Hamilton, Sara E
Mayo Clinic
Department of Laboratory Medicine and Pathology and Center of Immunology, University of Minnesota, Minneapolis, MN, USA. probbins@umn.edu kirkland.james@mayo.edu lniedern@umn.edu tchkonia.tamar@mayo.edu hamil062@umn.edu.
Citations 2
Senolytics reduce coronavirus-related mortality in old mice
Camell, Christina D. , Yousefzadeh, Matthew J. , Zhu, Yi , Prata, Larissa , Huggins, Matthew A. , Pierson, Mark , Zhang, Lei , O’Kelly, Ryan, Pirtskhalava, Tamar , Xun, Pengcheng , Ejima, Keisuke , Xue, Ailing, Tripathi, Utkarsh , Espíndola‐Netto, Jair Machado , Giorgadze, Nino, Atkinson, Elizabeth J. , Inman, Christina L., Johnson, Kurt O. , Cholensky, Stephanie H., Carlson, Timothy W. , O’Sullivan, M. Gerard , Jameson, Stephen C. , Meves, Alexander , Li, Ming , Prakash, Y. S. , Hamilton, Sara E. , Niedernhofer, Laura J. , Kirkland, James L. , Prata, Larissa G P Langhi , LeBrasseur, Nathan K , Khosla, Sundeep , O'Sullivan, M Gerard , Allison, David B , Jameson, Stephen C , Meves, Alexander , Prakash, Y S , Chiarella, Sergio E , Hamilton, Sara E , Tchkonia, T , Niedernhofer, Laura J , Kirkland, James L , Robbins, Paul D , Zhang, Lei , Zhu, Yi , O'Kelly, Ryan D., LeBrasseur, Nathan K. , Khosla, Sundeep , Allison, David B. , Chiarella, Sergio E. , Tchkonia, Tamar , Robbins, Paul D.
Science | June 8, 2021 | Volume: 373 | Issue: 6552 | Pages: No page available
Senescent cells exacerbate COVID-19 Cellular senescence is a state elicited in response to stress signals and is associated with a damaging secretory phenotype. The number of senescent cells increases with advanced age and this in turn drives age-related diseases. Camell et al. show that senescent cells have an amplified inflammatory response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (see the Perspective by Cox and Lord). This response is communicated to nonsenescent cells, suppressing viral defense mechanisms and increasing the expression of viral entry proteins. In old mice infected with a SARS-CoV-2–related virus, treatment with senolytics to reduce the senolytic cell burden reduced mortality and increased antiviral antibodies. Science , abe4832, this issue p. eabe4832 ; see also abi4474, p. 281
Different T Cell Receptor Signals Determine CD8 + Memory Versus Effector Development
Teixeiro, Emma , Daniëls, Mark A. , Hamilton, Sara E. , Schrum, Adam G. , Bragado, Rafael, Jameson, Stephen C. , Palmer, Ed, Daniels, Mark A , Schrum, Adam G , Jameson, Stephen C , Hamilton, Sara E
Science | January 22, 2009 | Volume: 323 | Issue: 5913 | Pages: 502-505
Following infection, naïve CD8 + T cells bearing pathogen-specific T cell receptors (TCRs) differentiate into a mixed population of short-lived effector and long-lived memory T cells to mediate an adaptive immune response. How the TCR regulates memory T cell development has remained elusive. Using a mutant TCR transgenic model, we found that point mutations in the TCR β transmembrane domain (βTMD) impair the development and function of CD8 + memory T cells without affecting primary effector T cell responses. Mutant T cells are deficient in polarizing the TCR and in organizing the nuclear factor κB signal at the immunological synapse. Thus, effector and memory states of CD8 + T cells are separable fates, determined by differential TCR signaling.