Autoimmune disease and allergy
33 important questions on Autoimmune disease and allergy
Summarize the mechanisms of inflammation briefly
Inflammation can be induced by allergens.
How can a allergic reaction be recognized in the airways? (experiment saline/control and ragweed/allergen)
Eosinophils. in this case.
What are the four types of hypersensitivity reactions?
- I: typical allergy; mediated by IgE; IgE bounded to antigen binds mast cells; granules with histamine and cytokines.
- II: Antibody mediated hypersensitivity; mediated by IgG and IgM; surface antigens are recognizes by complement and ctls.
- III: Immune complex mediated hypersensitivity; antigen bound in immune complexes attrackt neutrophiles.
- IV: Delayed hypersensitivity; mediated by tcells; no antibodies involved.
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What can induce a hypersensitive reaction?
- Infectious agents (TB-mantoux).
- Environmental antivens (grass pollen)
- Auto-antigens
Explain the linkage between diseases ms, crohn, asthma and diabetes
Shared genes among distinct diseases may lead to common early diagnosis criteria and therapeutic strategies (anti TNFalfa).
Explain the difference between allergy and atopy.
How can atopy lead to allergy?
Allergy = Atopy + Tissue factors.
For disease, certain changes in the target organ are needed.
Also; triggers (for changes in target organs?)
What are the similarities and differences between psoriasis and atopic dermatitis?
The immunereaction is different.
What levels of dearrangment can can cause allergys/immunemediated disease?
Atopy genes
Tissue factors
What factors determine atopic dermatitis versus allergic asthma?
Which factors determine allergic dermatitis versus psoriasis?
Psoriasis never had atopy (?). Specific psoriasis gene cause hyper activation of endothelia.
Two groups of genes are differentially regulated in atopic dermatitis compared to the healthy control group. Which groups of genes?
Genes for proliferation, apoptosisn and polarization are downregulated..
This causes more cd4 tcell migration to the skin .
What is the effect of downregulation of GADD45a mrna and TNFAIP mrna in CD4 tcells in atopic dermatitis?
TNFAIP3: Is a global negative regulator of inflammation.
When mrna is downregulated; more tcell activation and more inflammation!
Which specific gene expression profiles are important to determine multifactorial atopic disease?
How can we distinguish a inflammed skin from a healthy skin under the microscope?
Lesional: Infiltration of tcells in the epidermis.
What happens when there are too much th1 cells? And too much th2? What can cause disbalance?
Too many th2 cells leads to allergy
Tregs normally regulate this balance. Hygiene theory; too much hygiene; less triggers for Treg; less tregs; disrupted balance; switch and Th2 expansion.
What are the different Th subsets and what diseases do they cause when upregulated?
Which cells regulate the Tcell differentiation?
- TGFbeta; Treg
- IL6; Th17 (TGFbeta also stimulates Th17)
- ICOS-ligand; Th2 (IL4 also stimulates Th2)
- IL12; Th1 (IFNgamma also stimulates Th1)
In the picture, the names shown above the cells represent the intracellular enzymes that react on the cytokines and induce differentiation intracellular.
What is the difference between acute allergic disease and inflammational allergic disease (?)
Which cells and other components are involved in a hypersensitivity reaction? What is the exact mechanism? (type I allergy)
- Mastcells in skin/gut/lungs (basophils in blood)
- Bcell (IgE)
- APC
- Tcell
- Allergen
- Cytokines (IL4,5,13 Tcells, histamine mastcells, LTL4, RAF, TNFalfa...)
Picture notes: Tcell not only produces IL4, but also IL13 and IL5.
IL13 activates skinn cells (tissue).
IL5 induces eosinophil differentiation; those cells are important for chronic inflammation.
The IgE mastcell interaction stays upon 6 months!
Left; sensitazation phase, lot of people have this.
How is type I hypersensitivity treated (astma, hooikoorts, non inflammed!)?
What are the characteristics of atopic dermatitis (atopic eczema)?
Histology: Spongiosis (holes in the skinn), infiltrated tcells, ancanthosis (diffuse epirdermal hyplasia=thickening of the skinn).
What is the difference between an intracutaneous test and atopy patch test (mechanism, outcomes etc).
Damage because of injection causes the neutrophile influx, so this has nothing to do with the disease mechanism. ICT shows a drop in mast cells; this is because degranulation takes place and therefore the mast cells are not shown.
Acute vs. chronic allergic reactions:
What is the difference between auto-immunity and auto-immune disease?
Auto-immune disease is a disease as a result of tissue damage due to autoimmune reactions
What mechanisms of selftolerance do you know?
- Central tolerance: elimination of autoreactive b and t cells.
- Peripheral tolerance: no costimulation for autoreactive t and bcells; autoreactive t and b cells are stimulated towards apoptosis. + regulatory cells can inhibit lymphocytes.
What is central tolerance (tcells) and where does it occur? Which protein is essential in central tolerance?
Where: In the thymus (tcells)
Positive selection: 90% of the tcells are lost. Double positive tcells that bind self HLA are selected.
Negative selection: 50% of the tcells are lost. Tcells with strong binding to self HLA and specific self antigen are eliminated.
AIRE: Autoimmuneregulator: Gene responsible for expression of tissue autoantigens in the medular epithelial cells. (AIRE deficiency APS1 leads to auto-antibodies against certain tissue types).
What is central tolerance for bcells and where does it occur?
Explain why central tolerance is not perfect
- Sometimes the antigen is not presented on AIRE or the concentration is too low.
- Antigen produced due to AIRE is not processed by the APC correctly.
Only antigens that are produced by AIRE are tested. When this doesnt occur correctly, autoreactive t and b cells will enter the periphery.
Explain two ways how the innate immune system is involved in autoimmunity due to activation autoreactive cells by inflammation
- During infection, pro-inflammatory cytokines are released, leading to tissue damage en release of auto-ag. These auto-ags are phagocytosed by APCs and presented to autoreactive tcells. Since the APC is already activated by the infection causing inflammation, co-stimulatory molecules are expressed and cytokines. This is called bystander activation.
- Molecular mimicry: the pathogen epitopes resemble auto-antigen; antibodies produced against pathogen after infection also recognize self-antigen,
Explain how the innate immune system is involved in autoimmunity by disrupted clearance of apoptotic debris
Disease: Too many apoptotic cells induce disrupted macrophagereceptor-ligand interactions. Now, immature dc's take up the apoptotic cell instead of the macropgafes.
Anti-inflammatory cytokines are not released. In presence of pro-inflammatory cytokines, the dc matures into an auto ag presenting cell, able to activate auto-ag specific tcells.
Explain how the innate immune system is involved in autoimmunity by activation netosis
Specific autoantibodies bond to neutophiles, inducing netosis. (SLE=higher rates of NET).The pDC can uptae the self DNA and induce upregulation of IFNalfa.; leading to auto-immunity?
Name some characteristics and examples of type II autoimmune disease
- Antibodies against cell-surface or matric antigens; immune complexes of antibodies and complement bind to the antigen. Mainly IgM and IgG.
- Example: Grave disease: Autoantigen thyroid stimulating hormone receptor is attacked, leading to hyperthyroidism; overproduction of thyroid hormone
Mind you; the circulating antibodies have stimulating activity on the receptor!!
Other examples are: acute rheumatic fever, pemphigus vulgaris (antibodies bind skin) and goodpasture syndrome. (anti GBM binds kidney).
Name some characteristics and examples of type III and IV autoimmune disease
- Type III is characterized by reaction due to formed immune complexes. Type IV is characterized by tcell mediated reaction. An example is SLE. Immune complexes in the circulation bind the endothelial cells. The recognized auto antigen is DNA/RNA.
- Type IV is characterized by the tcell mediated reaction. An example is diabetis: cytotoxic tcells react on pancreatic beta cell antigen.
Explain the role of genetics in auto-immune disease
For example SLE: mutations in different pathways such as immunecomplex processing, immune signal transduction and IFN pathways.
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