Innate Immune sensing of Chlamydia
Molecular Mechanisms of Chlamydial Immunopathology
Cell Autonomous Defenses Against Chlamydia
Memory CD8+ T Cell Responses to Chlamydia

Human Indoleamine 2,3-dioxygenase and the CD4+ T Cell Response

Memory CD8+ T Cell Responses to Chlamydia

Jennifer Helble


A previous study from the Starnbach lab demonstrated that Chlamydia trachomatis infection in the upper genital tract of mice causes an upregulation of PD-L1 on epithelial cells. This upregulation can be somewhat attributed to the inhibited CD8+ T cell response to C. trachomatis, as infected PD-L1-/- mice exhibit both faster bacterial clearance and a productive CD8+ T cell response in comparison to infected WT mice. In PD-L1-/- mice, CD8+ T cells have a higher effector memory to central memory (TEM/TCM) ratio than WT mice, indicating that the inhibition of the CD8+ T cells in WT mice could be attributed to the predominance of TCM cells. I am most interested in following up on several of these aspects, both from the host perspective and the bacteria perspective. First, I am interested in further characterizing the skewing of the TEM/TCM ratio and understanding how infection in the upper genital tract (in particular, upregulation of PD-L1) can lead to these differences in CD8+ T cell populations. Second, I am interested in screening for Chlamydia proteins (in particular, secreted effectors) that can directly manipulate PD-L1 expression using both gain of function and loss of function approaches.

Department of Microbiology and Immunobiology | Harvard Medical School | 77 Ave Louis Pasteur, Boston, MA 02115