{"id":23052,"date":"2026-09-07T11:21:01","date_gmt":"2026-09-07T09:21:01","guid":{"rendered":"https:\/\/www.biolife-publisher.it\/ejnd\/?p=23052"},"modified":"2026-09-10T10:42:36","modified_gmt":"2026-09-10T08:42:36","slug":"using-car-t-therapy-in-cns-autoimmune-diseases-can-cause-cytokine-storms-and-possible-death","status":"publish","type":"post","link":"https:\/\/www.biolife-publisher.it\/ejnd\/2026\/09\/07\/using-car-t-therapy-in-cns-autoimmune-diseases-can-cause-cytokine-storms-and-possible-death\/","title":{"rendered":"USING CAR-T THERAPY IN CNS AUTOIMMUNE DISEASES CAN CAUSE CYTOKINE STORMS AND POSSIBLE DEATH"},"content":{"rendered":"

Letter to the Editor<\/em><\/p>\n

 <\/p>\n

TO THE EDITOR:<\/strong><\/p>\n

Chimeric Antigen Receptor T cell (CAR-T) therapy is a system in which T lymphocyte activation against target cells can trigger severe inflammation, including a cytokine storm (1). CAR-T cells recognize target cell antigen through the CAR’s scFv domain. The CAR receptor has an antigen-recognition transmembrane domain and the intracellular signaling domains CD3\u03b6 + CD28, or CD137 (4-1BB), which is a protein belonging to the tumor necrosis factor (TNF) receptor family (2). When the CAR recognizes the target antigen, a cascade is activated, starting from the CAR, inducing CD3\u03b6, Lck\/ZAP70, LAT\/SLP-76, Ca\u00b2\u207a\/calcineurin, and NFAT (3). The CD28, PI3K, and mTOR pathways, as well as NF-\u03baB, are also activated. These reactions lead to the release of inflammatory mediators that can cause a cytokine storm, that can also lead to death. The most responsible cytokines for activating the inflammatory network are interleukin (IL)-1, TNF, interferon-gamma (IFN-\u03b3), IL-2 (which induces IL-1), IL-6, and granulocyte-macrophage colony-stimulating factor (GM-CSF) (4).<\/p>\n

Chemokines are a functional subclass of cytokines that also participate in inflammation. They create signals that cause immune cells to migrate towards the inflammatory site, further fuelling the local and systemic inflammatory response (5).<\/p>\n

CAR-T cells are emerging as an experimental approach in the treatment of both cancer and autoimmune diseases of the central nervous system, especially when autoimmunity is due to B cell dysfunction. In autoimmune diseases, CAR-T cells are not used to cells as they do with cancer but are used to prevent abnormal B cells from producing autoantibodies. B cells and plasma cells express the CD19 receptor, which CAR-T cells target through B cell recognition (6).\u00a0 CAR-T cells eliminate these autoimmune B cells, promoting replacement with non-autoreactive B cells.<\/p>\n

Blocking inflammatory cytokines with anti-inflammatory cytokines or anti-receptor cytokines such as IL-1RA, monoclonal antibodies, or corticosteroids has become an important experimental therapeutic target (5).\u00a0 Additionally, the use of tocilizumab, an antibody directed against the IL-6 receptor, can reduce the inflammatory cascade.<\/p>\n

The application of CAR-T cells to autoimmune neurological diseases such as autoimmune encephalitis, multiple sclerosis, and myasthenia gravis, amongst others, is a very active field of research and holds great promise for therapy. However, the severe inflammatory effect of CAR-T treatment, which can lead to a cytokine storm, must be resolved before these engineered cells are used for therapies.<\/p>\n

 <\/p>\n

Pio Conti*<\/sup><\/p>\n

Postgraduate Medical School, University \u201cGabriele d\u2019Annunzio\u201d of Chieti\/Pescara, Chieti, Italy.<\/p>\n

*Correspondence to<\/em>:
\nProf. Pio Conti,
\nPostgraduate Medical School,
\nUniversity \u201cGabriele d\u2019Annunzio\u201d of Chieti\/Pescara,
\nChieti, Italy.
\ne-mail: pioconti@yahoo.it<\/p>\n\n\n\n
Received: 05 August, 2026
\nAccepted: 07 September, 2026
\n\"adobe-pdf-download-icon\"<\/a><\/td>\n		ISSN 2279-5855 print \/ 3103-7364 [online]
\nCopyright 2026 \u00a9 by Biolife Publisher
\nThis publication and\/or article is for individual use only and may not be further reproduced without written permission from the copyright holder. Unauthorized reproduction may result in financial and other penalties. Disclosure: All authors report no conflicts of interest relevant to this article.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Conflict of interest <\/em><\/p>\n

The author declares that they have no conflict of interest.<\/p>\n

 <\/p>\n

REFERENCES<\/strong><\/p>\n

    \n
  1. Hughes AD, Teachey DT, Diorio C. Riding the storm: managing cytokine-related toxicities in CAR-T cell therapy. Seminars in Immunopathology<\/em>. 2024;46(3-4). doi:10.1007\/s00281-024-01013-w<\/li>\n
  2. Long AH, Haso WM, Shern JF, et al. 4-1BB costimulation ameliorates T cell exhaustion induced by tonic signaling of chimeric antigen receptors. Nature Medicine<\/em>. 2015;21(6):581-590. doi:10.1038\/nm.3838<\/li>\n
  3. Okada R, Reyes-Gonz\u00e1lez JM, Rodriguez C, et al. GPC2-Targeted CAR T Cells Engineered with NFAT-Inducible Membrane-Tethered IL15\/IL21 Exhibit Enhanced Activity against Neuroblastoma. Cancer Immunology Research<\/em>. 2025;13(9):1363-1373. doi:10.1158\/2326-6066.cir-24-0975<\/li>\n
  4. Zanza C, Romenskaya T, Manetti AC, et al. Cytokine Storm in COVID-19: Immunopathogenesis and Therapy. Medicina<\/em>. 2022;58(2):144. doi:10.3390\/medicina58020144<\/li>\n
  5. Zhang PF, Wang C, Zhang Le, Li Q. Reversing Chemokine\/Chemokine Receptor Mismatch to Enhance the Antitumor Efficacy of CAR-T Cells. Immunotherapy<\/em>. 2022;14(6):459-473. doi:10.2217\/imt-2021-0228<\/li>\n
  6. Norelli M, Camisa B, Barbiera G, et al. Monocyte-derived IL-1 and IL-6 are differentially required for cytokine-release syndrome and neurotoxicity due to CAR T cells. Nature Medicine<\/em>. 2018;24(6):739-748. doi:10.1038\/s41591-018-0036-4<\/li>\n
  7. Schett G, Mackensen A, Mougiakakos D. CAR T-cell therapy in autoimmune diseases. The Lancet<\/em>. 2023;402(10416). doi:10.1016\/s0140-6736(23)01126-1<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"

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