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Refractory autoimmune mutilineage cytopenias can present in childhood associated with chronic nonmalignant lymphoproliferation (splenomegaly, hepatomegaly, and/or lymphadenopathy). Cytopenias due to peripheral destruction and sequestration have been well recognized since the 1950s and are often lumped together as eponymous syndromes, such as Evans syndrome and Canale-Smith syndrome. Though their clinical and genetic diagnostic workup may appear daunting, it can provide the basis for early intervention, genetic counseling, and empirical and targeted therapies.

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Self-catalyzed nitric oxide nanocomplexes induce ferroptosis for cancer immunotherapy.

J Control Release

January 2025

MoE Frontiers Science Center For Precision Oncology, Cancer Centre, Faculty of Health Sciences, University of Macau, Macau, SAR 999078, China. Electronic address:

Ferroptosis, triggered by membrane lipid peroxidation (LPO) and diminished antioxidants, can be induced by intracellular iron (II, Fe). However, the role of nitric oxide (NO) in causing Fe overload for ferroptosis remains uncertain. This study reveals that NO can stimulate endogenous Fe release by upregulating heme oxygenase 1 (HMOX1) expression.

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The cytokine IL-18 has immunostimulatory effects but is negatively regulated by a secreted binding protein, IL-18BP, that limits IL-18's anticancer efficacy. A decoy-resistant form of IL-18 (DR-18) that avoids sequestration by IL-18BP while maintaining its immunostimulatory potential has recently been developed. Here, we investigated the therapeutic potential of DR-18 in renal cell carcinoma (RCC).

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Article Synopsis
  • Dengue virus (DENV) infection is a major global health concern, and a new whole-blood model using hirudin has been developed to study its immunopathogenesis more effectively.
  • This model shows that all major leukocyte populations, especially monocytes and granulocytes, are highly susceptible to DENV, with granulocytes identified as new key targets for the virus.
  • The study also confirms that B, NK, and T cells can be infected, indicating complex interactions within the immune response, and highlights the potential for this model to improve understanding of dengue disease and aid in developing new treatments.
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Dendritic cells (DCs) within the tumor microenvironment (TME) have an insufficient capacity to activate T cells through antigen presentation. Furthermore, the programmed cell-death ligand 1 (PD-L1), abundantly expressed on tumor-associated DCs, binds the programmed cell-death 1 (PD-1)-positive T cells and suppresses their immune function. The binding of PD-L1 to CD80 (B7.

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