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23 Cards in this Set
- Front
- Back
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What cell is necessary for peripheral tolerance and what is this process? |
T regulatory cells are required for peripheral tolerance. This process enables for the removal of any t-cells that may have become self-reactive or were not recognized to be in the thymus |
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What distinguishes T reg cells? |
They express CD25, CD4 and FoxP3 (modified T helper cell) |
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What is the mechanism of B-cell tolerance? |
If they bind self antigen strongly in the bone marrow they either go through apoptosis or receptor editing to lose affinity for the self antigen |
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What is anergy and how is receptor editing correlated? |
Anergy means that the T-cell is unable to mount an immune response against the antigen
Receptor editing causes the B-cell to lose affinity for the self-antigen and can therefore no longer mount an immune response against it (anergy) |
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Can tolerance be reversible? |
Yes, an immune cell can become sensitive to something it was once tolerant to |
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How can sequestered antigens lead to autoimmunity? |
They are stored/hidden within organs and therefore lymphocytes would not be selected against them during the selection process During trauma these antigens can be released and enter the bloodstream resulting in activation of T-cells against these antigens because they were never selected against them |
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How can a streptococcal infection result in autoimmunity? |
The cell wall antigens on the streptococcal bacteria mimic the heart wall surface proteins and therefore the antibodies released against the bacterial infection will also bind the heart wall |
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What is the disease caused by aberrant antibody binding? |
Rheumatic fever |
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What is a major result of rheumatic fever? |
carditis |
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What was the created in the transgenic mouse experiment? |
A mouse embryo was transfected with a viral protein hybridized to the insulin promoter so that it would only be expressed in the pancreatic B-cells Goal was to demonstrate that the mouse immune system would not attack the antigen despite it being foreign because it was born with it |
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What happened during the experiment and what does this demonstrate about tolerance? |
Mouse was infected with the virus corresponding with the transfected antigen and it was noted that the immune system began to destroy the beta cells (demonstrating that the tolerance was reversed). It demonstrated that the t-cells must have only constructed peripheral tolerance to the viral antigen (anergy: functional unresponsiveness) which can be reversed. Central tolerance cannot be reversed because any T-cells that act unfavourably with the self antigens are destroyed. In peripheral tolerance T-cell can still bind the antigen but it doesn't respond to it. |
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What is the mechanism of Grave's disease? |
B-cells secrete self-antigens that attack the thyroid stimulating hormone receptors on the thymus follicles which cause activation of the receptor and release of thyroid hormone (therefore occurs even if not stimulated) and we get overproduction of thyroid hormones |
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Why is the negative feedback loop damaged in Grave's disease? |
Because the thyroid hormone actually does feedback to prevent from further TSH release although the antibodies are unaffected by this and continue to stimulate the thymus |
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What autoimmune reaction occurs during myasthenia gravis? |
Autoreactive antibodies target the acetylcholine receptors on the neuromuscular junction and destroy them, therefore there is no activation occurring (no muscular contraction) |
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What diseases are examples of Type-II autoimmunity? And what is the mechanism of this? |
Grave's Disease, Myasthenia Gravis, and Rheumatic Fever. The mechanism is cell bound antigen recognition. |
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What disease in an example of Type-III and what is the mechanism? |
Rheumatoid arthritis, where a circulating antigen is recognized and attacked |
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What is the antigen commonly recognized in rheumatoid arthritis? |
Antibodies are often produced that recognize a certain antigen on the Fc receptor of other antibodies resulting in immune complex formation |
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How many patients express the rheumatoid factor? |
80% of patients have the rheumatoid factor which is the antigen on the Fc receptor that can be reacted against |
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What is the mechanism of inflammation in rheumatoid arthritis? |
The formation of large immune complexes that build up in the joints and produce inflammation because of taking up space, activating complement etc. |
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What do the antibodies react against in Lupus? |
The antibodies are reacting against self-DNA although there must be some sort of cell damage first that causes the DNA to leak out |
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What is the mechanism of Lupus inflammation and what is it similar to? |
It is the result of immune complex formation which is similar to what occurs in rheumatoid arthritis |
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What is a standard treatment for Lupus? |
Prophylactic steroid treatment |
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How do MHC alleles increase autoimmunity risk? |
Certain HLA molecules are more likely to bind self-antigens and present them to T-cells and therefore increase the risk of making a self-immune response |
