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CD8+ T cells differentiate into effector CTLs during chronic infections like HIV or HCV.
False
Exhausted CTLs exhibit enhanced cytokine production and reduced expression of inhibitory receptors like PD-1.
False
T cell exhaustion is a phenomenon observed only during acute infections.
False
T cell exhaustion can contribute to the persistence of chronic infections but not cancer.
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CTLs kill target cells mainly through fas/FasL-mediated cell killing.
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Effector CTLs recognize and engage with infected target cells displaying the specific antigen on their surface through binding of CD4 molecules.
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CTLs release cytokines, such as interferons, which directly induce apoptosis in the target cell.
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Perforin forms pores in the target cell membrane, allowing the entry of granzymes into the nucleus.
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CTLs play a minimal role in immune surveillance against cancer due to the specificity of tumor antigens.
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T helper cells can inhibit the differentiation of CTLs into effector cells.
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Effector CTLs recognize and eliminate only infected cells, not abnormal cells.
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Perforin forms pores in the target cell membrane, allowing the release of granzymes into the cytosol.
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Effector CTLs produce cytokines that inhibit inflammation and suppress immune responses.
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Naïve CD8+ T cells are most effectively activated by antigens presented by B cells.
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Class I MHC molecules present extracellular antigens to CD8+ T cells.
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Perforin is a pore-forming protein that causes target cell death by inducing apoptosis.
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CTLs primarily kill target cells by releasing granzymes, which are serine proteases.
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Cytotoxic granules in CTLs store molecules that are essential for inducing programmed cell death in target cells.
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CTLs form an immune synapse with helper T cells to promote the differentiation of CTLs.
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Fas/FasL-mediated cell killing is the primary mechanism through which CTLs induce apoptosis in target cells.
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FasL is expressed on the surface of target cells that are being killed by CTLs.
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Fas is a ligand for FasL in the process of CTL-mediated cell killing.
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The interaction between FasL on CTLs and Fas on the target cell surface triggers apoptosis in the target cell.
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The Fas/FasL-mediated cell killing pathway involves the interaction between Fas and FasL expressed on the same cell type.
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CTLs can induce apoptosis in target cells through perforin/granzyme-mediated cell killing.
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Perforin-mediated membrane disruption allows the entry of Bcl-2 into the cytoplasm of the target cell.
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Granzyme-mediated cleavage of substrates leads to the inactivation of caspases.
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Apoptosis is characterized by DNA duplication, nuclear expansion, and membrane expansion.
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The process of CTL-mediated killing is slow, often taking days for the death of the target cell after CTL-target cell interaction.
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CTLs kill target cells mainly through fas/FasL-mediated cell killing.
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Effector CTLs acquire cytotoxic capabilities and migrate to the site of infection or inflammation.
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Effector CTLs can release cytokines like interleukin-2 (IL-2) to induce apoptosis in target cells.
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Naïve CD8+ T cells undergo clonal expansion upon activation, leading to the generation of a large pool of effector and memory T cells.
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Chemokines guide the migration of effector CTLs and other leukocytes to the site of antigenic challenge in tissues or organs.
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CTLs play a significant role in immune surveillance against cancer due to their ability to recognize and engage with tumor antigens on target cells.
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T helper cells inhibit the differentiation of CTLs into effector cells during chronic infections like HIV or HCV.
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Antigen cross-presentation occurs when DCs present endogenous antigens on MHC-I molecules to activate CD8+ T cells.
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T cell exhaustion is only observed during chronic infections, not cancer.
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Perforin forms pores in the target cell membrane that allow the entry of cytokines like interferons into the nucleus.
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Effector CTLs primarily kill target cells through fas/FasL-mediated cell killing rather than perforin/granzyme-mediated killing.
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