Sickle hemoglobin activates monocytes via TLR4, germinal center B cells provide a niche for T-cell lymphoma, and a combination immunosuppression regimen for acquired hemophilia A

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In this week’s episode, we will review a study that cell-free hemoglobin S was found to induce high levels of pro-inflammatory cytokine production in monocytes. The effect is mediated by Toll-like receptor 4, or TLR4, suggesting intriguing therapeutic possibilities for sickle cell disease.  Secondly, germinal center B cells with aberrant expression profiles undergo independent clonal evolution in the microenvironment of angioimmunoblastic T-cell lymphoma. New findings published in Blood elucidate mechanisms of disease pathogenesis and uncover a new potential target for treatment. Finally, an upfront combination of three immunosuppressive agents was highly effective and well tolerated in patients with acquired hemophilia A. Although prospective studies are needed, the triple regimen could be an attractive treatment option, particularly for elderly and frail patients.

Sickle hemoglobin activates monocytes via TLR4, germinal center B cells provide a niche for T-cell lymphoma, and a combination immunosuppression regimen for acquired hemophilia A

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Sickle hemoglobin activates monocytes via TLR4, germinal center B cells provide a niche for T-cell lymphoma, and a combination immunosuppression regimen for acquired hemophilia A
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