Immunology Case Reports

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (202) 780-3397

Editorial - Immunology Case Reports (2025) Volume 8, Issue 3

Vaccines and the Brain: Neuroimmune Responses to Immunization and Infection

Asif Ahmed *

Department of Virology, Wuhan Institute of Virology, China

*Corresponding Author:
Asif Ahmed
Department of Virology,
Wuhan Institute of Virology,
China
E-mail: aahmed@wits.ac

Received:02-Jan-2025, Manuscript No. AAICR-25-171206; Editor assigned:03-Jan-2025, PreQC No. AAICR-25-171206(PQ); Reviewed:18-Jan-2025, QC No. AAICR-25-171206; Revised:24-Jan-2025, Manuscript No. AAICR-25-171206(R); Published:31-Jan-2025, DOI:10.35841/aaicr-8.3.206

Citation: Ahmed A. Vaccines and the brain: Neuroimmune responses to immunization and infection. Immunol Case Rep. 2025;8(3):206

Visit for more related articles at Immunology Case Reports

Introduction

Vaccines have revolutionized public health by preventing infectious diseases and reducing mortality worldwide. While their primary role is to stimulate systemic immunity, growing evidence suggests that vaccines also influence neuroimmune responses—interactions between the immune system and the central nervous system (CNS). These responses can be protective, modulating brain inflammation and enhancing resilience to infection, but they may also contribute to transient neurological symptoms or, in rare cases, adverse events. Understanding how vaccines and infections affect the brain’s immune landscape is essential for optimizing vaccine safety, efficacy, and public trust. The CNS was once considered immune-privileged, shielded from peripheral immune activity by the blood-brain barrier (BBB). However, it is now clear that the brain maintains active communication with the immune system. Microglia, the brain’s resident immune cells, respond to peripheral signals, while cytokines and chemokines can cross the BBB or be produced locally in response to systemic immune activation. Vaccination and infection both trigger systemic immune responses that can influence neuroimmune signaling. These effects are typically transient and beneficial, but under certain conditions, they may lead to neuroinflammation or behavioral changes [1].

Infections such as influenza, SARS-CoV-2, and bacterial meningitis can provoke robust neuroimmune responses. Pathogens may directly invade the CNS or induce systemic inflammation that disrupts the BBB and activates microglia. This can result in elevated levels of pro-inflammatory cytokines like IL-6, TNF-α, and IL-1β in the brain, contributing to symptoms such as fatigue, cognitive dysfunction, and mood disturbances. For example, COVID-19 has been associated with neurological complications ranging from anosmia and encephalopathy to long-term cognitive impairment. Advances in neuroimmunology are inspiring novel vaccine strategies. Researchers are exploring vaccines that modulate neuroimmune pathways to treat neurological diseases. For example, therapeutic vaccines targeting amyloid-beta or tau proteins are under investigation for Alzheimer’s disease. These effects are thought to arise from a combination of viral neuroinvasion and cytokine-mediated neuroinflammation. Vaccines mimic infection to train the immune system without causing disease. In doing so, they can transiently activate neuroimmune pathways. Most vaccine-induced neuroimmune responses are mild and self-limiting, such as fever, headache, or fatigue. These symptoms reflect cytokine signaling and immune activation rather than direct CNS involvement [2].

Importantly, vaccines may also confer neuroprotective effects. By preventing infection, they reduce the risk of pathogen-induced neuroinflammation and its long-term consequences. For instance, influenza vaccination has been linked to a lower risk of Alzheimer’s disease and stroke, possibly due to reduced systemic inflammation and vascular damage. Cytokines play a central role in neuroimmune communication. Following vaccination, peripheral cytokines can signal to the brain via neural pathways (e.g., vagus nerve), humoral routes (crossing the BBB), or by activating endothelial cells and perivascular macrophages. This signaling can influence mood, cognition, and behavior. Studies have shown that IL-6 and IFN-γ levels rise temporarily after vaccination, correlating with mild neurobehavioral symptoms such as fatigue or irritability. These effects are typically short-lived and reflect the immune system’s engagement rather than pathology [3].

While vaccines are overwhelmingly safe, rare neurological adverse events have been reported. These include Guillain-Barré syndrome (GBS), transverse myelitis, and seizures, often occurring in the context of autoimmune responses or molecular mimicry. For example, GBS has been associated with influenza and COVID-19 vaccines, though the risk remains extremely low compared to the risk from infection itself. Vaccine safety monitoring systems such as VAERS and VigiBase play a crucial role in detecting and investigating these events. Understanding the immunological mechanisms behind them can inform safer vaccine design and personalized risk assessment. Age, genetics, and pre-existing conditions influence neuroimmune responses to vaccination. Older adults may exhibit blunted immune responses due to immunosenescence, while individuals with autoimmune or neurodegenerative diseases may have altered neuroimmune reactivity [4].

For example, patients with multiple sclerosis (MS) may experience transient symptom exacerbation following vaccination, though vaccines do not increase relapse risk and are recommended to prevent infection-related complications. Similarly, children with neurodevelopmental disorders may show heightened sensitivity to immune activation, warranting careful monitoring. In early life, the immune system and brain undergo rapid development. Vaccination during this period is critical for disease prevention, but concerns have been raised about potential neurodevelopmental effects. Extensive research has found no link between vaccines and autism or other developmental disorders. In fact, preventing infections like measles and rubella—known to cause encephalitis and developmental delays—protects neurodevelopment. Maternal vaccination during pregnancy also supports fetal brain health by reducing the risk of congenital infections [5].

Conclusion

Additionally, vaccines may be used to prevent neurotropic infections such as Zika virus, which causes microcephaly, or Japanese encephalitis. These efforts highlight the intersection of immunology and neuroscience in addressing complex health challenges. Vaccines influence the brain’s immune environment in subtle but important ways. While most neuroimmune responses to immunization are transient and protective, understanding their mechanisms is essential for ensuring safety, especially in vulnerable populations. As science advances, vaccines may not only prevent infectious diseases but also serve as tools to modulate neuroimmune function and treat neurological disorders. The brain and immune system are deeply interconnected—and vaccines are at the frontier of this dynamic relationship.

References

  1. Rabe H, Malmquist M, Barkman C, et al. Distinct patterns of naive, activated and memory T and B cells in blood of patients with ulcerative colitis or Crohn’s disease. Clin Expl Immunol. 2019;197(1):111-29.

    2. Indexed at, Google Scholar, Cross Ref

  2. Gerlach K, Hwang Y, Nikolaev A, et al. Th9 cells that express the trancription factor PU.1 drive T cel-mediated colitis via IL-9 receptor signaling in intestinal epithelial cells. Nat Immunol. 2014;15(7):676-86.

    3. Indexed at, Google Scholar, Cross Ref

  3. Heller F, Fromm A, Gitter A.H, et al. Epithelial apoptosis is a prominent feature of the epithelial barier disturbance in intedtinal inflammation: Effect of pro-inflammatory interlekin-13 on the epithelial cell function. Mucosal Immunol. 2008;1:S58-61.

    4. Indexed at, Google Scholar, Cross Ref

  4. Seidelin J.B, Coskun M, Kvist P.H, et al. IL-33 promotes GATA-3 polarization of gut-derived T cells in experimental and ulcerative colitis. J. Gastroenterol. 2015;50:180-90.

    5. Indexed at, Google Scholar, Cross Ref

  5. Travers J, Rochman M, Miracle C.E, et al. Chromatin regulates IL-33 release and extracellular cytokine activity. Nat Commun. 2018;9(1):3244.

    6. Indexed at, Google Scholar, Cross Ref

Get the App