Pre-cancerous blood clones reshape bone marrow in their favour
Mutant blood clones drove bone-marrow support cells into senescence, creating an environment that increased clone growth over healthy blood production; removing senescent cells decreased clone growth in mice. Allergic asthma also worsened in mice lacking the CD97 receptor, while receptor levels in airway cells from asthma patients decreased after an attack. The findings expose feedback loops in diseased tissues without establishing a treatment effect in people.
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Mutant blood clones turn marrow support to their advantage
A study led by The Jackson Laboratory reports that mutant blood cells in clonal haematopoiesis drive the bone marrow's stromal support cells into senescence. The aged environment then favours expansion of the mutant clone over healthy blood production. When researchers removed senescent support cells from mice, clone growth fell across several tests; mice carrying fewer of those cells also progressed more slowly toward blood cancer. Human samples show an association between mutant clones and senescent support cells, but the effect of clearing those cells was tested only in mice.[1]
Loss of CD97 worsens allergic asthma in mice
In Nature Communications experiments, mice lacking the CD97 receptor developed worse asthma across several models. Blocking the receptor with an antibody before sensitisation also strengthened the allergic response. The effect ran chiefly through immune cells rather than lung epithelium: dendritic cells without CD97 became more active, increased T-cell proliferation and type 2 cytokine secretion, and produced stronger airway inflammation when transferred. Lower ADGRE5 levels in airway phagocytes collected from people with asthma after an allergen-induced attack provide an observational human counterpart rather than a clinical test.[2]
Clonal haematopoiesis becomes common in later life
Clonal haematopoiesis affects roughly one in five people over 70, according to the source. Study leader Jennifer Trowbridge says the condition can accelerate the accumulation of senescent cells in bone marrow beyond what a person's age would predict. Human samples show mutant clones and senescent stromal support cells occurring together, but do not directly test that acceleration. Slower clone growth after senescent support cells were cleared has been shown only in mice.[1]
