All of this is hard to believe. The fact that my lab survived for 20 years, I was blessed with incredible trainees, such diverse people and science that supported the lab, and the next generation of scientists it fostered. Grateful does not begin to describe how I feel. (3/)
Well, but we are just getting started 😎 I feel honored and energized to continue doing science with amazing people. I want to continue to mentor more young scientists and create a better world in academia, where women and URM are truly empowered to unleash their potential. (4/)
A fascinating new study by Vishnu Shankar et al. @stanfordimmuno shows that oxidative stress is a shared characteristic of ME/CFS and Long COVID in lymphocytes due to inability to clear reactive oxygen species. This happens in sex-specific manner. (1/) pnas.org/doi/abs/10.107…
Females show higher mtROS levels and insufficient antioxidant levels, while males show mitochondrial lipid oxidative damage. While the reason for this is unclear, it may explain the sex differences in lymphocyte dysfunction we see in PAIS in general. (2/) science.org/doi/10.1126/sc…
ROS-targeting therapies were tested. Metformin treatment in vitro showed some impact on CD4 T cell proliferation. I suspect that other therapies to induce autophagy/mitophagy might also benefit restoration of T cell phenotype. #LowDoseRapamycin 👇🏼 (3/) polybio.org/projects/long-…
Published today! Victoria Bastos, @KerrieGreene_ et al found two distinct immunotypes of ME/CFS based on the cerebrospinal fluid analysis. Great collaboration with @MBVanElzakker @microbeminded2 and the Bragée clinic in Sweden. (1/) academic.oup.com/jimmunol/artic…
This is perfect timing as Victoria will present these data at the @polybioRF symposium today. (2/)
Based on cerebrospinal fluid cytokines, we identified two clusters of ME/CFS patients. Cluster 1 had elevated matrix metalloproteinases & many cytokines compared to cluster 2. Other than older age (Cluster 1), clinical presentation of these clusters was similar. (3/)
Published today📣
Our nasal booster in the "Prime & Spike" vaccine works without adjuvants (which are needed to induce adaptive immunity but also cause inflammation). @Kwon_Dongil @tianyangmao @BenIsraelow et al. asked how this is possible. (1/) nature.com/articles/s4159…
Prime & Spike is a vaccine strategy that leverages preexisting immunity primed by conventional vaccines to elicit mucosal IgA and T cell responses that prevent COVID infection and transmission in rodents. The nasal booster is simply the spike protein (2/) science.org/doi/10.1126/sc…
Our new study shows that the nasal spike protein booster converts lymph node memory B cells into IgA-secreting cells in the lung with the help of memory CD4 T cells. Ag-specific CD4 T cells replace all the necessary functions of adjuvants without nonspecific inflammation! (3/)
This prospective observational study led by @connorbgrady @bornali_27 @SilvaJ_C @hmkyale examined the impact of the primary COVID-19 vaccination on the symptoms and immune signatures of 16 people with #longCOVID. Here is what we found 👇🏼 (1/)
This study asked: Does COVID vaccination improve symptoms of long COVID? If so, is the improvement due to robust T and B cell responses leading to the clearance of the viral reservoir? If not, is there an immune feature that predicts worsening of LC? (2/)
The self-reported impact of vaccination was variable. Of the 16 long COVID patients, 10 felt better, 3 had no change, and 3 had worse health (1 hospitalized) 12 weeks after vaccination. Both physical and social effects of symptom burden appeared to decrease after vaccination. (3/)
Our preprint on post-vaccination syndrome is out. We studied immune signatures and examined spike protein in the blood of people who have developed chronic illnesses after COVID-19 vaccination. (1/) medrxiv.org/content/10.110…
Vaccines have saved countless lives and inspired me to become an immunologist. While generally safe, some people experience adverse effects, including Post-Vaccination Syndrome (PVS). Studying PVS is crucial for improving patient care and enhancing vaccine safety & acceptance. (2/) pubmed.ncbi.nlm.nih.gov/37986769/
Happy to share our latest work by @YYexin et al. on antibody-mediated control of endogenous retroviruses in mice. In the process, we found “natural antibodies” with broad reactivity against enveloped viruses. Here is how “panviral” antibodies work 🧵(1/)
Endogenous retroviruses (ERV) are remnants of genetic invaders that have integrated into our ancestors' genomes over millions of years. ERVs occupy ~8% of the human genome and are under constant host immune surveillance. (2/) nature.com/articles/nrg31… nature.com/articles/nrmic…
This work started over 7 years ago when @YYexin and @rebecca_treger began to examine why ERVs reactivate in certain mouse strains. Through many genetic crosses, we figured out that secreted IgM recruits complement to suppress infectious ERV from emerging. (3/)