lecture 16 true and false quiz- immunology

CD8+ T cells differentiate into effector CTLs during chronic infections like HIV or HCV.

Exhausted CTLs exhibit enhanced cytokine production and reduced expression of inhibitory receptors like PD-1.

T cell exhaustion is a phenomenon observed only during acute infections.

T cell exhaustion can contribute to the persistence of chronic infections but not cancer.

CTLs kill target cells mainly through fas/FasL-mediated cell killing.

Effector CTLs recognize and engage with infected target cells displaying the specific antigen on their surface through binding of CD4 molecules.

CTLs release cytokines, such as interferons, which directly induce apoptosis in the target cell.

Perforin forms pores in the target cell membrane, allowing the entry of granzymes into the nucleus.

CTLs play a minimal role in immune surveillance against cancer due to the specificity of tumor antigens.

T helper cells can inhibit the differentiation of CTLs into effector cells.

Effector CTLs recognize and eliminate only infected cells, not abnormal cells.

Perforin forms pores in the target cell membrane, allowing the release of granzymes into the cytosol.

Effector CTLs produce cytokines that inhibit inflammation and suppress immune responses.

Naïve CD8+ T cells are most effectively activated by antigens presented by B cells.

Class I MHC molecules present extracellular antigens to CD8+ T cells.

Perforin is a pore-forming protein that causes target cell death by inducing apoptosis.

CTLs primarily kill target cells by releasing granzymes, which are serine proteases.

Cytotoxic granules in CTLs store molecules that are essential for inducing programmed cell death in target cells.

CTLs form an immune synapse with helper T cells to promote the differentiation of CTLs.

Fas/FasL-mediated cell killing is the primary mechanism through which CTLs induce apoptosis in target cells.

FasL is expressed on the surface of target cells that are being killed by CTLs.

Fas is a ligand for FasL in the process of CTL-mediated cell killing.

The interaction between FasL on CTLs and Fas on the target cell surface triggers apoptosis in the target cell.

The Fas/FasL-mediated cell killing pathway involves the interaction between Fas and FasL expressed on the same cell type.

CTLs can induce apoptosis in target cells through perforin/granzyme-mediated cell killing.

Perforin-mediated membrane disruption allows the entry of Bcl-2 into the cytoplasm of the target cell.

Granzyme-mediated cleavage of substrates leads to the inactivation of caspases.

Apoptosis is characterized by DNA duplication, nuclear expansion, and membrane expansion.

The process of CTL-mediated killing is slow, often taking days for the death of the target cell after CTL-target cell interaction.

CTLs kill target cells mainly through fas/FasL-mediated cell killing.

Effector CTLs acquire cytotoxic capabilities and migrate to the site of infection or inflammation.

Effector CTLs can release cytokines like interleukin-2 (IL-2) to induce apoptosis in target cells.

Naïve CD8+ T cells undergo clonal expansion upon activation, leading to the generation of a large pool of effector and memory T cells.

Chemokines guide the migration of effector CTLs and other leukocytes to the site of antigenic challenge in tissues or organs.

CTLs play a significant role in immune surveillance against cancer due to their ability to recognize and engage with tumor antigens on target cells.

T helper cells inhibit the differentiation of CTLs into effector cells during chronic infections like HIV or HCV.

Antigen cross-presentation occurs when DCs present endogenous antigens on MHC-I molecules to activate CD8+ T cells.

T cell exhaustion is only observed during chronic infections, not cancer.

Perforin forms pores in the target cell membrane that allow the entry of cytokines like interferons into the nucleus.

Effector CTLs primarily kill target cells through fas/FasL-mediated cell killing rather than perforin/granzyme-mediated killing.