T-cell immune attack of cancer cells underlies the efficacy of immune checkpoint inhibitors in many cancer subtypes, but is not yet well established in the primary brain cancer glioblastoma. Immune checkpoint inhibitor treatments that disinhibit the immune system to enhance immune clearance of cancer have in rare cases resulted in T-cell attack of peripheral ganglia causing lymphocytic ganglionitis. In glioblastoma, lymphocytic ganglionitis has not been reported and checkpoint inhibitors are not routinely used. Here we report a case of glioblastoma not treated with checkpoint inhibitors in which the primary tumor and peripheral ganglia of the celiac and sympathetic chains, as well as myenteric plexus, are infiltrated by CD8 cytotoxic T-cells. In addition to the marked lymphocytic infiltrates, this case is also notable for an unusually long survival (8 years) after diagnosis with glioblastoma, but an ultimately fatal outcome due to ileus. The findings suggest T-cell immune attack of glioblastoma may prolong survival, but also suggest T-cell autoimmune diseases such as lymphocytic ganglionitis could become a risk with the future use of immune-targeted therapies for glioblastoma.
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http://dx.doi.org/10.1016/j.jneuroim.2019.577075 | DOI Listing |
Eur J Neurosci
January 2025
Department of Neurology, the Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
To summarise the clinical characteristics, radiological features, treatments and prognosis of patients with myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) overlapped with NMDA receptor (NMDAR) encephalitis. We retrospectively analysed patients who exhibited dual positivity for MOG antibodies and NMDAR antibodies in serum/CSF from Jan 2018 to Jun 2023. Ten patients with MOGAD and NMDAR encephalitis were enrolled.
View Article and Find Full Text PDFNeurorehabil Neural Repair
January 2025
Medical School of Nantong University, Nantong, Jiangsu, P.R. China.
Background: The peripheral nervous system (PNS) exhibits remarkable regenerative capability after injury. PNS regeneration relies on neurons themselves as well as a variety of other cell types, including Schwann cells, immune cells, and non-neuronal cells.
Objectives: This paper focuses on summarizing the critical roles of immune cells (SCs) in the injury and repair processes of the PNS.
Mol Genet Metab Rep
December 2024
Eye Center, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Background: Variants in have been reported to be associated with Leigh syndrome. However, further expansion of the -phenotype and variants spectrum of -related Leigh syndrome are still required.
Methods: Two patients diagnosed with Leigh syndrome were recruited, and whole-exome sequencing was performed to identify the genetic variants responsible for the abnormal gait, dystonia, and bilateral basal ganglia lesions, followed by validation using Sanger sequencing.
Mult Scler J Exp Transl Clin
December 2024
Department of Neurology, Tokyo Women's Medical University, Tokyo, Japan.
Background: Few studies have examined B cells among patients with anti-myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD), including brain pathology.
Objective: To describe cases of tumefactive MOGAD with B-cell dominant central nervous system (CNS) infiltration.
Methods: In this study, we reviewed three cases with clinical and brain histopathological features with tumefactive MOGAD.
Proc Natl Acad Sci U S A
November 2024
Innate Immunity Laboratory, Institute of Experimental Medicine (National Scientific and Technical Research Council/National Academy of Medicine of Buenos Aires), Buenos Aires 1425, Argentina.
Dry eye disease (DED) is characterized by a dysfunctional tear film in which the corneal epithelium and its abundant nerves are affected by ocular desiccation and inflammation. Although adaptive immunity and specifically CD4 T cells play a role in DED pathogenesis, the exact contribution of these cells to corneal epithelial and neural damage remains undetermined. To address this, we explored the progression of a surgical DED model in wild-type (WT) and T cell-deficient mice.
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