Immunology Flashcards
Mneumonic for vaccines
Live attenuated
BOY Loves The CR_ME
BCG
Oral polio
Yellow fever
Live attenuated
Typhoid
Chickenpox
Rotavirus
MMR
Epidemic thypus
TOXOID - D&T class in school used toxic substances
- Diptheria
- Tetanus
Inactivated ones are HIP
- Hep A
- Influenza
- Pertussus
Genetically modified
- Hep B
Polysacharide
- HOW MEN POSE THREATS
- HIB
- Meningococcal A/C
- Pneumococcal
- Thyphoid
Which cytokines decrease and increase in pregnancy?
Th1 cells decrease
Th2 cells increase
Th1 produces:
- TNF-a
- IL2
- IFN-y
Th2 produces:
- IL 4/5/9/10/13
Which cells are professional antigen presenting cells?
Explain how they work?
What can other cells do?
Macrophages
Dendritic cells
B-cells
T cells cannot readily detect free antigens.
APCs have MHC class 2 and take the free antigens and present them to recruit the CD4 and CD8 T cells.
Most cells have MCH 1 and can present antigens via this. They are called non-professional APCs
Which Ig is the one that can cross the placenta?
Which is the one that fetuses make themselves?
Which is the one they get from breast milk?
IgG crosses the placenta
Fetuses can make IgM
IgA is from breast milk
What is the function of all the Ig’s
IgA - found on mucosal surfaces. Prevent pathogens from getting onto surfaces. BREAST MILK and resistant to stomach acids so key for neonatal immunity
IgD - something to do with B-cells
IgE - key in allergic response
IgG - most prevalent Ig. Key to neonatal immunity as cross placenta.
IgM - Made quicker in response to new pathogen. Before IgG. Neonates can make this one first
What are all the types of hypersensitivity reaction?
Which Igs are involved?
What are examples of conditions?
1 - IgE - allergic reaction
2 - IgG, IgM, complement - Ig’s bind to antigens and cause recruitment of cytotoxic mediators - Goodpastures, ITP, haemolytic disease of newborn
3 - IgG - IgG binds to antigens and forms immune complex which collects in vasculature to cause inflammation - RA, SLE
4 - T-cells - Delayed hypersensitivity. Recruitment of macrophages and memory T-cells. T1DM, graft rejection, MS, mantoux test
5 - IgG - instead of binding to antigens, antibodies bind to ligands which cause prevention of cell signalling - myasthenia gravis, graves disease
How does the baby not cause an immune response?
Many mechanisms via the placenta.
- Progesterone - stimulates blocking of cytokines
- Trophoblast cells have no MHC2 - less presentation of antigens. There is also upregulation of HLA-G which has an important role. HLA A and B are downregulated, HLA E and G are upregulated
- PDL-1 - cell signalling olecule which downregulates T cell response
- Complement is inhibited
- Changes to T cell populations. Th1 is downregulated. Th2 is upregulated
Do rheumatoid arthritis flares increase or decrease in pregnancy?
Why?
Decrease
Because of downregulation of Th1 cells
Do SLE flares increase or decrease in pregnancy?
Why?
Increase. This is because of the UPregulation of th2 cells
Do hyperthyroidism flares increase or decrease in pregnancy?
Increase
Do IBD flares increase or decrease in pregnancy?
Why?
Increase
What are these tumour markers typically associated with?
CEA
Ca 19-9
Ca 15-3
Ca125
AFP
Calcitonin
Ca 27-19
HCG
CEA - bowel Ca
Ca 19-9 - pancreatic Ca, colon cancer
Ca 15-3 - breast Ca
Ca125 - ovarian Ca, peritoneal cancer
AFP - HCC
Calcitonin - medullary thyroid cancer
Ca 27-29 - breast Ca
HCG - trophoblastic disease, non-seminomatous germ cell tumour
When does IgG transfer begin via the placenta?
When do fetusus start to make IgM
IgG transfer - 12 weeks
IgM creation - 10 weeks
Which Ig has the largest and heaviest structure and a pentamer structure?
What shape are the others?
IgM - think LAST ONE in the alphabet and therefore the heaviest
Describe the complement pathway
Classic pathway:
- C1,2,4 –> C3
Leptin pathway
- C2,4 –> C3
Alternative pathway
- Factors B and D –> C3
C3 splits into C3a and C3b
C3b makes C5b which is involved in recruiting C6-9 to make MAC
