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Deficient NK cell activation
5%
27/566
Deficient presentation of pathogens to CD4 T-cells
81%
459/566
Deficient presentation of pathogens to CD8 T-cells
8%
43/566
Deficient cell extravasation
4%
22/566
Deficient expression of B7
1%
8/566
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A defect in antigen processing would result in deficient presentation to CD4 T-cells. The MHC class II pathway of antigen presentation begins with pathogen endocytosis by an antigen presenting cell followed by degradation in the acidic environment of a phagolysosome. The process proceeds with fusion with a vesicle containing MHC II molecules leading to the formation of antigen:MHC II complexes which are then presented on the surface for contact with CD4 T-cells. Landsverk et al. discuss how MHC class II molecules are assembled and trafficked to endosomes. Here, they are bound to the foreign peptides which they are meant to present. MHC class II molecules are present exclusively on antigen presenting cells while MHC class I molecules are present on all the cells of the body. MHC class I molecules interact with CD8 T-cells while MHC class II molecules interact with CD4 cells. Cooper et al. examine primary immunodeficiencies. They note that disorders of phagocytosis tend to result in presentation in infancy or early childhood as unusually severe infections by common pathogens. Granuloma formation, poor would healing, and abscess formation are present. Skin, oral cavity, and anorectal infections are common. Illustration A is a diagram depicting antigen processing. Incorrect Answers: Answer 1: NK cell activation is mediated by a balance of activating signals and inactivating signals (MHC class I molecules). Answer 3: Antigen:MHC class I complexes are presented to CD8 T-cells and are loaded in the ER not the phagolysosome. Answer 4: Cell extravasation is dependent on interactions with selectins and integrins; both of these interactions are not dependent on phagolysosome acidity. Answer 5: B7 expression is not dependent on phagolysosome aciditiy.
3.0
(3)
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