Immunology and disease
Index:
Immunopathologic reaction types ————————————————— page 2
Inflammation —————————————————————————— page 3
Pathogen responses ——————————————————————— page 4
Things that can go wrong ————————————————————— page 6
Vaccines ———————————————————————————— page 7
Immunoassays
- Immunohistochemistry —————————————————— page 9
- Flow cytometry ————————————————————— page 10
- ELISA ————————————————————————— page 11
Transplantology ————————————————————————— page 12
Cancer ————————————————————————————— page 15
Immunodeficiency ———————————————————————— page 17
Autoimmunity —————————————————————————— page 19
Mucosal immunity ———————————————————————— page 21
Allergies ————————————————————————————page 23
Bonus: Effects of old age on the immune system —————————— page 26
Page 1
,Immunopathologic reaction types:
There are in total 4 different types and in my opinion they go from least serious to
deadly serious;
Type 1: immediate hypersensitivity
It is an immune reaction against (sometimes harmless) agents. Upon first expo-
sure, B cells produce IgE antibodies that bind to Fcε receptors on mast cells
and basophils, sensitizing them. Upon re-exposure, the allergen cross-links IgE,
triggering mast cell degranulation and the release of histamine.
This is also what happens with allergies.
Type 2: antibody mediated toxicity
The IgM and IgG antibodies bind against the cell surface or extracellular matrix.
This can lead to opsonization and subsequent phagocytosis by macrophages,
activation of the complement system.
Type 3: immune complex mediated
This occurs when IgM or IgG antibodies form immune complexes with soluble
antigens. These complexes deposit in tissues, particularly in blood vessels.
Then the complement activation and leukocyte recruitment (especially neu-
trophils) lead to tissue inflammation and damage.
Type 4: T-cell mediated
Unlike the other types, this reaction is mediated by T cells rather than antibod-
ies. CD4+ T-cells recruit and activate macrophages and other immune cells,
leading to delayed inflammation. CD8+ T-cells can directly kill infected or ab-
normal cells. This reaction typically manifests 24–72 hours after antigen expo-
sure.
Page 2
, Inflammation:
Signs of inflammation:
• Tumor: Swelling
• Rubor: Redness
• Calor: Heat
• Dolor: Pain
• Functio Laesa: Loss of function
There are different types of inflammation; acute and chronic.
Acute inflammation response works in 7 steps;
1. A physical barrier (e.g. epithelial layer) breaks which allows entry for microbes.
2. The microbes activate sentinel cells*.
3. Sentinel cells secrete inflammatory cytokines.
4. Then the blood vessels dilate (vasodilation), which increases the blood flow, this
causes fluid and proteins to enter this area.
5. Complement, antibodies and antimicrobial protein kill the microbes.
6. Adhesion molecules cause leukocyte migration to the tissue.
7. Which then finally leads to the phagocytosis of the microbes.
*sentinel cells are dendritic cells (DC), macrophages and mast cells.
To stop the inflammatory response, regulatory T-cells (Treg) are the most important.
When sentinel cells can no longer sense PAMPs or DAMPs, the switch from pro-
inflammatory to anti-inflammatory mode, and they will start producing anti-
inflammatory cytokines.
Treg cells will also start producing anti-inflammatory cytokines. If it didn’t do this, then
it could lead to chronic inflammation.
Important pro-inflammatory cytokines are; TNF, IL-1, IL-6
Important anti-inflammatory cytokines are; IL-10, TGF-ß
They are produced by macrophages, mast cells and epithelial cells
Chronic inflammation stays active for weeks, months or even years! Instead of
resolving the issue, the immune system stays constantly activated, which will lead to
tissue damage and fibrosis, which is a fancy word for scarring.
Page 3
Index:
Immunopathologic reaction types ————————————————— page 2
Inflammation —————————————————————————— page 3
Pathogen responses ——————————————————————— page 4
Things that can go wrong ————————————————————— page 6
Vaccines ———————————————————————————— page 7
Immunoassays
- Immunohistochemistry —————————————————— page 9
- Flow cytometry ————————————————————— page 10
- ELISA ————————————————————————— page 11
Transplantology ————————————————————————— page 12
Cancer ————————————————————————————— page 15
Immunodeficiency ———————————————————————— page 17
Autoimmunity —————————————————————————— page 19
Mucosal immunity ———————————————————————— page 21
Allergies ————————————————————————————page 23
Bonus: Effects of old age on the immune system —————————— page 26
Page 1
,Immunopathologic reaction types:
There are in total 4 different types and in my opinion they go from least serious to
deadly serious;
Type 1: immediate hypersensitivity
It is an immune reaction against (sometimes harmless) agents. Upon first expo-
sure, B cells produce IgE antibodies that bind to Fcε receptors on mast cells
and basophils, sensitizing them. Upon re-exposure, the allergen cross-links IgE,
triggering mast cell degranulation and the release of histamine.
This is also what happens with allergies.
Type 2: antibody mediated toxicity
The IgM and IgG antibodies bind against the cell surface or extracellular matrix.
This can lead to opsonization and subsequent phagocytosis by macrophages,
activation of the complement system.
Type 3: immune complex mediated
This occurs when IgM or IgG antibodies form immune complexes with soluble
antigens. These complexes deposit in tissues, particularly in blood vessels.
Then the complement activation and leukocyte recruitment (especially neu-
trophils) lead to tissue inflammation and damage.
Type 4: T-cell mediated
Unlike the other types, this reaction is mediated by T cells rather than antibod-
ies. CD4+ T-cells recruit and activate macrophages and other immune cells,
leading to delayed inflammation. CD8+ T-cells can directly kill infected or ab-
normal cells. This reaction typically manifests 24–72 hours after antigen expo-
sure.
Page 2
, Inflammation:
Signs of inflammation:
• Tumor: Swelling
• Rubor: Redness
• Calor: Heat
• Dolor: Pain
• Functio Laesa: Loss of function
There are different types of inflammation; acute and chronic.
Acute inflammation response works in 7 steps;
1. A physical barrier (e.g. epithelial layer) breaks which allows entry for microbes.
2. The microbes activate sentinel cells*.
3. Sentinel cells secrete inflammatory cytokines.
4. Then the blood vessels dilate (vasodilation), which increases the blood flow, this
causes fluid and proteins to enter this area.
5. Complement, antibodies and antimicrobial protein kill the microbes.
6. Adhesion molecules cause leukocyte migration to the tissue.
7. Which then finally leads to the phagocytosis of the microbes.
*sentinel cells are dendritic cells (DC), macrophages and mast cells.
To stop the inflammatory response, regulatory T-cells (Treg) are the most important.
When sentinel cells can no longer sense PAMPs or DAMPs, the switch from pro-
inflammatory to anti-inflammatory mode, and they will start producing anti-
inflammatory cytokines.
Treg cells will also start producing anti-inflammatory cytokines. If it didn’t do this, then
it could lead to chronic inflammation.
Important pro-inflammatory cytokines are; TNF, IL-1, IL-6
Important anti-inflammatory cytokines are; IL-10, TGF-ß
They are produced by macrophages, mast cells and epithelial cells
Chronic inflammation stays active for weeks, months or even years! Instead of
resolving the issue, the immune system stays constantly activated, which will lead to
tissue damage and fibrosis, which is a fancy word for scarring.
Page 3
