Up, down, and all around: immune cells are constantly in motion as they seek to defend the host against pathogens. Dramatic cell shape changes induced by alterations in the underlying actin cytoskeleton provide the structural framework required for cell motility. The Morley lab is interested in defining how elements of the actin cytoskeleton regulate immune cell shape and motility, and how impairments in motility then alter immune cell development and activation.
We work on both adaptive and innate immune responses, with current projects investigating B cells and alveolar macrophages. Our primary model system uses mice lacking an actin-binding protein called L-plastin (don’t worry, no one else has heard of it either – though we are trying to change that!). L-plastin is only expressed in cells of the immune system (the “L” stands for “leukocyte”), so mice missing L-plastin are perfectly fertile and viable and there is no need to do complicated fetal liver transplants or anything annoying like that. I am quite sure that other immune cell types will also have defects, so if your interest is in dendritic cells or NK cells or Langerhans cells or whatever, those areas are open, too! Additionally, we are working with a pneumococcal model of infection and are interested in exploring other infectious models in the future.
We have a variety of fascinating projects to work on that range from signal transduction and protein structure-function analysis to cytoskeletal dynamics to cellular immunology and host-pathogen interactions to a clinical-translational project looking for variant alleles in L-plastin-associated proteins in patients. See our Projects page for details!
Division of Pediatric Infectious Diseases
Office Phone: 314-286-2136
Lab Phone: 314-286-0241
e-mail (Dr. Morley): firstname.lastname@example.org