Associate Professor
Research Interest: Adaptive immunity to Chlamydia
Ph.D., University of Minnesota
Postdoctoral: University of California, Davis
Office: 501-686-6949
Lab: 501-686-6546
Fax: 501-686-5359
Email: lxli@uams.edu
Currently accepting new students
Research Description
Chlamydia is a gram-negative obligate intracellular bacterium that leads to the most prevalent sexually transmitted infection worldwide. According to the CDC, Chlamydia infection is now the most commonly reported infectious disease in the US with more than three million new cases occurring annually. Although Chlamydia infections can be readily treated, in young women most are initially subclinical and therefore remain untreated. These untreated Chlamydia infection can often cause severe reproductive problems, such as pelvic inflammatory disease, ectopic pregnancy, and infertility. To date, no Chlamydia vaccine is available.
The primary focus of my laboratory is to understand the development and maintenance of CD4 T cell memory in a mouse model of Chlamydia female reproductive tract (FRT) infection. To track Chlamydia-specific CD4 T cells in vivo, we recently developed several new tools called Chlamydia-specific MHC Class II tetramers. These new reagents allow for the first time direct visualization of endogenous, antigen-specific CD4 T cells during Chlamydia infection in the FRT. We are currently employing a variety of immunological methods, including flow cytometry and immunofluorescence imaging, in conjunction with cellular approaches and gene ablation mouse models to characterize the memory CD4 T cell responses in the FRT during Chlamydia reinfection.
Our secondary focus is on deciphering the role B cells play in bacterial containment within the FRT. We recently showed that mice lacking B cells experience disseminated Chlamydia infection and develop ascites during Chlamydia primary infection. These unexpected observations lead us to actively seek the precise effector function of host B cells during initial encounter of Chlamydia at the FRT mucosa. We hope that improved understanding of host adaptive immune responses to Chlamydia infection will provide important insights into the rational design of an urgently needed Chlamydia vaccine.
Publications
- Li, L.X., Labuda J. C., Imai D. M., Griffey S. M. and McSorley S. J. 2017. CCR7 deficiency allows accelerated clearance of Chlamydia from the female reproductive tract. J Immunol doi: 10.4049/jimmunol.1601314. (PMID: 28801359).
- Qualai, J.*, Li, L. X.*, Cantero, J., Tarrats, A., Fernández, M. A., Sumoy, L., Rodolosse, A., McSorley, S. J., Genescà, M. 2016. Expression of CD11c is associated with unconventional activated T cell subsets with high migratory potential. PLoS One. 11(4):e0154253. (PMCID: PMC4847787) *co-first author
- Li, L. X., and McSorley, S. J. 2015. A re-evaluation of the role of B cells in protective immunity to Chlamydia infection. Immunol Lett 164: 88-93. (PMCID: PMC4402208)
- O’Donnell, H., Pham, O. H., Li, L. X., Atif, S. M., Lee, S. J., Ravesloot, M. M., Stolfi, J. L., Nuccio, S. P., Broz, P., Monack, D. M., Baumler, A. J., and McSorley, S. J. 2014. Toll-like receptor and inflammasome signals converge to amplify the innate bactericidal capacity of T helper 1 cells. Immunity 40: 213-224. (PMCID: PMC3960852)
- Li, L. X., and McSorley, S. J. 2013. B cells enhance antigen-specific CD4 T cell priming and prevent bacteria dissemination following Chlamydia muridarum genital tract infection. PLoS Pathog 9: e1003707. (PMCID: PMC3814678)