Philadelphia University + Thomas Jefferson University

Snyder, Christopher

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Christopher M. Snyder, PhD

Contact Dr. Snyder

233 South 10th Street
Bluemle Life Sciences Building 526
Philadelphia, PA 19107

(215) 503-2543

Research and Clinical Interests

Our lab is interested in understanding how T cells respond to chronic antigen stimulation during persistent viral infections, particularly cytomegalovirus (CMV) infections. CMV is a ubiquitous herpesvirus that infects most people world-wide and persists for life. In immunocompromised individuals, CMV can be a major pathogen, causing severe morbidity and death. In healthy individuals, CMV is continuously controlled by the immune system and causes little or no pathology, thanks largely to a potent T cell response. The constant immune surveillance of CMV-infected cells results in a slow accumulation of virus-specific CD8+ T cells in healthy people such that on average, CMV-specific T cells comprise 4% to 5% of all T cells in circulation. However, the mechanisms by which these T cells are generated and maintained are not understood. This is important for two reasons. First, CMV-specific T cells isolated from healthy donors are being used experimentally to control CMV infection in immune compromised patients. Second, CMV has been proposed as a vaccine vector to stimulate large T cell populations specific for recombinant antigens encoded in the CMV genome. In both cases, a better understanding of how these populations develop and persist as well as how they respond to new antigen encounters will improve these therapeutic approaches. To study the immune response to CMV, we use murine cytomegalovirus (MCMV), a homologue of human CMV (HCMV) and a natural mouse pathogen. Like HCMV, infection of mice with MCMV results in the slow accumulation of functional, virus-specific T cells over time. Currently we focus on two broad areas of research: 1) the homeostasis of MCMV-specific T cells that enables their maintenance over time and 2) the response of MCMV-specific T cells to re-stimulation in the context of adoptive immunotherapy.


Most Recent Peer-Reviewed Publications

  1. The chemokine receptor CXCR3 promotes CD8+t cell accumulation in uninfected salivary glands but is not necessary after murine cytomegalovirus infection
  2. Intratumoral infection by CMV may change the tumor environment by directly interacting with tumor-associated macrophages to promote cancer immunity
  3. Virus-specific CD8+T cells infiltrate melanoma lesions and retain function independently of PD-1 expression
  4. Blocking virus replication during acute murine cytomegalovirus infection paradoxically prolongs antigen presentation and increases the CD8+T cell response by preventing type I IFN-dependent depletion of dendritic cells
  5. CMV-specific CD8 T cell differentiation and localization: Implications for adoptive therapies
  6. Intratumoral Infection with Murine Cytomegalovirus Synergizes with PD-L1 Blockade to Clear Melanoma Lesions and Induce Long-term Immunity
  7. Cytomegalovirus and immunotherapy: Opportunistic pathogen, novel target for cancer and a promising vaccine vector
  8. Murine CMV Infection Induces the Continuous Production of Mucosal Resident T Cells
  9. Memory T cells specific for murine cytomegalovirus re-emerge after multiple challenges and recapitulate immunity in various adoptive transfer scenarios
  10. Front-Line Memory T Cells Think Outside the T-box. . . Mostly
  11. Virus-specific CD8+ T cells infiltrate melanoma lesions and retain function despite high PD-1 expression
  12. Resolving the titer of murine cytomegalovirus by plaque assay using the M2-10B4 cell line and a low viscosity overlay
  13. Systemic Hematogenous Maintenance of Memory Inflation by MCMV Infection
  14. Competition for antigen at the level of the APC is a major determinant of immunodominance during memory inflation in murine cytomegalovirus infection
  15. Competition between T cells maintains clonal dominance during memory inflation induced by MCMV
  16. Editorial: Once more unto the breach, dear friends: CMV reactivates when the walls come down
  17. Buffered memory: A hypothesis for the maintenance of functional, virus-specific CD8+T cells during cytomegalovirus infection
  18. Sustained CD8+ T cell memory inflation after infection with a single-cycle Cytomegalovirus
  19. Aborted germinal center reactions and B cell memory by follicular T cells specific for a B cell receptor V region peptide
  20. Cross-presentation of a spread-defective MCMV is sufficient to prime the majority of virus-specific CD8+ T cells