Empty MHC class I and MHC class II molecules are rapidly removed from the cell surface. This process prevents: The accumulation of empty MHC molecules on the cell surface which would interfere with T cells recognizing pathogen-derived peptide:MHC complexes Pathogens from evading the immune response by inducing peptide release from cell surface MHC molecules MHC class I molecules from being internalized into endosomes and binding endosome-derived peptides HLA-DM from trafficking to the cell surface with MHC class II Inappropriate T cell recognition of healthy cells that are not infected, nor have ingested a pathogen

Empty MHC class I and MHC class II molecules are rapidly removed from the cell surface. This process prevents: The accumulation of empty MHC molecules on the cell surface which would interfere with T cells recognizing pathogen-derived peptide:MHC complexes Pathogens from evading the immune response by inducing peptide release from cell surface MHC molecules MHC class I molecules from being internalized into endosomes and binding endosome-derived peptides HLA-DM from trafficking to the cell surface with MHC class II Inappropriate T cell recognition of healthy cells that are not infected, nor have ingested a pathogen

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter12: Body Defenses

Section: Chapter Questions

Problem 15RE

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During MHC class I synthesis and folding in the endoplasmic reticulum (ER), a process of peptide editing takes place as the newly synthesized MHC class I protein is held in a ‘peptide receptive’ state by binding to the calreticulin:ERp57:tapasin complex. Peptide editing ensures that the MHC class I molecules that reach the cell surface have stable, high affinity binding for their peptide cargo. Peptide editing is important to the immune response because it: Maintains high levels of surface MHC class I expression Ensures that MHC class I molecules are not degraded in the ER Retains the nascent MHC class I molecule in a peptide receptive state Allows surface MHC class I molecules to bind new peptides from the extracellular milieu Prevents surface MHC class I molecules from undergoing peptide exchange at the cell surface
During MHC class I synthesis and folding in the endoplasmic reticulum (ER), a process of peptide editing takes place as the newly synthesized MHC class I protein is held in a 'peptide-receptive state' by binding to the calreticulin:ERp57:tapasin complex. Peptide editing ensures that the MHC class I molecules that reach the cell surface have stable, high-affinity binding for their peptide cargo. Peptide editing is important to the immune response because it maintains high levels of surface MHC class I expression. ensures that MHC class I molecules are not degraded in the ER. prevents surface MHC class I molecules from undergoing peptide exchange at the cell surface. retains the nascent MHC class I molecule in a peptide-receptive state. 000
Peptide editing is an important component of antigen presentation for both MHC class I and MHC class II pathways, as it drives the preferential presentation of high-affinity binding peptides. For MHC class II peptide editing, HLA-DM plays a key role. In the absence of HLA-DM: MHC class II molecules traffic to the cell surface with CLIP in their binding sites. No MHC class II molecules are released to traffic to the cell surface. MHC class II molecules bind to HLA-DO and are inhibited from binding peptides. Pathogens can evade the immune system by blocking peptide exchange on MHC class II. HLA-DO competes for high-affinity binding peptides with MHC class II molecules and blocks antigen presentation.
The innate immune response together with antibodies are generally not effective at clearing infections established by pathogens that replicate inside host cells. The evolution of T cells has provided a means for the immune response to ‘see’ intracellular infections based on the ability of T cells to: Secrete cytokines that diffuse into the infected tissue Activate type I interferon production by macrophages and dendritic cells Activate macrophages to induce inflammation Recognize pathogen-derived peptides on host MHC surface molecules Express cytoplasmic sensors for detecting pathogen-derived nucleic acids
Which of the following statements are NOT TRUE about Antigen Presenting Cells (APCs)? (Select all that apply) An APC can become activated from antigen binding as well as MHC binding APCs can carry mutliple MHCs Antigen presenting is due to APC activation Adaptive, innate, and non-immune cells can be APCs APCs travel to the sites of resident macrophages to recruit effector immune cells An APC that binds via their expressed MHC II will be killed
Cancer cells often underexpress MHC class 1 molecules. Due to these characteristics, they may be the target of: B cells Eosinophils Neutrophils NK cells OMacrophages
Indicate whether each of the cell components or processes given is involved the processing and presentation of exogenous antigens, endogenous antigens, or both. (Assume n cross-presentation here.) Exognenous Both Possible answers proteasomes MHC class II molecules No Answers Chosen No Answers Chosen phagocytosis or endocytosis invariant chains calnexin tapasin Endogenous No Answers Chosen vesicular transport from RER to Golgi lysosomal hydrolases TAP1 and TAP2 proteins MHC class I molecules
Cytotoxic effector T cells also produce inflammatory cytokines such as IFN-g and TNF-a when their T-cell receptor recognizes peptide:MHC on a target cell. One effect of this cytokine secretion is to enhance the ability of CD8 effector T cells to recognize and kill other infected cells in the nearby vicinity. This enhanced activity is due to: The increased production of perforin and granzymes by CD8 cells The up-regulation of MHC class I protein expression by IFN-g The ability of TNF-a to induce vascular leakage The effect of cytokines on promoting target cell apoptosis The effect of IFN-g to enhance viral replication leading to increased viral antigen presentation
You can choose one or more than one option Antibodies: IMMUNOLOGY basic have two identical antigen-binding sites. consist of two identical heavy chains and two identical light chains. are secreted by plasma cells are produced by T lymphocytes during adaptive immune response can bind their constant heavy chain region to phagocytes Which of the following proteins are transmembrane proteins? CELL BIOLOGY basic integrin oestrogen receptor phospholipase C adenosine triphosphate (ATP) synthase growth factor receptor What are the correct statements? MOLECULAR BIOLOGY advanced A mutation located within a promoter can change the gene expression. An mRNA can be differentially spliced according to the tissue. RNA transcribed by the RNA polymerase II are translated The end of the transcription process requires a specific DNA sequence A reverse transcriptase can polymerise either a DNA or an RNA strand. Which of the following cells kill other cells by exocytosis of…
The diagram shows a pathogen (in red) that is present in different cellular compartments of each of the cell types shown. In each case, a specific T cell subset will recognize peptides of that pathogen presented on MHC molecules on the surface of the cell, and will execute its effector function. From the list below, match the appropriate T cell effector response to the cell type and location of the pathogen. CD4 T cell killing of target cell CD8 T cell killing of target cell CD4 T cell activation of target cell’s antibody production CD8 T cell activation of target cell’s antibody production CD4 T cell activation of target cell’s ability to kill intracellular pathogen CD8 T cell activation of target cell’s ability to kill intracellular pathogen
Individuals or mice with defects in the biochemical pathways needed for loading peptides onto MHC molecules show greatly increased susceptibility to virus infections. Experiments examining the MHC molecules present on the surface of host cells in these individuals would show: Normal numbers of MHC molecules expressed on host cells, but no peptides bound to them. Very low levels of total MHC proteins expressed on the cell surface. Normal numbers of MHC proteins on the surface but all of them bound to self-peptides not pathogen peptides. Very high levels of total MHC proteins expressed on the cell surface. Only virus-infected cells expressing high levels of MHC proteins on the cell surface.
MHC class I proteins: present endogenous antigens to the immune system both are on all nucleated cells and present endogenous antigens to the immune system are on all nucleated cells