ArticleNoro psikiyatri arsivi2022
A Rare Central Nervous System Involvement Due to CTLA-4 Gene Defect.
Article in Noro psikiyatri arsivi, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Clinical, Genetic, and Immunological Spectrum of CHAI and LATAIE Patients from a Tertiary Referral Centre in India.International journal of molecular sciences · 2025Article
- Neuroinflammation in CTLA-4 Haploinsufficiency: Case Report of a New Variant with Remarkable Response to Targeted Therapy.International journal of molecular sciences · 2025Article
- A novelFrontiers in immunology · 2025Article
- Management of Autoimmune Encephalitis in a 7-Year-Old Child With CTLA-4 Haploinsufficiency and AMPA Receptor Antibodies: A Case Report.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
Corrections and comments
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Authors and funding
12 authors.
Funding
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Abstract
Cytotoxic T-lymphocyte antigen-4 (CTLA-4) haploinsufficiency is the defect of one of the checkpoint inhibitory molecules and defined as a primary immunodeficiency characterized by immune dysregulation. A 26-year-old female with a history of autoimmune hemolytic anemia, autoimmune thrombocytopenia, and hypogammaglobulinemia was admitted with an inability to walk, urinary hesitancy, and bowel incontinence. Neurological examination revealed mild weakness, pyramidal, and deep sensorial involvement of the left lower extremity. Brain MRI revealed periventricular, juxtacortical, and cerebellar inflammatory lesions. Thoracic spinal MRI showed a longitudinaly extensive cord lesion. Additionally, thoracal CT showed parenchymal opacities and bilateral hilar lymph nodes. The biopsy from mediastinal lymph nodes and lung parenchyma demonstrated a low-grade lymphoproliferation and grade 1 "Lymphomatoid granulomatosis". Detailed laboratory analyses indicated the diagnosis of ''common variable immunodeficiency''. Next-generation sequencing with primary immunodeficiency panel revealed a heterozygous mutation in CTLA-4 (c.436G>A(p.G146R)(p.Gly146Arg)). After molecular diagnosis, abatacept therapy was started as a targeted therapeutic approach with subcutaneous immunoglobulin therapy.
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