I. L. Weissman

P66 is a bacterial mimic of CD47 that binds the anti-phagocytic receptor SIRPα and facilitates macrophage evasion by Borrelia burgdorferi

This study identifies P66, a bacterial protein mimicking CD47, which binds SIRPα to evade macrophage phagocytosis, and shows its role in Lyme Disease pathogenesis.

SIRPα controls CD47-dependent platelet clearance in mice and humans

This study shows that the CD47-SIRP axis regulates platelet homeostasis and that blocking this interaction affects platelet levels in mice and humans.

Engineered CD47 protects T cells for enhanced antitumor immunity

This paper engineers a CD47 variant to protect T cells from macrophage clearance, enhancing antitumor efficacy by combining T cell and macrophage activation.

Novel Association of Lyme Disease, Age, and Atopic Dermatitis

This study identifies a novel association between Lyme disease, age, and atopic dermatitis using both murine models and human epidemiological data.

Anti-GD2 antibody disrupts GD2:Siglec-7 interactions and synergizes with CD47 blockade to mediate tumor eradication

This study shows that combining anti-GD2 and anti-CD47 antibodies enhances anti-tumor responses by recruiting macrophages and disrupting the GD2:Siglec-7 interaction in GD2+ cancers.

Mass spectrometry analysis of mouse hematopoietic stem cells and their progenitors reveals differential expression within and between proteome and transcriptome throughout adult and aged hematopoiesis

The paper reports a proteomics resource analyzing protein expression in mouse adult and aged hematopoietic stem cells and their progenitors, revealing differential expression and gene regulation.

Neogenin-1 distinguishes between myeloid-biased and balanced Hoxb5+ mouse long-term hematopoietic stem cells

This paper identifies Neogenin-1 as a marker distinguishing myeloid-biased from balanced Hoxb5+ long-term hematopoietic stem cells in mice, revealing their functional heterogeneity and hierarchical relationship.

Heme oxygenase-1 deficiency affects bone marrow niche and triggers premature exhaustion of hematopoietic stem cells.

This study shows that HO-1 deficiency in the bone marrow niche leads to premature HSC exhaustion and aging features, which can be reversed by transplanting HO-1-expressing HSCs.