S. Celeste Morley, M.D., Ph.D.

Assistant Professor
Pediatrics
Infectious Diseases

Immunology Program
Molecular Microbiology and Microbial Pathogenesis Program
Molecular Cell Biology Program

Research Abstract:

The Morley lab investigates how immune cells regulate their shape and migration patterns to combat pathogenic infections. Current projects in the lab include:

1. Identification of cells and genes required for resistance to pneumococcal infections. Severe pneumococcal infection is the leading killer of infants under aged 1 worldwide, and a major killer of children under aged 5. Little is known about elements of the immediate lung immune response that enables some children to resist infection while others succumb. Evidence in the Morley lab points to a critical role of actin regulation in specific immune cell populations in clearing pneumococcal infections in the early stages. Ongoing basic research in our mouse models is aimed at understanding the critical cell types involved in disease resistance and the precise nature of the cytoskeletal organization required for bacterial clearance.

2. Structure-function analysis of the actin-bundling protein L-plastin: We have shown that L-plastin is essential for T and B lymphocyte motility and activation. Detailed analysis of the structural domains essential to the function of L-plastin is being pursued to determine how L-plastin regulates immune cell development and function. This work is designed to illuminate the basic biological processes required for vaccine responses.

Selected Publications:

Zhou JY, Isaacson-Schmid M, Utterson EC, Todd EM, McFarland M, Sivapalan J, Niehoff JM, Burnham, CAD, Morley SC. (2015). Prevalence of nasopharyngeal pneumococcal colonization in children and antimicrobial susceptibility profiles of carriage isolates. International Journal of Infectious Diseases, in press.

Deady LE, Todd EM, Davis CG, Zhou JY, Topcagic N, Edelson BT, Ferkol TW, Cooper MA, Muenzer JT, Morley SC. (2014). L-plastin is essential for alveolar macrophage production and control of pulmonary pneumococcal infection. Infection and Immunity, 82(5): 1982-93. PMCID: PMC3993441.

Todd EM, Deady LE, Morley SC. Intrinsic T- and B-cell defects impair T-cell-dependent antibody responses in mice lacking the actin-bundling protein L-plastin. Eur J Immunol 2013; 43(7):1735-1744.

Morley SC. The actin-bundling protein L-plastin: a critical regulator of immune cell function. Int J Cell Biol 2012; 2012: 935173.

Todd EM, Deady LE, Morley SC. The actin-bundling protein L-plastin is essential for marginal zone B cell development. J Immunol 2011; 187: 3015-3025.

Morley SC, Wang C, Lo WL, Lio CW, Zinselmeyer BH, Miller MJ, Brown EJ, Allen PM. The actin-bundling protein L-plastin dissociates CCR7 proximal signaling from CCR7-induced motility. J Immunol 2010 184: 3628-3638.

Morley SC, Weber SK, Kao H, Allen PM. Protein kinase C theta is required for efficient positive selection. J Immunol 2008 181: 4696-4708.

Morley SC, Sung J, Sun GP, Martelli MP, Bunnell S, Bierer BE. Gelsolin overexpression alters actin dynamics and tyrosine phosphorylation of raft-associated proteins. Mol Immunol 2007 44: 2469-2480.

Morley SC, Sun GP, Bierer BE. Inhibition of actin polymerization enhances commitment to and execution of apoptosis induced by withdrawal of trophic support. J Cell Biochem 2003 88: 1066-1076.

Posey SC, Martelli MP, Azuma T, Kwiatkowski DJ, Bierer BE. Failure of gelsolin overexpression to regulate lymphocyte apoptosis. Blood 2000 95: 3483-3488.

Last Updated: 9/4/2015 12:32:36 PM

Wild-type T cells (left) polarize in response to chemotactic signals. T cells from a mouse missing the actin-bundling protein L-plastin cannot polarize (right). Impaired motility disrupts T cell development and function.
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