Institute Affiliations

Honors & Awards

  • Learners to LeAders in Urology, Nephrology, and non-Cancer Hematology (LAUNCH) Fellow, NIH/NIDDK
  • NRSA in Pediatric Nonmalignant Hematology and Stem Cell Biology (T32) Fellow, NIH/NIDDK
  • Predoctoral Ruth L. Kirschstein National Research Service Award (F31) Recipient, NIH/NCI
  • Patel Scholar Award for Cancer Research Recipient, AFCRI/Cancer Biology - Penn Medicine
  • Chancellor’s Research Scholarship - Science Award Recipient, UCSD
  • The Fate and Function of Duplicate Genes in Developmental Regulation Grant Recipient, US Grants
  • Member, Sigma Xi
  • Member, Phi Beta Kappa
  • Finalist and Scholar, National Merit

Professional Education

  • Doctor of Philosophy, University of Pennsylvania (2022)
  • Ph.D., University of Pennsylvania, Cell and Molecular Biology (CAMB) - Cancer Biology
  • B.S., University Of California - San Diego, Molecular Biology

Stanford Advisors

Contact

  • Academic
    University - Scholar Department: Stem Cell Operations Position: Postdoctoral Scholar

Additional Info

Graduate and Fellowship Programs

  • Pediatric Nonmalignant Hematology and Stem Cell Biology Training Grant (Fellowship Program)

All Publications

  • Depleting myeloid-biased haematopoietic stem cells rejuvenates aged immunity. Nature Ross, J. B., Myers, L. M., Noh, J. J., Collins, M. M., Carmody, A. B., Messer, R. J., Dhuey, E., Hasenkrug, K. J., Weissman, I. L. 2024

    Abstract

    Ageing of the immune system is characterized by decreased lymphopoiesis and adaptive immunity, and increased inflammation and myeloid pathologies1,2. Age-related changes in populations of self-renewing haematopoietic stem cells (HSCs) are thought to underlie these phenomena3. During youth, HSCs with balanced output of lymphoid and myeloid cells (bal-HSCs) predominate over HSCs with myeloid-biased output (my-HSCs), thereby promoting the lymphopoiesis required for initiating adaptive immune responses, while limiting the production of myeloid cells, which can be pro-inflammatory4. Ageing is associated with increased proportions of my-HSCs, resulting in decreased lymphopoiesis and increased myelopoiesis3,5,6. Transfer of bal-HSCs results in abundant lymphoid and myeloid cells, a stable phenotype that is retained after secondary transfer; my-HSCs also retain their patterns of production after secondary transfer5. The origin and potential interconversion of these two subsets is still unclear. If they are separate subsets postnatally, it might be possible to reverse the ageing phenotype by eliminating my-HSCs in aged mice. Here we demonstrate that antibody-mediated depletion of my-HSCs in aged mice restores characteristic features of a more youthful immune system, including increasing common lymphocyte progenitors, naive T cells and B cells, while decreasing age-related markers of immune decline. Depletion of my-HSCs in aged mice improves primary and secondary adaptive immune responses to viral infection. These findings may have relevance to the understanding and intervention of diseases exacerbated or caused by dominance of the haematopoietic system by my-HSCs.

    View details for DOI 10.1038/s41586-024-07238-x

    View details for PubMedID 38538791

    View details for PubMedCentralID 3250139

https://orcid.org/0000-0002-5961-0722