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Effect of hypoxia and treatment with cyclosporine A on chemotaxis of RAMOS B cells

ABSTRACT: To investigate the effect of changes in oxygen tension and treatment with cyclosporine A on the chemotactic migration of B cells, we grew RAMOS B cells at 19% and 1% oxygen levels, and at 19% and 1% oxygen levels after treatment with cyclosporine A. We then performed RNA-seq on these RAMOS B cells and subequently gene expression profiling analysis on this RNA-seq data.

ORGANISM(S): Homo sapiens

PROVIDER: GSE212853 | GEO | 2023/02/13

REPOSITORIES: GEO

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Effect of hypoxia and treatment with cyclosporine A on chemotaxis of RAMOS B cells

Project description:Background: Hypoxia is a potent molecular signal for cellular metabolism, mitochondrial function, and migration. Conditions of low oxygen tension trigger regulatory cascades mediated via the highly conserved HIF-1 α post-translational modification system. In the adaptive immune response, B cells (Bc) are activated and differentiate under hypoxic conditions within lymph node germinal centers, and subsequently migrate to other compartments. During migration, they traverse through changing oxygen levels, ranging from 1-5% in the lymph node to 5-13% in the peripheral blood. Interestingly, the calcineurin inhibitor cyclosporine A is known to stimulate prolyl hydroxylase activity, resulting in HIF-1 α destabilization and may alter Bc responses directly. Over 60% of patients taking calcineurin immunosuppressant medications have hypo-gammaglobulinemia and poor vaccine responses, putting them at high risk of infection with significantly increased morbidity and mortality. Results: We demonstrate that oxygen tension is a previously unrecognized Bc regulatory switch, altering CXCR4 and CXCR5 chemokine receptor signaling in activated Bc through HIF-1 α expression, and controlling critical aspects of Bc migration. Our data demonstrate that calcineurin inhibition hinders this oxygen regulatory switch in primary human Bc. Conclusion: This previously unrecognized effect of calcineurin inhibition directly on human Bc has significant and direct clinical implications.

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