltrated the CNS prior to gamma delta T cells and were more abundant. Gamma delta T cell trafficking to the CNS occurred before onset of clinical signs of disease and peaked early during the acute phase of disease. • Showed that gamma delta T cells, particularly those in the CNS, produced more IFN-gamma and TNF- alpha than alpha beta T cells throughout the course of EAE. Gamma delta T cell-mediated production of IFN-gamma and TNF-alpha is critical for EAE development, suggesting these cells may set the stage for activation of other subsets of infiltrating effector cells. • Results suggest unique roles for beta2-integrins in the trafficking of gamma delta versus alpha beta T cells during disease. Furthermore, the data suggest that alpha beta T cells rapidly infiltrate the CNS early in EAE and produce cytokines that modulate acute disease. • These data suggest that gamma delta T cells may represent a new therapeutic target in demeylinating disease.

Springfield, Illinois Area

Examined transgenic expression of Ly49A on islet-reactive CD4 T cells and their regulation of T cell activity and Type I diabetes. • Demonstrated that antigen-mediated activation of Ly-49A T cells was inhibited in vitro when the Ly-49A ligand, H-2Dd, was present on antigen presenting cells. • Antigen-driven T cell proliferation, cytokine production, and changes in cell surface receptor expression were significantly reduced by Ly49A ligand binding. Inhibition was also evident during secondary antigenic challenge. • Showed that the addition of exogenous IL-2 did not rescue cells from inhibition, suggesting that Ly-49A engagement does not lead to T cell anergy. • Importantly, in a bone marrow chimeric adoptive transfer model, Ly-49A significantly delayed the onset of diabetes and many recipients of Ly49A CD4 T cells remained euglycemic. These results demonstrated that the inhibitory receptor Ly-49A effectively limited antigen-specific CD4 cell responses even in the presence of sustained autoantigen expression in vivo.

Doctor Of Philosophy - Phd, Molecular Biology, Microbiology, Biochemistry, Immunology

Bachelor Of Science (Bs), Psychology/Biology