Christine J. Hastey, Ph.D.
Affiliations: | 2012 | Microbiology | University of California, Davis, Davis, CA |
Area:
Microbiology Biology, ImmunologyGoogle:
"Christine Hastey"Parents
Sign in to add mentor| Nicole Baumgarth | grad student | 2012 | UC Davis | |
| (Subversion of Humoral Immunity Following Borrelia burgdorferi Infection.) | ||||
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Publications
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| Hastey CJ, Olsen KJ, Elsner RA, et al. (2023) Borrelia burgdorferi Infection-Induced Persistent IgM Secretion Controls Bacteremia, but Not Bacterial Dissemination or Tissue Burden. Journal of Immunology (Baltimore, Md. : 1950). 211: 1540-1549 |
| Waffarn EE, Hastey CJ, Dixit N, et al. (2015) Infection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation. Nature Communications. 6: 8991 |
| Elsner RA, Hastey CJ, Olsen KJ, et al. (2015) Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection. Plos Pathogens. 11: e1004976 |
| Lee CY, Thompson Iii GR, Hastey CJ, et al. (2015) Coccidioides Endospores and Spherules Draw Strong Chemotactic, Adhesive, and Phagocytic Responses by Individual Human Neutrophils. Plos One. 10: e0129522 |
| Elsner RA, Hastey CJ, Baumgarth N. (2015) CD4+ T cells promote antibody production but not sustained affinity maturation during Borrelia burgdorferi infection. Infection and Immunity. 83: 48-56 |
| Wangdi T, Lee CY, Spees AM, et al. (2014) The Vi capsular polysaccharide enables Salmonella enterica serovar typhi to evade microbe-guided neutrophil chemotaxis. Plos Pathogens. 10: e1004306 |
| Hastey CJ, Ochoa J, Olsen KJ, et al. (2014) MyD88- and TRIF-independent induction of type I interferon drives naive B cell accumulation but not loss of lymph node architecture in Lyme disease. Infection and Immunity. 82: 1548-58 |
| Hastey CJ, Elsner RA, Barthold SW, et al. (2012) Delays and diversions mark the development of B cell responses to Borrelia burgdorferi infection. Journal of Immunology (Baltimore, Md. : 1950). 188: 5612-22 |
| Tunev SS, Hastey CJ, Hodzic E, et al. (2011) Lymphoadenopathy during lyme borreliosis is caused by spirochete migration-induced specific B cell activation. Plos Pathogens. 7: e1002066 |