Molecular Microbiology, University of Texas at San Antonio

Cardona, Astrid, Ph.D.

Adjunct Associate Professor

Personal Statement:

Dr. Cardona’s research is focused on understanding the mechanisms of tissue damage in Multiple Sclerosis and Diabetic retinopathy. Her laboratory focuses on the functional interactions between immune cells, microglia, neurons and blood vessels, utilizing experimental mouse models of disease, immunological assays, flow cytometry, fluorescent activated cell sorting, microscopy and molecular biology approaches.

Dr. Cardona’s research program is concentrated in translational approaches for the treatment of diabetic retinopathy and multiple sclerosis. She teaches immunology and works with students and faculty to promote outcomes of educational attainment, academic achievement and student advancement. Students in her lab build skills for careers in biomedical research, medicine, academia, industry and pedagogy at the undergraduate and graduate levels.


Ph.D., Microbiology & Immunology at the University of Texas Health Science Center San Antonio


Dr. Cardona is particularly interested in determining the contribution of fractalkine signaling on myeloid cells during neuroinflammation. Although fractalkine and its receptor CX3CR1, are mainly expressed in the CNS by neurons and microglia respectively, they also have a distinctive peripheral pattern of expression. Fractalkine is found at in endothelial and epithelial cells and circulating monocytes, dendritic cells and NK cells express CX3CR1. Some of the questions we are addressing include: Does CX3CR1 play a role in the trafficking of microglial precursors? Does CX3CR1-deficiency on microglia or peripheral cells enhance neuronal/axonal pathology? How does CX3CR1-deficiency alter CNS immune responses? We intend to clarify the role of fractalkine/CX3CR1 in the brain, research that is instrumental for potential development of therapeutic agents.


  • Cardona AE, Li M, Liu L, Savarin C and Ransohoff RM. 2008. Chemokines in and out of the central nervous system: much more than chemotaxis and inflammation. J. Leukoc. Biol. 84(3):587-94.
  • Lee S, Varvel N, Konerth M, Xu G, Cardona AE, Ransohoff RM, Lamb BT. 2010. CX3CR1 deficiency alters microglial activation and reduces beta-amyloid deposition in two Alzheimers disease mouse models. Am.J.Pathol. Am.J.Pathol.177(5) :2549-62
  • Bhaskar K, Konerth M, Kokiko ON, Cardona AE, Ransohoff RM, Lamb BT. 2010. Regulation of tau pathology by the microglial fractalkine receptor. Neuron. 68(1):19-31.
  • Ransohoff, RM, Cardona AE. 2010. Nature. Microglia : Myeloid cells of the central nervous system parenchyma. Nature. 468(7321) :253-62
  • Saederup and Cardona AE, Croft K, Mizutani M, Cotleur AC, Tsou CL, Ransohoff RM, Charo IF. 2010. Selective chemokine receptor usage by central nervous system myeloid cells in CCR2-red fluorescent protein knock-in mice. PLoS One. 5(10):e13693.
  • Hamann I, Uterwalder N, Cardona AE, Meisel C, Zipp F, Ransohoff RM, Infante-Duarte C. 2011. Analyses of phenotypic and functional characteristics of CX3CR1-expressing natural killer cells. Immunology. 133(1):62-73.
  • Pino PA and Cardona AE. 2011. Isolation of brain and spinal cord mononuclear cells using percoll gradients. J. Vis. Exp. Feb 2;(48).pii 2348. Doi 10.3791/2348.
  • Mizutani M, Pino PA, Saederup N, Charo I, Ransohoff, RM, Cardona AE. 2012. The fractalkine receptor but not CCR2 is present on microglia from embryonic development throughout adulthood. J. Immunol. 188(1):29-36.