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Article Synopsis
  • Current kidney transplant regimens often struggle to prevent antibody-mediated rejection (ABMR) in sensitized individuals, leading to graft failure.
  • Research showed that anti-CD154 monoclonal antibody (mAb) treatment for kidney transplants in nonhuman primates was more effective at controlling rejection and post-transplant immune responses than standard tacrolimus-based therapy.
  • The anti-CD154-treated group had significantly longer survival rates, better suppression of harmful antibodies, and fewer complications post-transplant, suggesting that anti-CD154 mAbs could enhance outcomes in sensitized kidney transplant patients.
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Impaired hemostatic and immune functions of platelets after acute thrombocytopenia.

J Thromb Haemost

December 2024

Institute of Vascular Biology and Thrombosis Research, Center of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria. Electronic address:

Background: Platelets are pivotal in maintaining vascular integrity, hemostasis, and immune modulation, with newly generated, immature platelets being the most responsive in fulfilling these tasks. Therefore, the immature platelet fraction provides insights into thrombopoiesis dynamics and clinical prognostication. However, it is currently unclear how immature platelet functions change in settings of acute thrombocytopenia.

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Altering Bacille Calmette-Guérin (BCG) immunization from low-dose intradermal (i.d.) to high-dose intravenous (i.

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Herpes simplex virus (HSV) encodes surface glycoproteins that are host defense evasion molecules, allowing the virus to escape immune clearance. In addition to their role in neuropathogenesis and cell-cell spread, glycoproteins E and I (gE/gI) form a viral Fc receptor (vFcR) for most subclasses and allotypes of human IgG and promote evasion of humoral immune responses. While monoclonal antibodies (mAbs) protect mice from neonatal HSV (nHSV) infections, the impact of the vFcR on mAb-mediated protection by binding to IgG is unknown.

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CD4 T cells have been established as central orchestrators of cellular and humoral immune responses to infection or vaccination. However, the need for CD4 T cell help to generate primary CD8 T cell responses is variable depending on the infectious agent or vaccine and yet consistently required for the recall of CD8 T cell memory responses or antibody responses. Given the deployment of new vaccine platforms such as nucleoside-modified mRNA vaccines, we sought to elucidate the requirement for CD4 T cell help in the induction of cellular and antibody responses to mRNA and adenovirus (Ad)-vectored vaccines against SARS-CoV-2.

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