Publications by authors named "J Bohlen"

Article Synopsis
  • T follicular helper (Tfh) cells, which are important for antibody production, rely heavily on the immunoreceptor PD-1, and its deficiency leads to weakened Tfh functions and impaired immune responses in mice.
  • Individuals lacking PD-1 or PD-L1 demonstrate fewer memory B cells and diminished antibody responses, highlighting the critical role of these molecules in immune system functionality.
  • PD-1 influences both the intrinsic and extrinsic aspects of B cell memory and antibody production, suggesting that disruptions in PD-1 signaling can lead to complications in immune responses, especially during anti-PD-1-PD-L1 therapies.
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Chiral 3,6-dihydroborolo[3,2-]boroles are obtained in one diastereoselective step from the reactions of -(dihaloboryl)arenes with stannole derivatives a complex rearrangement of 1-borolyl-2-(dihaloboryl)arene intermediates.

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Patients heterozygous for germline CBL loss-of-function (LOF) variants can develop myeloid malignancy, autoinflammation, or both, if some or all of their leukocytes become homozygous for these variants through somatic loss of heterozygosity (LOH) via uniparental isodisomy. We observed an upregulation of the inflammatory gene expression signature in whole blood from these patients, mimicking monogenic inborn errors underlying autoinflammation. Remarkably, these patients had constitutively activated monocytes that secreted 10 to 100 times more inflammatory cytokines than those of healthy individuals and CBL LOF heterozygotes without LOH.

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Article Synopsis
  • Some babies with a specific mutation in the IL7R gene have a serious immune problem called SCID, where they lack a certain type of immune cells called T cells, but still have normal B and NK cells.
  • In a study of 6 adults who have a similar genetic issue, they showed low levels of T cells but had relatively normal levels of other immune cells, indicating a more specific problem in T cell development.
  • Even though their T cells didn’t grow well in the lab, the study hints that there might be another way T cells can develop that doesn’t depend solely on the IL-7 cytokine.
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Article Synopsis
  • Inborn errors or autoantibodies (auto-Abs) against type I interferons (IFNs) can lead to severe viral infections.
  • Researchers developed a straightforward blood test that can identify these conditions by stimulating blood with glycosylated IFN-α2, -β, or -ω and measuring IP-10 levels.
  • The study found that IP-10 levels in patients with inherited deficiencies only increase with type II IFN (IFN-γ), while those with auto-Abs can still respond to non-neutralized type I IFNs.
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