The Hidden Power of Normalization: Exponential Capacity Control in Deep Neural Networks

arXiv:2511.00958v1 Announce Type: cross Abstract: Normalization methods are fundamental components of modern deep neural networks (DNNs). Empirically, they are known to stabilize optimization dynamics and

FeNN-DMA: A RISC-V SoC for SNN acceleration

arXiv:2511.00732v1 Announce Type: cross Abstract: Spiking Neural Networks (SNNs) are a promising, energy-efficient alternative to standard Artificial Neural Networks (ANNs) and are particularly well-suited to

Parameter Interpolation Adversarial Training for Robust Image Classification

arXiv:2511.00836v1 Announce Type: cross Abstract: Though deep neural networks exhibit superior performance on various tasks, they are still plagued by adversarial examples. Adversarial training has

Region-Aware Reconstruction Strategy for Pre-training fMRI Foundation Model

arXiv:2511.00443v1 Announce Type: cross Abstract: The emergence of foundation models in neuroimaging is driven by the increasing availability of large-scale and heterogeneous brain imaging datasets.

FlashEVA: Accelerating LLM inference via Efficient Attention

arXiv:2511.00576v1 Announce Type: cross Abstract: Transformer models have revolutionized natural language processing, achieving state-of-the-art performance and demonstrating remarkable scalability. However, their memory demands, particularly due

Astrocytes control the Neuroinflammation and ILC2 response through IL-33/ST2 signaling, during protection against Cerebral Malaria in Toxoplasma-P. berghei coinfected Mice

October 25, 2025

Cerebral malaria (CM) is a complex multi-systemic disorder defined by diffuse encephalopathy and acute neurological manifestations, including altered consciousness, deep coma, and seizures preceding death. During infection, astrocytes undergo profound morphological and molecular changes, adopting a reactive state that alters their normal functions. This reactivity involves a shift from a neuroprotective (A2) to a neurotoxic (A1) phenotype, influencing the outcome of the neuroimmune response. The balance between these phenotypes may vary depending on the chronicity or recurrence of infection in the same host. In this study, we investigated how latent Toxoplasma gondii (Tg) brain infection influences the course of experimental cerebral malaria (ECM) in mice infected with Plasmodium berghei ANKA (PbA). Our findings highlight an immunomodulatory role of GFAP positive astrocytes, which exhibited marked morphological and molecular alterations and adopted a unique intermediate reactive state (A1/A2). This hybrid state was associated with increased production of CXCL10 and TGF beta, which together controlled neuroinflammation without exacerbating parasitemia. Moreover, we identified a pivotal role of the IL33-ST2 signaling axis induced by Tg brain infection in protection against ECM. Astrocyte-derived IL33 promoted the recruitment and activation of type 2 innate lymphoid cells (ILC2s), contributing to the host antiparasitic defense. Additionally, we observed a distinctive intermediate M1/M2 phenotype in CD86 positive, CD206 positive, CD163 positive, MHCII high microglia, along with enhanced infiltration of inflammatory monocytes, both contributing to controlled inflammation and parasite restriction. This study demonstrates, for the first time, that latent T. gondii brain infection confers protection against severe cerebral malaria by positioning astrocytes as central regulators of neuroinflammatory balance. These findings broaden our understanding of host pathogen interactions and underscore astrocytic pathways as potential therapeutic targets for preventing CM.

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