Journal of Clinical Immunology Research

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Mini Review - Journal of Clinical Immunology Research (2023) Volume 6, Issue 3

Neuroimmune Interactions in Neurodevelopmental Disorders: Implications for Neuroimmunology

Smith Olive*

Department of Pediatric Oncology, Utrecht University, Middelburg, The Netherlands

Corresponding Author:
Smith Olive
Department of Pediatric Oncology
Utrecht University, Middelburg
The Netherlands

Received: 02-Jul-2023, Manuscript No. AACIR-23-104166; Editor assigned: 04-Jul-2023, Pre QC No. AACIR-23-104166(PQ); Reviewed: 18-Jul-2023, QC No. AACIR-23-104166; Revised: 21-Jul-2023, Manuscript No. AACIR-23-104166 (R); Published: 25-Jul-2023, DOI: 10.35841/aacir-6.3.152

Citation: Olive S. Neuroimmune interactions in neurodevelopmental disorders: Implications for neuroimmunology. J Clin Immunol. 2023;6(3):152

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Neurodevelopmental disorders encompass a group of conditions characterized by atypical brain development and functioning that impact early childhood development and persist into adulthood. Recent research has highlighted the critical role of neuroimmune interactions in the pathogenesis of these disorders. Neuroimmune interactions involve the complex interplay between the immune system and the developing nervous system. This essay aims to explore the role of neuroimmune interactions in neurodevelopmental disorders, focusing on Autism Spectrum Disorder (ASD) and attention deficit Hyperactivity Disorder (ADHD). Understanding the intricate relationship between the immune system and brain development in these disorders can provide insights into their etiology, potentially leading to the development of novel therapeutic strategies [1].

ASD is a neurodevelopmental disorder characterized by persistent deficits in social communication and interaction, as well as the presence of restricted and repetitive patterns of behavior. Increasing evidence suggests that immune dysregulation and altered neuroimmune interactions contribute to the pathogenesis of ASD [2].

Maternal immune activation (MIA): Maternal immune activation during pregnancy, resulting from maternal infection or inflammation, has been associated with an increased risk of ASD in offspring. Immune activation in the maternal system can lead to the release of pro-inflammatory cytokines, chemokines, and antibodies that can cross the placenta and affect fetal brain development. Animal studies have demonstrated that MIA can induce neurodevelopmental abnormalities and behavioral changes resembling ASD in offspring [3].

Altered cytokine profiles: Individuals with ASD often exhibit alterations in immune cell function and cytokine profiles. Studies have reported elevated levels of pro-inflammatory cytokines, such as interleukin-6 (IL-6), tumor necrosis factoralpha (TNF-alpha), and interferon-gamma (IFN-gamma), in the blood and brain of individuals with ASD. These cytokines can disrupt normal neural development, synaptic connectivity, and neuronal communication, potentially contributing to the core symptoms of ASD [4].

Microglial activation: Microglia, the resident immune cells of the Central Nervous System (CNS), play a crucial role in brain development and immune surveillance. Dysregulated microglial function has been implicated in ASD. Postmortem studies have revealed increased microglial activation and altered gene expression patterns in the brains of individuals with ASD. Activated microglia release pro-inflammatory mediators, neurotoxic molecules, and reactive oxygen species, which can impact synaptic pruning, neuronal connectivity, and neurodevelopmental processes.

Autoantibodies and neuroinflammation: Autoantibodies targeting brain proteins have been detected in a subset of individuals with ASD. These autoantibodies can contribute to neuroinflammation and disrupt neuronal function. Autoimmune-related processes, such as neuroinflammation and the presence of brain-reactive antibodies, have been associated with altered brain development and behavioral abnormalities in ASD.

Neuroimmune Interactions in Attention Deficit Hyperactivity Disorder (ADHD): ADHD is a neurodevelopmental disorder characterized by persistent patterns of inattention, hyperactivity, and impulsivity that impair daily functioning. Neuroimmune interactions have been implicated in the pathogenesis of ADHD, highlighting the role of immune dysregulation in the disorder.

Inflammatory markers: Studies have identified alterations in inflammatory markers in individuals with ADHD. Increased levels of pro-inflammatory cytokines, such as IL-6, TNF-alpha, and C-Reactive Protein (CRP), have been reported in the blood of individuals with ADHD. These inflammatory markers can influence neural functioning, disrupt neurotransmitter systems, and impair cognitive processes associated with ADHD [5].

Dysregulated immune response genes: Genetic studies have identified immune-related genes associated Prognostic estimates can be extremely accurate when used on large statistical populations; for instance, it is possible to say with some confidence that "45% of patients with severe septic shock will die within 28 days" because prior studies have shown that this percentage of patients did indeed pass away. Because patient-specific factors can significantly alter the expected course of the disease, this statistical information does not apply to the prognosis for each individual patient. Additional information is required to determine whether a patient belongs to the 45% who will die or the 55% who will survive.


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