ArticlebioRxiv : the preprint server for biology2026
CD3, CD28, TCRαβ expression and IL-2 production in a spontaneous glycosylphosphatidylinositol-deficient Jurkat T cell line.
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Glycosylphosphatidylinositol (GPI) anchors are involved in the organization of membrane microdomains that support T cell receptor (TCR) signaling. However, their role in regulating expression of TCR-related proteins and downstream functional output remains unclear. This study aimed to characterize the effects of GPI-deficiency on TCR, cluster of differentiation 3 (CD3), and CD28 expression as well as interleukin-2 (IL-2) production using a GPI-deficient Jurkat T cell line (S12). Flow cytometry confirmed the complete loss of GPI anchors and GPI-anchored proteins (GPI-APs) in the S12 cell line. Compared to GPI-producing parental Jurkat, S12 had significantly higher expression of CD3 and TCRαβ while CD28 had similar expression. IL-2 production by S12 was assessed following stimulation with anti-CD3/anti-CD28 beads and following stimulation with phorbol 12-myristate 13-acetate (PMA) and ionomycin. Neither S12 nor parental Jurkat produced detectable IL-2 in response to anti-CD3/anti-CD28 bead-mediated stimulation. Both parental Jurkat and S12 produced IL-2 following PMA/ionomycin-mediated stimulation. No significant difference in IL-2 production was observed between S12 and parental Jurkat following PMA/ionomycin-mediated stimulation. These findings demonstrate that GPI-deficiency influences surface receptor expression but does not significantly impair downstream IL-2 production under PMA/ionomycin stimulation. This finding suggests that GPI anchors and GPI-APs contribute to proximal signaling organization but are not required for cytokine production when downstream pathways are directly activated.
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