By contrast, KLRB1 stratification was primarily linked to immune effector pathways: in SLE, the KLRB1-high subgroup displayed higher activity of the Natural killer cell mediated cytotoxicity pathway ( P = 4 × 10 −6 ); a directionally consistent trend was observed in IPF, although the association did not reach statistical significance ( P = 0.32) ( Fig. 6 F), implying that this relationship may be less stable in the IPF cohort due to heterogeneity or sample size limitations.
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GRN and KLRB1 define a shared peripheral-blood transcriptomic signature linking SLE and IPF.
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