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New treatment rejuvenates defenses in older people

New treatment rejuvenates defenses in older people
New treatment rejuvenates defenses in older people


In a recent study published in NatureResearchers have developed a younger immune system that includes fewer myeloid-biased hematopoietic stem cells (my-HSCs), more HSCs, and a balanced generation of myeloid and lymphoid cells (bal-HSCs). We have developed a treatment to restore the condition.

study: Depleting myeloid-biased hematopoietic stem cells rejuvenates the aging immune system. Image credit: Lightspring /

Effects of aging on the immune system

Aging of the immune system is associated with decreased lymphopoiesis, increased inflammation, and myeloid disease due to changes in self-renewing HSCs. During childhood, bal-HSCs become predominant, promoting lymphopoiesis and adaptive immune responses.

Aging increases my-HSC, decreases lymphopoiesis, and promotes myelopoiesis. The origin and interconversion potential of myeloid HSCs is unknown. However, ablation of my-HSCs in aged mice can reverse the aging phenotype.

About research

Researchers asked whether antibody-controlled my-HSC depletion could cure age-related immunological decline by limiting bone marrow cell-induced inflammation and restoring lymphopoiesis. I investigated whether. To this end, the impact of my-HSC depletion on the hematopoietic system, immunological phenotype, and functional response to incident infection was evaluated.

Several cell surface antigen molecules have been developed and validated to identify potential targets for therapeutic my-HSC reduction. Levels of my-HSC and balanced HSC were measured using antibodies and flow cytometry.

some my-HSC antigenSubsequently, those including neogenin 1 (NEO1), cluster of differentiation 62p (CD62p), and CD150 were targeted to determine their role in reducing my-HSC levels. Individual antibody conditioning treatments for each targeted my-HSC depletion were then developed, focusing on cellular clearance regulators such as anti-phagocytic signals, isotype, and antibody density.

To establish the role of CD150 targeting and the ability of CD150-targeting antibodies to reduce my-HSC alive It was evaluated. To target CD62p or NEO1, goat anti-mouse NEO1 antiserum was mixed with anti-CD47 and anti-KIT antibodies.

Gene expression analysis of pure whole HSCs extracted from 11-month-old mice was performed to determine changes in HSC composition after my-HSC removal. Transplant studies using pure HSCs were also performed to compare the myeloid and lymphoid lineage potential of recipient mice.
Myeloid and common lymphoid progenitor cells (CLPs) were measured in mouse bone marrow after conditioning with antibodies. These analyzes were performed after 1 week to assess acute effects, and also after 8 and 16 weeks to determine long-term effects. The effect of this treatment on non-self-renewing progenitor cells was also evaluated after 8 weeks.

T cells Subsets were analyzed using standard markers or cluster-based analysis. The impact of my-HSC depletion in aged animals on pro-inflammatory mediators and functional immunity to infection has also been shown to influence mouse immune responses to live attenuated virus using mouse friend retrovirus (FV) and subsequent pathogenic virus infection. This was investigated by analyzing the attacks. model.

research result

Antibody-mediated depletion of my-HSC in aged mice restored characteristics of the young immune system, such as increases in CLPs, naive T cells, and B cells, while at the same time reducing indicators of age-related immune decline. Depleting my-HSCs in old mice increased primary and secondary adaptive immune responses to viral infection.

Twelve potential genes encoding cell surface proteins significantly expressed in aged HSCs and my-HSCs were identified. Additionally, CD150, CD4, CD6, CD62p20, and NEO1 were identified as markers for my-HSCs.

Antibodies against CD41 and NEO1 increase the frequency of my-HSC staining, thus indicating a myeloid bias. CD62p targeting resulted in the highest my-HSC enrichment.

The most abundant protein molecules on my-HSCs were NEO1, CD41, and CD62p. Flow cytometry analysis did not identify any surface proteins strongly expressed by the subgroups, except for CD41, which is highly expressed by megakaryocyte progenitors.

Anti-CD150 antibodies significantly reduced my-HSCs in mice, thereby increasing naïve T cell and mature B cell levels. In aged mice, CD4+ T lymphocytes with an exhausted phenotype (PD1+ CD62L-) proliferated more than lymphocytes with a non-exhausted phenotype (PD1- CD62L+).

Antibody training reduced CD4+ PD1+ CD62L- cells compared to CD4+ PD1- CD62L+. Older mice also acquired age-associated B cells associated with impaired humoral immunity.

Antibody training reduced the levels of proinflammatory proteins such as interleukin-1 alpha (IL-1α) and CXC-motif chemokine ligand 5 (CXCL5), which were higher in older animals. Older animals depleted of my-HSCs exhibit higher virus-specific CD8+ T cell responses in the spleen after vaccination, thus indicating a better initial response to live-attenuated virus infection.


Increased my-HSC levels with aging may lead to inadequate adaptive immune and inflammatory responses. Therefore, depleting my-HSCs may promote the synthesis of new T and B cells and improve immune responses while reducing the production of inflammatory myeloid cells. In this study, we show that depletion of my-HSC in aged animals allows bal-HSC to exhibit youthful immunological characteristics such as enhanced lymphocyte progenitors and naïve cells, lymphocyte dysfunction and exhaustion indicators, and decreased inflammatory mediators. was able to recover.

Further research can refine conditioning techniques and examine their effects on differentiated cells, such as regulatory T cells.

Reference magazines:

  • Ross, J.B., Myers, L.M., No., J.J. other. (2024). Depleting myeloid-biased hematopoietic stem cells rejuvenates the aging immune system. Nature. doi:10.1038/s41586-024-07238-x




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