Immune Flashcards
1
Q
Parts of immune sxs
A
- innate and adaptive immunity
2
Q
Active immunity
- naturally acquired
- artifically acquired
A
- you get sick and produce antibodies
- vaccine
3
Q
Passive immunity
- naturally acquired
- artificially acquired
A
- mother passes IgG through placenta to baby or IgA through breast milk
- IV Ig
4
Q
Innate immune system
- parts
- also called
A
- physical barrier, complement, phagocytes
- tissue immunity
5
Q
Acquired immune system
- parts
- also called
A
- B and T cells
- humoral immunity
6
Q
Complement system
- classic: pathway, part
- alternative: pathway, importance, part
- mannose binding lectin
A
- IgG/ M activates C1 esterase -> Splits C2 into C2a and b, and C4 into C4a and b -> C2b and C4b combine -> split C3 into C3a and B -> C2b/3b/4b combine to become c5 convertase -> turns c5 into c5a and b -> c5b goes to MAC complex; part of acquired
- C3 spontaneously splits into C3a and b -> c3b will become c3bBb -> splits C5 -> MAC complex forms; dont need Ig to be activated, part of innate
- mannose is displayed on cell surface and bound by MBL, turns C2 and C4 into their peice; candida, salmonella, cryptococcus, listeria, nisseria
7
Q
Complement deficiences
- C1 esterase def causes
- C3 def causes
- MAC def
- decay accelerating factor def
A
- angioedema
- sinus and resp track infections
- recurring nisseria infections
- Paroxsymal Nocturnal Hemoglobinuria
8
Q
C1 esterase def
- normally
- C1 esterase inhibitor normally
- c2 b other product
A
- splits C2 and C4
- regulates C1 esterase and prevents plaminogen to plasmin to cause fibrin split products which also activate C1
- can be turned into c2 kinin by plasmin -> vasoactive peptide -> vasodilation and capillary leak
9
Q
Paroxsymal Nocturnal Hemoglobinuria
- genetics
- pathogen
- why just night
- tx
A
- acquired mutation to PIG-A gene that encodes for GPI
- GPI anchors CD55 (decay accelerating factor) and 59 (MIRL) to RBC so complement can destroy RBC
- RBC getting destroyed while you sleep and collects in urine making it red
- eculizumab against complement
10
Q
Organs of immune sxs
- thymus
- spleen
- peyer patch
- bone marrow
- appendix
- LN
A
- produce T cells
- have B and T cells to filter blood
- immune cells of immune sxs live
- where B cells made
- lymph organ but idk
- where naive B and T cells reside and plasma cells
11
Q
Spleen
- size
- location
- most
- blood supply
- red pulp function
- white pulp function
- role in gestation
A
- 4 in
- LUQ, between 9-11 rib
- injured in intraabdominal blunt trauma
- splenic a off celiac trunk
- consists of sinusoids which filter blood and have macrophages that destroy RBC
- humoral immunity, T cells in PALS, B cells in follicles and APC in marginal zones
- helps make RBC until 5th month
12
Q
LN
- function
- route
- outer most part: called, consists of, function
- paracortex: contain
- medulla: contain
A
- proliferation and storage B and T cells
- mult afferent and 1 efferent
- cortex -> primary (dormant B cells) and secondary follicles (proliferating B cell)
- contains t cells
- B tells, t cells, plasma cells
13
Q
MCC leukocytosis
- stress demargination: what is it, when will it be fixed
- infection: what will you see
- leukemia: what will you see
- lymphoma
- myelodysplastic
- leukemoid
A
- when there is stress PMNs come off wall and go into circulation; should return to normal in about a day
- elevated WBC, left shift -> increase in PMNs and bands, fever, chills, etc
- elevated WBC and blasts, night sweat, weight loss, etc
- everything will be raised
- exaggerated stress demargination -> stressor has caused elevated WBC for weeks (DKA)
14
Q
Viruses that cause leukopenia
A
- Parvo, Hep E and C
15
Q
lymph development
- b cell: location dev, location maturation, differentiation
- t cell: location dev, location maturation, differentiation
A
- BM, spleen, LN
- BM, thymus, LN
16
Q
T cells in thymus
- positive selection: location
- negative selection
- t suppressor
- CD4 function
A
- cortex, makes sure it can bind to MHC; those that can bind to MHC II -> CD4, those that only bind MHCI -> CD8
- medulla, makes sure CD8 doesn’t bind to self antigen too tightly (want weakest) and CD4 binds to MHCII very tightly (want strongest)
- select few of CD8 cells that bind too tightly to MHCI that reg t cells
- produce memory cells, activate CD8, activate B cells, produce inflamm mediators to bring PMN and macro to area
17
Q
NK cells
- express
- function
- how
- activation
A
- CD 16 and 56
- respond to MHC class I
- perforation, apoptosis or opsinozation
- normal cell expresses MHC1 and NK ligand which bind to activating receptor and inhibitory receptor normally but when infected the cell will stop expressing MHCI and onlt the activating recptor on NK cell will be bound causing it to kill the cell
18
Q
T helper cells
- Th1: how does it differentiate, cytokines secreted, function
- Th2: how does it differentiate, cytokines secreted, function
- Th17: how does it differentiate, cytokines secreted, function
- T reg: where is it made, what does it secrete, function
A
- IL12 -> IFN gamma, lymphotoxin A; viral/bacterial infection, AI
- IL4 -> 1L4, 5, 10, 13; parasite and asthma/allergy
- IL6, TGF beta -> IL 12, 21; fungal and AI
- made in thymus -> IL 10, TGF beta -> immunosuppression and AI
19
Q
Antigen processing Viral infected cell
- CD8
- macrophage
A
- CD8 cannot recognize as self and will destroy
- macrophage sees antigen -> processes it -> presents on MHC II, secretes IL1 (fever and recruit t cell), secretes IL6 -> MHCII binds to CD4 -> macrophage produced B7 and binds to CD28 on CD4 activating it -> CD4 will activate B cells and CD8 cells
20
Q
MHC
- made up of
- I
- II
A
- alpha subunit and beta subunit
- alpha has binding cleft, embedded in cell membrane
- alpha and beta make up binding cleft and both embedded in cell membrane
