Hypersensitivity disorders (Stegeman)
21 important questions on Hypersensitivity disorders (Stegeman)
What does auto-immunity imply in the adaptive and innate immune system?
Innate --> auto-inflammatory disorders
Which receptors interact during T cell - B cell interaction?
Which cytokines do T cells produce in reaction to this interaction and what do they promote?
B cell: CD40 receptor
T cell expressed cytokines: TNF-alpha, Interferon-gamma, IL-10.
--> They promote the B cell to form antibodies
Describe the interaction between a T cell and an APC. Which interaction are present and which are stimulative of inhibitive?
T cell: CD28 receptor, binds to B7 on APC -> stimulatory -> cytokine release, B cell help, inflammation
T cell: CTLA-4 receptor, binds to B7 on APC -> inhibitory -> activation suppressed
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What is the difference between tolerance and ignorance in a T-cell response?
Ignorance: T cell + Nonimmunogenic antigen = no response
What is the difference between central and peripheral tolerance?
Peripheral tolerance takes place in the peripheral tissue when mature lymphocytes recognize self antigens
Name the two mechanisms of central tolerance of T cells
The development of regulatory T cells
What are the mechanisms behind central tolerance of B cells?
Low avidity -> reduced receptor expression, signalling block -> leads to anergic B cells in peripheral tissue.
Why is selection during central tolerance not absolute?
On what receptor interaction is central tolerance dependent?
Peripheral tolerance: what mechanism causes unresponsive (anergic) T cells?
- Signaling block, or
- Engagement of inhibitory receptors (ex: CTLA4)
-> anergic T cell
In what ways can apoptosis be induced during peripheral tolerance of T cells?
- Role of pro-apoptotic proteins: pro-apoptotic proteins outweigh anti-apoptotic proteins.
Why is anergy not absolute?
- can be overruled by sufficient co-stimulation
Regulatory T-cells can suppress the immune system. What are the characteristics of Treg-cells? (how many, transcription factor, centrally or peripherally induced)
- approx. 5% of circulating CD4+ lymphocytes
- transcription factor FoxP3
- can be induced both centrally and peripherally
How do Treg cells conduct peripheral tolerance?
- Contact dependent inhibition of T cell response
How does auto-immunity develop?
- Loss of tolerance
- reversal of anergy
- loss of/insufficient T-reg activity
- Auto-antigen had to become available/accessible
- For a disease to form, the auto-immunity reaction has to result in (tissue) damage
Auto-immunity can be a result of genetic susceptibility, where there is a failure of self-tolerance creating self-reactive lymphocytes.
This can result in auto-immune disease caused by infection or injury, how does this mechanism work?
2) Activation of tissue APCs
3) Influx of self-reactive lymphocytes (generated by genetic susceptibility) into tissues
4) Activation of self-reactive lymphocytes
5) Tissue injury: autoimmune disease
Why are most auto-immune diseases only marginally associated with genetics?
- many auto-immune diseases show extreme variation in manifestation, course and response to therapy
What do the armamentum of drugs for auto-immune disease predominantly target?
What is the induction phase and what treatment principle applies to it?
Name five types of immune suppressive drugs/therapies for auto-immune diseases
- Glucocorticosteroids
- Alkylating agents
- Anti-metabolites
- Calcineurin inhibitors (inhibition of T-lymphocytes)
- Therapy with (monoclonal) antibodies
What is a diagnostic tool for auto-immune diseases?
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