Study Identifies Altered Immune Receptor Expression on Blood-Forming Cells in Rheumatoid Arthritis Model
Researchers using a mouse model of rheumatoid arthritis found that key immune receptors — including TREM1, PD-L1, TLR2, and CD14 — are significantly upregulated on hematopoietic stem and progenitor cells (HSPCs) during chronic inflammation. HSPCs are the source of hundreds of billions of new blood and immune cells daily, and their receptor expression normally helps them sense inflammatory signals. The findings suggest that chronic inflammation may reprogram these stem cells in ways that alter immune cell production, potentially contributing to the pathology of rheumatoid arthritis and similar diseases.
A study posted to bioRxiv investigated how chronic inflammation in rheumatoid arthritis affects the receptor landscape of hematopoietic stem and progenitor cells (HSPCs), which continuously generate the body's blood and immune cells. Using a murine arthritis model, researchers found elevated expression of microbial sensors TLR2 and CD14, the orphan inflammatory receptor TREM1, and the immune checkpoint receptor PD-L1 on HSPCs — particularly on myeloid progenitor subsets. When these receptors were stimulated in cell culture, they produced measurable changes in cell expansion and differentiation dynamics, and the responses differed notably between HSPCs from arthritic mice versus healthy controls. This suggests that chronic inflammatory conditions do not merely act on mature immune cells but may fundamentally alter the behavior of upstream progenitor cells. The authors hypothesize that this receptor induction on HSPCs could shape the functional properties of the immune cells they produce, positioning HSPCs as active contributors to — rather than passive bystanders in — chronic inflammatory disease. The work opens potential new avenues for understanding and possibly targeting the root of dysregulated immune cell production in rheumatoid arthritis.
What's missing
As a preprint, this study has not yet undergone peer review. The work is conducted entirely in a mouse model, and it remains unknown whether the same receptor upregulation and functional changes occur in human HSPCs in rheumatoid arthritis patients. The study does not address whether these HSPC changes are reversible upon treatment or disease remission, nor does it establish a direct causal link between HSPC reprogramming and clinical disease outcomes.
What different sources said
- bioRxivCenter
Increased Expression and Altered Functional Activities of Immune Receptors TREM1, PD-L1, and Others on Hematopoietic Progenitor Cells in a Mouse Model of Rheumatoid Arthritis
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