13th lecture (immunology) Flashcards
SCHEDULE: -cells of immune system -hypersensitive reactions -transplant rejection -autoimmune disorders -immundeficiency
what are the antigen presenting cells?
- plasmacidic dendritic cell (called plasmacidic because it looks like a plasma cells, they are everywhere): PRODUCE: INF-gamma (protect against viral infection.
- follicular dendritic cells (lymph nodes in the germinal centers, they provide antigen stimuli for B-cells)
- interdigitation reticulum cells (MHC II receptors)
- Monocytes: macrophage cells.
what are the 2 categories of T-cells?
Th (CD4) T-helper
-Th1: (cellular immunity) IL2, INF-gamma
-Th2: (B-cell reaction) IL4, IL5, IL10
Ts (CD8) T-suppressor
(cell mediated cytotoxicity) MHC1 this receptor recognize mine and not mine.
NK cells: have granules containing perforins and granzymes.
Fc receptors
Type 1 hypersensitivity (immediate reaction) anaphalaxia = infection with a sudden onset that can cause death.
INITIAL PHASE:
Antigen -> APC detect and present via MHC2 to Th2 cells with secrete IL4/5 and act on B-cells to make IgE secretion.
Detection of antigen also occurs by B-cells and stimuli from T-cells create IgE secretion.
IgE binds to mast cells which have Fc receptors for it.
Type 1 hypersensitivity (immediate reaction) anaphalaxia = infection with a sudden onset that can cause death.
EARLY PHASE:
no clinical reaction upon 1st encounter with the antigen, but upon the 2nd encounter the mast cells are already sensitized to IgE. Thus IgE can bind to the mast cells which will degranulation releasing: Histamine, Seratonin (vasoactive substances) mucus secretion, vasospasm, increased permeability making edema.
They are also chemotactic factors that help migrate eosinophils to the area and neutorphil to the area.
In the cell membrane phospholipase A2 and arachidoinic acid make leukotrienes and prostaglandins (same affect as histamine and serotonin). Affect on vessels is extended.
Type 1 hypersensitivity (immediate reaction) anaphalaxia = infection with a sudden onset that can cause death.
LATE PHASE:
the degranulation of eosinophils -> Major basic proteins -> cause cell necrosis
PROBLEM: we have no idea that this is happening until the 2nd exposure.
what are the disease for type I hypersensitivity reaction?
LOCAL anaphylaxis:
Local anaphylaxis: only one organ affected. (allergy to spring time pollen or food allergy causing runny nose, etc.
ASTHMA BRONCHITITS: hyper-reactive airways, bronchospasm, and overproduction of mucus.
Curschmann spirals: microscopic findings in the sputum of asthmatics (spiral plug)
massive inflammatory/eosinophilic infiltration and degranulation occurs, there is a precipitation of crystals (charcot leyden crystals)
RESULT: expiatory disphnea
what are charcot leyden crystals?
exagonal bipyramidal structures localised in the primary granules of the cytoplasm of eosinophils and basophils. Their presence, along with eosinophilic infiltrate, is an indirect evidence of parasitic infestation.
What is asthma?
overfiltrated air in the alveoli increasing pressure causing destroying the septum causing emphysema (destruction of the air-sacs)
leads to cor-pulmonale.
what are the disease for type I hypersensitivity reaction?
SYSTEMIC anaphylaxis:
ALL organs are affected. Bee-bites, drugs (penicillin), nuts.
severity of the reaction is INDEPENDENT of the dose of the antigens.
RESULT: general increase in the permeability of the vessels, generalized edema. Edema in the larynx may cause obstruction and lead to suffocation.
The patient can also die from acute right sided heart failure as the edema develops in the lungs.
What is type II hypersensitive reaction; antibody mediated reaction?
related to antigens that are fixed on the cells surface.
Cells that have antigens on their surface (exogenous or part of the cell surface), the antibodies bind to it. The antibody-antigen reaction occurs on the cell surface.
1. in this cell the compliment system reaction will occur. C1, C3, C3b are opsonins. Macrophages eliminates it.
2. C5 and C9 membrane-attack-complex and cell lysis occurs.
3. NK receptors with Fc receptors can bind to it.
4. the antigen can be a receptor. TSH (thyroid stimulating hormone) receptor. If you have an antibody against it, it can up-regulate or down-regulate the hormone.
what are the pathological disease for type II hypersensitivity reaction? In the context of a fetus.
erythroblastosis fetalis: abnormal presence of erythroblasts in the blood. Rh+ father and an Rh- mother and the child is Rh+. the blood does not mix during pregnancy, but after birth the Rh+ antigens go into the Rh- mother causing antibodies to form against them. This could attack the RBC’s of the fetus of the 2nd child.
The resulting cell lysis of the RBC’s the erythroblasts will be hyperplastic (over-proliferation). The patient will have icterus (jaundice). hydrops fetalis: general edema of fetus do to lack of RBC causes hypoxia which makes edema.
-A/B missmatch transfusion
what are the pathological disease for type II hypersensitivity reaction?
- Erythroblastosis fetalis
- A/B missmatch transfusion
- autoimmune hemolitic anemia
- goodpasture syndrome (antibodies against glomeruli basement membrane)
- Anemia pernicioasa
Type III hypersensitive reactions?
immune-complex mediated reaction.
-systemic: antigens make their way into the circulation through the wall of the vessels. Antibody is produced against it. thus antigen and antibody complexes forms.
The immune-complexes have a certain size and charge allowing them to attach to certain areas; large size, they may end up in the glomeruli filtration, positive charge may attach to negative endothelium. The complement system will be activated and destroy the areas that have the immune complexes.
glomerulonephritis (immune complex trapped in the kidney)
arthritis (attach to joints)
-local:
Type IV hypersensitive reaction description?
cell mediated hypersensitive reaction. 2 types;
Delayed: tuberculin reaction (used to test for tuberculosis on the skin)
MECHANISM:
Bacteria injected -> macrophages take them up -> phagocyte them and present them to the immune-component cells via MHCII molecule. CD4 cells recognize them. The IL12 produced by the macrophages they (T-cells) will transform to Th1 cells (memory cell)
when the test is done a 2nd time same thing occurs but this time the Th1 (memory cells) recognize them and makes a blastic-tranformation that makes INF-gamma, TNF-alpha. These help the migration of the monocyte and macrophages cells. These can fuse to make giant cells and granulomas.
what type of reaction is seen in granulomas?
any granulomatous reaction is related to type IV reaction.
