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Cytotoxic T lymphocyte antigen-4 (CTLA-4) limits the expansion of encephalitogenic T cells in experimental autoimmune encephalomyelitis (EAE)-resistant BALB/c mice

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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

inferredcites →https://doi.org/10.1007/978-3-642-50059-6_35openalex-snapshot

Genetic Analysis of BALB/cJ Subline Resistance to Actively Induced Experimental Allergic Orchitis (EAO) and Experimental Allergic Encephalomyelitis (EAE)

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Acute experimental allergic encephalomyelitis in radiation bone marrow chimeras between high and low susceptible strains of mice

inferredcites →https://doi.org/10.1016/0008-8749(87)90124-9openalex-snapshot

Differential susceptibility to actively induced experimental allergic encephalomyelitis and experimental allergic orchitis among BALB/c substrains

inferredcites →https://doi.org/10.1016/0165-5728(93)90168-xopenalex-snapshot

T cell responses to myelin basic protein in experimental autoimmune encephalomyelitis-resistant BALB/c mice

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CTLA-4 gene polymorphism may modulate disease in Japanese multiple sclerosis patients

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Specific blockade of CTLA-4/B7 interactions results in exacerbated clinical and histologic disease in an actively-induced model of experimental allergic encephalomyelitis

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The CTLA-4 gene is associated with multiple sclerosis

inferredcites →https://doi.org/10.1016/s0165-5728(99)00189-7openalex-snapshot

Cytokine, chemokine and chemokine receptor mRNA expression in different strains of normal mice: implications for establishment of a Th1/Th2 bias

inferredcites →https://doi.org/10.1016/s1074-7613(01)00259-xopenalex-snapshot

Cytotoxic T Lymphocyte Antigen-4 Accumulation in the Immunological Synapse Is Regulated by TCR Signal Strength

inferredcites →https://doi.org/10.1034/j.1399-0039.1999.530112.xopenalex-snapshot

CTLA4 promoter and exon 1 dimorphisms in multiple sclerosiso

inferredcites →https://doi.org/10.1073/pnas.220423597openalex-snapshot

Cytotoxic T lymphocyte antigen-4 (CTLA-4) regulates the size, reactivity, and function of a primed pool of CD4 + T cells

inferredcites →https://doi.org/10.1073/pnas.94.2.599openalex-snapshot

Increased interleukin 12 production in progressive multiple sclerosis: Induction by activated CD4 + T cells via CD40 ligand

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Defective CTLA-4 cycling pathway in Chediak–Higashi syndrome: A possible mechanism for deregulation of T lymphocyte activation

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IL-12 unmasks latent autoimmune disease in resistant mice.

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CTLA-4: a negative regulator of autoimmune disease.

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Regulation of Interleukin (IL)-12 Receptor β2 Subunit Expression by Endogenous IL-12: A Critical Step in the Differentiation of Pathogenic Autoreactive T Cells

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Combination Immunotherapy of B16 Melanoma Using Anti–Cytotoxic T Lymphocyte–Associated Antigen 4 (Ctla-4) and Granulocyte/Macrophage Colony-Stimulating Factor (Gm-Csf)-Producing Vaccines Induces Rejection of Subcutaneous and Metastatic Tumors Accompanied by Autoimmune Depigmentation

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Elucidating the Autoimmune and Antitumor Effector Mechanisms of a Treatment Based on Cytotoxic T Lymphocyte Antigen-4 Blockade in Combination with a B16 Melanoma Vaccine

inferredcites →https://doi.org/10.1111/j.1744-313x.1976.tb00583.xopenalex-snapshot

EXPERIMENTAL AUTOIMMUNE ENCEPHALO‐MYELITIS IN MICE: GENETIC CONTROL OF SUSCEPTIBILITY*

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CTLA-4-Mediated Inhibition in Regulation of T Cell Responses: Mechanisms and Manipulation in Tumor Immunotherapy

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CTLA-4 gene polymorphism associated with Graves' disease in a Caucasian population

inferredcites →https://doi.org/10.4049/jimmunol.139.6.1834openalex-snapshot

Comparison of antigen specificity, class II major histocompatibility complex restriction, and in vivo behavior of myelin basic protein-specific T cell lines and clones derived from (BALB/c x SJL/J) mice.

inferredcites →https://doi.org/10.4049/jimmunol.140.6.1868openalex-snapshot

Myelin proteolipid protein-induced experimental allergic encephalomyelitis. Variations of disease expression in different strains of mice.

inferredcites →https://doi.org/10.4049/jimmunol.154.1.388openalex-snapshot

Experimental autoimmune encephalomyelitis-resistant mice have highly encephalitogenic myelin basic protein (MBP)-specific T cell clones that recognize a MBP peptide with high affinity for MHC class II.

inferredcites →https://doi.org/10.4049/jimmunol.156.1.371openalex-snapshot

Immunogenic and encephalitogenic epitope clusters of myelin proteolipid protein

inferredcites →https://doi.org/10.4049/jimmunol.157.4.1333openalex-snapshot

CTLA-4 blockade enhances clinical disease and cytokine production during experimental allergic encephalomyelitis

inferredcites →https://doi.org/10.4049/jimmunol.157.5.2186openalex-snapshot

Genetic analysis of susceptibility to experimental autoimmune encephalomyelitis in a cross between SJL/J and B10.S mice

inferredcites →https://doi.org/10.4049/jimmunol.161.4.1860openalex-snapshot

New Genetic Loci That Control Susceptibility and Symptoms of Experimental Allergic Encephalomyelitis in Inbred Mice

inferredcites →https://doi.org/10.4049/jimmunol.162.7.4328openalex-snapshot

Autoantibodies to T Cell Costimulatory Molecules in Systemic Autoimmune Diseases

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Incoming claims: where this work appears in other papers’ reference lists and arguments.

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Experimental autoimmune encephalomyelitis can be prevented and cured by infection with Trypanosoma cruzi

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PD-1/PD-L1, but not PD-1/PD-L2, interactions regulate the severity of experimental autoimmune encephalomyelitis

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