T Cell Immunology in Autoimmune Encephalomyelitis

Autoimmune encephalomyelitis, modelled experimentally as EAE, provides profound insights into how autoreactive T cells breach tolerance and drive central nervous system inflammation. In this paradigm, naïve CD4+ T cells recognise myelin‐derived autoantigens presented by antigen‐presenting cells in lymphoid organs, differentiate into pro‐inflammatory subsets such as Th1 and Th17 cells, and traffic to the CNS. There, they orchestrate demyelination and neuroaxonal injury through cytokine secretion and recruitment of additional immune effectors. Regulatory T cells (Tregs) act as critical brakes on this process by suppressing autoreactive clones and maintaining tissue homeostasis. Advances in single‐cell transcriptomics and high‐dimensional flow cytometry have revealed the heterogeneity of CNS‐infiltrating T cells, the plasticity between pathogenic and regulatory phenotypes, and the role of co‐stimulatory and co‐inhibitory signals in fine‐tuning disease course. Understanding these dynamics not only elucidates fundamental mechanisms of CNS autoimmunity but also informs strategies for antigen‐specific tolerance induction and selective modulation of T cell effector functions.

Research from Nature Portfolio

One seminal study developed a recombinant human myelin basic protein (rhMBP) nanoparticle formulation as an antigen‐specific vaccine in murine EAE. Subcutaneous administration of rhMBP‐loaded polycaprolactone nanoparticles prior to disease induction significantly reduced clinical scores, preserved myelin architecture and shifted the cytokine milieu towards anti‐inflammatory profiles characterised by increased interleukin-10 and reduced interferon-γ. This work establishes a proof of concept for nano‐engineered delivery of disease‐relevant autoantigens to induce tolerogenic responses in CNS autoimmunity.

T Cell Immunology in Autoimmune Encephalomyelitis publication trend

The graph below shows the total number of articles in t cell immunology in autoimmune encephalomyelitis across all publications each year (not limited to Nature Index journals).

Technical terms

Experimental Autoimmune Encephalomyelitis (EAE): An animal model of CNS autoimmunity induced by immunisation with myelin antigens to study mechanisms of demyelination and neuroinflammation.

Regulatory T cells (Tregs): A subset of CD4+ T cells that suppress autoreactive lymphocytes and maintain immune tolerance through cytokine production and cell–cell interactions.

Th17 cells: A pro‐inflammatory CD4+ T cell lineage characterised by interleukin-17 secretion, implicated in driving tissue inflammation in autoimmune disorders.

Autoantigen: A self‐derived protein or peptide recognised by autoreactive T cells or B cells that contributes to the breakdown of immune tolerance.

Myelin Oligodendrocyte Glycoprotein (MOG): A myelin surface protein used experimentally to induce EAE and as a target in antigen‐specific immunotherapies.

References

1. Transcriptomic profiling after B-cell depletion reveals central and peripheral immune cell changes in multiple sclerosis. Journal of Clinical Investigation (2025).
2. An engineered Fc fusion protein that targets antigen-specific T cells and autoantibodies mitigates autoimmune disease. Journal of Neuroinflammation (2023).
3. Mimicking the brain: Epstein-Barr virus and foreign agents as drivers of neuroimmune attack in multiple sclerosis. Frontiers in Immunology (2023).
4. Development and Pre-Clinical Evaluation of Recombinant Human Myelin Basic Protein Nano Therapeutic Vaccine in Experimental Autoimmune Encephalomyelitis Mice Animal Model. Scientific Reports (2017).