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Questions and Answers
Which of the following mechanisms of peripheral tolerance occurs when self-antigens are not present in sufficient quantities to reach the threshold of activation for TCR?
Which of the following mechanisms of peripheral tolerance occurs when self-antigens are not present in sufficient quantities to reach the threshold of activation for TCR?
What is the term for the lack of TCR activation due to the lack of co-stimulation by APCs?
What is the term for the lack of TCR activation due to the lack of co-stimulation by APCs?
Which of the following is an example of an immunologically privileged site where self-antigens remain sequestered?
Which of the following is an example of an immunologically privileged site where self-antigens remain sequestered?
What is the purpose of central tolerance in the thymus?
What is the purpose of central tolerance in the thymus?
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Which of the following mechanisms of peripheral tolerance involves the action of negative co-stimulatory pathways?
Which of the following mechanisms of peripheral tolerance involves the action of negative co-stimulatory pathways?
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What is the term for the process by which T cells are not activated due to the lack of self-antigens during early +/- selection in the thymus?
What is the term for the process by which T cells are not activated due to the lack of self-antigens during early +/- selection in the thymus?
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What is the primary reason why the body maintains a state of immunological tolerance?
What is the primary reason why the body maintains a state of immunological tolerance?
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Where do B cells undergo 'education' in the process of central tolerance?
Where do B cells undergo 'education' in the process of central tolerance?
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What is the function of thymic nurse cells in the thymic cortex?
What is the function of thymic nurse cells in the thymic cortex?
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What is the outcome of T cells that fail to bind to MHC molecules during positive selection in the thymic cortex?
What is the outcome of T cells that fail to bind to MHC molecules during positive selection in the thymic cortex?
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What is the primary function of the medullar epithelial cells in the thymic medulla?
What is the primary function of the medullar epithelial cells in the thymic medulla?
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What is the limitation of central tolerance in preventing autoimmune diseases?
What is the limitation of central tolerance in preventing autoimmune diseases?
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What is the consequence of low affinity for self-antigens during central tolerance?
What is the consequence of low affinity for self-antigens during central tolerance?
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Why is it essential to maintain some self-reactive immune cells in the periphery?
Why is it essential to maintain some self-reactive immune cells in the periphery?
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What is the fate of B cells with high affinity for self-antigens in the bone marrow?
What is the fate of B cells with high affinity for self-antigens in the bone marrow?
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What is the primary function of central tolerance in T cells?
What is the primary function of central tolerance in T cells?
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What is the result of weak recognition of self-antigens by B cells in the bone marrow?
What is the result of weak recognition of self-antigens by B cells in the bone marrow?
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What is the outcome of deleting all self-reactive T cells?
What is the outcome of deleting all self-reactive T cells?
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What is the primary function of CTLA-4 in T cells?
What is the primary function of CTLA-4 in T cells?
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What is the outcome of repeated TCR stimulation in self-reactive T cells?
What is the outcome of repeated TCR stimulation in self-reactive T cells?
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Which type of regulatory T cells are generated in the periphery and can be induced by antigen presentation?
Which type of regulatory T cells are generated in the periphery and can be induced by antigen presentation?
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What is the mechanism of B cell tolerance in chronic infections?
What is the mechanism of B cell tolerance in chronic infections?
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What is the function of FcgR2b in B cells?
What is the function of FcgR2b in B cells?
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What is the primary mechanism of central tolerance in the thymus?
What is the primary mechanism of central tolerance in the thymus?
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What is the outcome of breaking tolerance in the immune system?
What is the outcome of breaking tolerance in the immune system?
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What is the primary mechanism of peripheral tolerance in B cells?
What is the primary mechanism of peripheral tolerance in B cells?
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What is the association between autoimmune diseases and genetic factors?
What is the association between autoimmune diseases and genetic factors?
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What is the role of vitamin D deficiency in autoimmune diseases?
What is the role of vitamin D deficiency in autoimmune diseases?
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T cells are ‘educated’ in the bone marrow during central tolerance.
T cells are ‘educated’ in the bone marrow during central tolerance.
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The limitation of central tolerance is that it cannot eliminate all self-reactive T cells.
The limitation of central tolerance is that it cannot eliminate all self-reactive T cells.
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Negative selection in the thymic medulla results in the activation of T cells with low affinity for self-antigens.
Negative selection in the thymic medulla results in the activation of T cells with low affinity for self-antigens.
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The primary function of cortical epithelial cells is to present self-antigens to T cells during negative selection.
The primary function of cortical epithelial cells is to present self-antigens to T cells during negative selection.
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Peripheral tolerance is more effective than central tolerance in preventing autoimmune diseases.
Peripheral tolerance is more effective than central tolerance in preventing autoimmune diseases.
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The thymic capsule is involved in the positive selection of T cells in the thymic cortex.
The thymic capsule is involved in the positive selection of T cells in the thymic cortex.
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All self-reactive T cells that escape central tolerance are eliminated in the periphery.
All self-reactive T cells that escape central tolerance are eliminated in the periphery.
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Receptor editing in B cells can lead to the deletion of the B cell if the process fails.
Receptor editing in B cells can lead to the deletion of the B cell if the process fails.
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Central tolerance can account for all innocuous environmental antigens.
Central tolerance can account for all innocuous environmental antigens.
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A high affinity for self-antigens in B cells always leads to receptor editing.
A high affinity for self-antigens in B cells always leads to receptor editing.
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Peripheral tolerance is not necessary for maintaining a healthy immune system.
Peripheral tolerance is not necessary for maintaining a healthy immune system.
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Self-reactive B cells undergo selection only in the thymus.
Self-reactive B cells undergo selection only in the thymus.
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Some self-antigens are only expressed during early +/- selection in the thymus.
Some self-antigens are only expressed during early +/- selection in the thymus.
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Immunologically privileged sites are normally accessible to T cells.
Immunologically privileged sites are normally accessible to T cells.
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Tolerance is maintained when self-antigens are present in sufficient quantities to reach the threshold of activation for TCR.
Tolerance is maintained when self-antigens are present in sufficient quantities to reach the threshold of activation for TCR.
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Anergy involves the action of positive co-stimulatory pathways.
Anergy involves the action of positive co-stimulatory pathways.
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Tolerogenic or immature DCs can provide co-stimulation to T cells.
Tolerogenic or immature DCs can provide co-stimulation to T cells.
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Central tolerance is the primary mechanism of tolerance in the periphery.
Central tolerance is the primary mechanism of tolerance in the periphery.
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CTLA-4 expression is induced upon TCR stimulation and has low affinity for CD80/86.
CTLA-4 expression is induced upon TCR stimulation and has low affinity for CD80/86.
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Repeated activation of the TCR induces expression of anti-apoptotic proteins such as Bcl-2.
Repeated activation of the TCR induces expression of anti-apoptotic proteins such as Bcl-2.
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Regulatory T cells can directly kill APCs and other T cells via Fas and FasL secretion.
Regulatory T cells can directly kill APCs and other T cells via Fas and FasL secretion.
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Peripheral tolerance mechanisms include ignorance, anergy, deletion, and the effects of regulatory B cells.
Peripheral tolerance mechanisms include ignorance, anergy, deletion, and the effects of regulatory B cells.
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Autoimmune diseases are thought to have a environmental trigger but no genetic component.
Autoimmune diseases are thought to have a environmental trigger but no genetic component.
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HLA-DQ, DR, and other genes are associated with reduced risk of autoimmune diseases.
HLA-DQ, DR, and other genes are associated with reduced risk of autoimmune diseases.
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Vitamin D deficiency is a protective factor against autoimmune diseases.
Vitamin D deficiency is a protective factor against autoimmune diseases.
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Breaking tolerance can lead to cancer.
Breaking tolerance can lead to cancer.
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The primary function of CTLA-4 is to enhance TCR signalling.
The primary function of CTLA-4 is to enhance TCR signalling.
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Central tolerance mechanisms remove all self-reactive T and B cells in the thymus and bone marrow.
Central tolerance mechanisms remove all self-reactive T and B cells in the thymus and bone marrow.
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Study Notes
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The immune system maintains a state of 'immunological tolerance' to prevent self-reactive immune cells from triggering autoimmunity, which is achieved through central and peripheral tolerance mechanisms.
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Central tolerance involves the 'education' of T cells in the thymus and B cells in the bone marrow, where self-reactive cells are removed through apoptosis.
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In the thymus, T cells undergo positive selection in the thymic cortex, where they are tested for MHC binding, and negative selection in the thymic medulla, where they are presented with self-antigen/MHC complexes and undergo apoptosis if they have high affinity for self antigen.
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Peripheral tolerance involves multiple mechanisms for B and T cells, including ignorance, anergy, deletion, and the effects of regulatory T cells.
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T cell peripheral tolerance mechanisms include ignorance, where some self-antigens are hidden or not present in sufficient quantities to trigger an immune response, anergy, where T cells are activated without co-stimulation, deletion, where self-reactive T cells are deleted through apoptosis, and the effects of regulatory T cells, which can suppress or kill self-reactive T cells.
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B cell peripheral tolerance mechanisms include anergy, where self-reactive B cells are unresponsive to antigen, deletion, where self-reactive B cells are deleted through apoptosis, and exclusion, where partially activated B cells are excluded from lymphoid follicles and cannot develop into mature plasma B cells.
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Breaking tolerance can lead to autoimmune disease, which occurs when the immune system responds to self-antigens, and can range from organ-specific to systemic diseases.
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Autoimmune diseases are thought to have a genetic component and an environmental trigger, and usually affect women more than men.
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Regulatory T cells play a crucial role in maintaining peripheral tolerance, and their dysfunction can contribute to autoimmune diseases.
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FcgR2b, a receptor with an ITIM motif, can inhibit B cell activation when crosslinked by Ab/Ag complexes, leading to a negative signal.
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BAFF, a survival factor, is important for B cell survival and can contribute to autoimmune diseases when dysregulated.
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CTLA-4, a negative regulatory molecule, is induced upon TCR stimulation and can inhibit T cell responses by binding to CD80/86 on APCs.
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Activation-induced cell death (AICD) can delete self-reactive T cells in the periphery through the expression of death receptors and pro-apoptotic proteins.
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Mucosal immunity is characterized by specialized structural and cellular features that contribute to immune tolerance and prevent excessive immune responses to innocuous antigens.
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Description
Test your knowledge of the immune system with this quiz on tolerance, hypersensitivity, and mucosal immunity. Learn about the mechanisms of central and peripheral tolerance, autoimmune diseases, and the different types of hypersensitivity responses. Identify the underlying mechanisms and diseases associated with each.