(Neuroimmunomodulation[TA])
1,294 results
  • Extracellular Matrix-Mediated Neuroendocrine Control of the Thymus. [Review]
    Neuroimmunomodulation. 2026; 33(1):304-314.Brito-Moreira J, Herculano EA, Savino WN
  • CONCLUSIONS: A key, yet underexplored, component of the thymic microenvironment is the extracellular matrix (ECM). It is very clear today that ECM is not a passive scaffold but a dynamic structure that presents critical signals for thymocyte migration, proliferation, and selection. This review synthesizes current evidence to propose a novel paradigm: the thymic ECM acts as a key mediator of neuroendocrine control. We explore how specific ECM molecules, such as laminins, collagens, and fibronectin, expressed by TECs and other microenvironmental cells, can be modulated by neuroendocrine ligands.Theses ECM modulations directly impact the presentation of key receptors, such as integrins, thereby influencing the critical crosstalk between a given thymic niche and developing lymphocytes. By delineating the ECM-mediated mechanisms, this review aimed to provide a more holistic understanding of how neuroendocrine factors govern thymic physiology, with implications for aging, stress-related immunosenescence, and therapeutic strategies aimed at thymic regeneration.
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  • The Participation of Prolactin in the Immunopathology of Experimental Pulmonary Tuberculosis. [Journal Article]
    Neuroimmunomodulation. 2026; 33(1):288-299.Mata-Espinosa DA, Quintero-Bustos G, … Hernández-Pando RN
  • CONCLUSIONS: Prolactin and its receptors appear to contribute to immune activation during pulmonary tuberculosis, particularly in the early stages of infection. Prolactin administration during late active disease reactivates immune protection. Although we do not demonstrate the mechanisms underlying these observations, these results could serve as a basis for expanding future experimental research.
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  • A Comprehensive Review of Worldwide Case Series of Neurocysticercosis and Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis. [Review]
    Neuroimmunomodulation. 2026; 33(1):225-235.Martínez-Juárez IE, Philibert-Rosas S, … Sotelo JN
  • CONCLUSIONS: A literature search was conducted in PubMed, Scopus, and ScienceDirect focusing on publications describing epilepsy due to NCC with HS. Twenty-three original articles, identified through 2023, were retrieved from Brazil, Ecuador, India, Mexico, and Korea. The proposed relationships between NCC and HS include incidental coexistence, NCC as an initial precipitating injury, and the presence of a third variable. While multiple hypotheses have been discussed and reported cases compiled, the precise nature of this association remains unresolved.Although the mechanisms underlying the relationship between NCC and HS are not fully elucidated, evidence supports their coexistence in patients with epilepsy. Recognition of this association is important for clinical evaluation and may guide future research on pathogenesis and management.
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  • NLRP3 Inflammasome Activation in Oxidative Stress: A Key Mechanism Driving Neuroinflammation. [Review]
    Neuroimmunomodulation. 2026; 33(1):236-263.Ramirez-Celis C, Martínez-Torres AM, Morán J
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  • CONCLUSIONS: In this review, we describe the key features of the NLRP3 inflammasome and explore the role of oxidative stress in its activation. Additionally, we discuss the evidence supporting the regulation of inflammasome activity by antioxidant molecules.Understanding the role of oxidative stress in NLRP3-mediated inflammation offers promising advantages for therapeutic strategies to reduce neuronal death.
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  • Glucocorticoids and Neutrophil Biology: Impact on the Development of Resistance to Glucocorticoid Therapy. [Review]
    Neuroimmunomodulation. 2026; 33(1):213-224.Pacheco FS, da Rocha Mota RG, … Carvalho VFN
  • CONCLUSIONS: Glucocorticoids (GCs), stress hormones, and potent anti-inflammatory agents exert complex effects on neutrophils. While they generally suppress immune responses, GCs can paradoxically enhance neutrophil survival and function under certain conditions. This duality is evident in their ability to delay neutrophil apoptosis and to induce a shift of neutrophils from the marginated to the circulating pool, increasing the neutrophil presence in the bloodstream. Th17 cells, a subset of T-helper cells, recruit neutrophils to sites of infection and inflammation. In addition, neutrophils promote Th17 cell differentiation. GCs can enhance Th17 differentiation and IL-17 production, exacerbating neutrophil accumulation. Nevertheless, in glucocorticoid-resistant diseases, including multiple sclerosis (MS), traumatic brain injury (TBI), and encephalomyelitis, Th17 cells and neutrophils contribute to persistent inflammation. This resistance complicates the treatment of autoimmune diseases and chronic inflammatory disorders, also in the central nervous system, where standard glucocorticoid therapy fails to mitigate symptoms effectively.In this context, we propose a mechanism for the development of resistance to GC driving by uncontrolled TH17 response and neutrophils induced by chronic stress. Understanding the interactions between neutrophils, Th17 cells, and GCs is essential for developing targeted therapies for diseases resistant to GC, such as MS, TBI, and encephalomyelitis.
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  • Interactions between Innate Immune Memory and the Central Nervous System. [Review]
    Neuroimmunomodulation. 2026; 33(1):180-199.Valerio RR, Bernardi A, … Frozza RLN
  • CONCLUSIONS: This review outlines both classical and newly described features of innate immune cells, highlighting the concepts of trained immunity and innate tolerance, along with their underlying molecular mechanisms. We also discuss the implications of innate immune memory in microglia and explore the potential therapeutic approaches for manipulating innate immunity in the context of neurodegenerative disorders.While trained immunity plays a crucial role in protecting the host against infections, its dysregulation can lead to chronic inflammation, autoimmune diseases, and potentially contribute to the development of neurodegenerative disorders. On the other hand, tolerance can reduce the inflammatory response and promote tissue regeneration but can also result in increased susceptibility to secondary infections. The long lifespan of microglia, coupled with their ability to learn and adapt their response to previously encountered pathogens or stimuli, underscores the potential long-term implications of their innate immune memory for the development of neuropathology.
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  • Autonomic-Immunoinflammatory-Cardiac Interplay during Lipopolysaccharide-Induced Systemic Inflammation. [Journal Article]
    Neuroimmunomodulation. 2026; 33(1):160-172.Akanksha K, Reyes-Lagos JJ, … Sinha RKN
  • CONCLUSIONS: LPS-induced endotoxemia in rats leads to pronounced autonomic and inflammatory dysregulation, accompanied by distinct ECG abnormalities and reduced VNIM. The integration of HRV, cytokine, and ECG profiling provides valuable insight into the autonomic-inflammatory-cardiac interplay during systemic inflammation, supporting their utility in early diagnosis and monitoring of sepsis and related conditions.
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  • Neuroinflammatory Aspects of Early Life Malnutrition and the Impacts on the Refinement of Neural Circuitry and Plasticity. [Review]
    Neuroimmunomodulation. 2026; 33(1):173-179.Serfaty CA, Coelho de Velasco P, … da Silva Chagas LN
  • CONCLUSIONS: However, chronic or excessive immune activation contributes to glial dysfunction and major disruption of synaptic pruning and adjustment of developing neural circuitry. Thus, inflammatory insults such as maternal infection, metabolic stress, or malnutrition such as lack essential nutrients (omega-3 fatty acids or tryptophan) or an excess of saturated fat and/or ultra-processed foods, alter inflammatory markers leading to abnormal microglial/astrocytic activation.Together, those findings underscore the dual nature of neuroinflammation as both a regulator of normal development and a driver of abnormal development when dysregulated. Understanding how neural, immune and metabolic cues converge to influence glial and neuronal function is essential for developing strategies to prevent or mitigate the long-term consequences of early life malnutrition on successful brain development during critical periods of postnatal life.
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  • Neurocysticercosis Is the Result of the Interplay between Parasites, Hormones, and Inflammation. [Review]
    Neuroimmunomodulation. 2026; 33(1):200-212.Romano MC, Aguirre-Pineda JA, … Valdez RAN
  • CONCLUSIONS: Here we review how the nervous, the immune, and the endocrine systems interact with T. solium and crassiceps cysticerci and influence the course and individualities of the disease that the parasites trigger in humans and animals. For example, a clear sexual dimorphism in cysticercosis has been found in experimental models of the disease, but the influence of gender in human patients needs further investigation. The synthesis of steroids by the brain cells and the cysticerci might influence the local immune response elicited by the presence of the parasites. Remarkably, cultured cysticerci can synthesize sex steroids and deoxycorticosterone, suggesting that these parasites can influence the local brain microenvironment, especially by producing dehydroepiandrosterone, estrogens, and androgens, which could modify the immune response. Treatment of neurocysticercosis includes cysticidal drugs and corticosteroids intended to control the inflammation caused by the parasite; however, these steroids represent a double-edged tool due to their side effects during prolonged administration and also because of some beneficial effects for the parasite itself.Parasite survival in the host depends on the inflammatory response and the local microenvironment, including steroid hormones that can promote their survival and even their development and proliferation. New strategies should be designed to manage the severe symptoms induced by the chronic presence or the death of parasites and the poor response to treatment that occurs in extraparenchymal neurocysticercosis.
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