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http://dx.doi.org/10.1016/0022-1759(75)90040-x | DOI Listing |
Bull Math Biol
January 2025
Information Technology Laboratory, National Institute of Standards and Technology, Gaithersburg, Maryland, 20899, USA.
Immune events such as infection, vaccination, and a combination of the two result in distinct time-dependent antibody responses in affected individuals. These responses and event prevalence combine non-trivially to govern antibody levels sampled from a population. Time-dependence and disease prevalence pose considerable modeling challenges that need to be addressed to provide a rigorous mathematical underpinning of the underlying biology.
View Article and Find Full Text PDFBull Math Biol
January 2025
Department of Theoretical Biology, Max Planck Institute for Evolutionary Biology, August-Thienemann-Strasse 2, 24306, Ploen, Germany.
The human immune system can recognize, attack, and eliminate cancer cells, but cancers can escape this immune surveillance. Variants of ecological predator-prey models can capture the dynamics of such cancer control mechanisms by adaptive immune system cells. These dynamical systems describe, e.
View Article and Find Full Text PDFAnn Hematol
January 2025
Department of Hematology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, China.
Background: Autoimmune hemolytic anemia (AIHA) following allogeneic hematopoietic stem cell transplantation (allo-HSCT) is often refractory and relapsing, leading to increased mortality post-HSCT.
Methods: We retrospectively analyzed the cases of patients with transfusion-dependent β-thalassemia (TDT) who underwent allo-HSCT to study their clinical features, the occurrence of AIHA post-HSCT, and treatment response and to explore the possible pathogenesis of AIHA.
Result: A total of 113 patients were registered in the study, out of whom 14 developed AIHA following allo-HSCT, resulting in a cumulative incidence of 12.
Background: A complex, multicellular disease with genetic and immunological elements, Alzheimer's disease (AD) affects millions worldwide. There has been previous research linking AD to the missense variants ABI3-rs616338-T and PLCG2-rs72824905-G, and the altered expression of these genes has been shown to disrupt microglial function. In our understanding of AD risk and resilience, limited research has been conducted on how these variants affect microglial subtypes and states in AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Knight Alzheimer Disease Research Center, St. Louis, MO, USA.
Background: Alzheimer's disease (AD) is characterized by the aggregation and accumulation of proteins including amyloid-β and tau. We previously compared the immunological milieus in the brain of mice with amyloid deposition or tau aggregation and found that mice with tauopathy but not amyloid developed a unique adaptive immune response with markedly increased activated T cells in areas with tau pathology. T cell depletion blocked tau-mediated neurodegeneration.
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