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SARS-CoV-2 Spike Does Not Possess Intrinsic Superantigen-like Inflammatory Activity.
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- Cells (2073-4409), 2022, v. 11, n. 16, p. 2526, doi. 10.3390/cells11162526
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- Article
T Helper Cells: The Modulators of Inflammation in Multiple Sclerosis.
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- Cells (2073-4409), 2020, v. 9, n. 2, p. 482, doi. 10.3390/cells9020482
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- Article
CD28 Autonomous Signaling Up-Regulates C-Myc Expression and Promotes Glycolysis Enabling Inflammatory T Cell Responses in Multiple Sclerosis.
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- Cells (2073-4409), 2019, v. 8, n. 6, p. 575, doi. 10.3390/cells8060575
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- Article
Astrocytes and Inflammatory T Helper Cells: A Dangerous Liaison in Multiple Sclerosis.
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- Frontiers in Immunology, 2022, v. 13, p. 1, doi. 10.3389/fimmu.2022.824411
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- Article
Targeting staphylococcal enterotoxin B binding to CD28 as a new strategy for dampening superantigen-mediated intestinal epithelial barrier dysfunctions.
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- Frontiers in Immunology, 2024, p. 1, doi. 10.3389/fimmu.2024.1365074
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- Article
Bivalent binding of staphylococcal superantigens to the TCR and CD28 triggers inflammatory signals independently of antigen presenting cells.
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- Frontiers in Immunology, 2023, p. 1, doi. 10.3389/fimmu.2023.1170821
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- Article
Bivalent binding of staphylococcal superantigens to the TCR and CD28 triggers inflammatory signals independently of antigen presenting cells.
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- Frontiers in Immunology, 2023, p. 1, doi. 10.3389/fimmu.2023.1170821
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- Article
Binding of Staphylococcal Enterotoxin B (SEB) to B7 Receptors Triggers TCR- and CD28-Mediated Inflammatory Signals in the Absence of MHC Class II Molecules.
- Published in:
- Frontiers in Immunology, 2021, v. 12, p. 1, doi. 10.3389/fimmu.2021.723689
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- Article