Inmunology Flashcards
1
Q
Deficiency associated with Neisserial infections:
A
Complement factors C5-C9
Because Neisseria has a very thin wall
2
Q
PGs, histamine, bradykinin and serotonin functions:
A
Vasodilation (arteriole)
Increased vascular permeability (post-capillary venule by perycite contraction)
Bradykinin and PGE2 contribute to pain!
PGs are released by arachidonic acid metabolism
Histamine is released by basophils, mast cells and platelets
Bradykinin is released by the kinin cascade, it dilates the arterioles but constricts the veins
Serotonin is released by the brain, GI and platelets
3
Q
Leukotrienes function:
A
Contraction:
Vasoconstriction
Bronchospasm
Increased vascular permeability (pericyte contraction)
4
Q
Complement functions:
A
C3a, C4a and C5a: trigger histamine release form mast cells, involved in anaphylaxis (anaphylatoxins)
C5a: attracts neutrophils
C3b: opsonin for phagocytosis and clear inmune response
C5b+C6-C9 from the membrane attack complex (hole)
5
Q
Thromboxane A2 function:
A
Made by platelets
Platelet aggregation!!
Vasoconstriction; contributes to angina!
Opposite to PGI2 prostacyclin
6
Q
IL4 (IL13) function and origin:
A
Made by T helper 2
Increases T helper 2 on the inflammation site
Inhibits T helper 1
Activates class switching to IgE, abundant in atopic disorders
IL13 is associated with minimal change disease!
7
Q
INF gamma function and origin:
A
Made by T helper 1
Recruits and activates macrophages
Converts macrophages into epithelioid histiocytes in granuloma (quantiferon test)
Activates T helper 1
Inhibits T helper 2
Activates class switching to IgG
Increases expression of MHC 1 and 2 in cells
Activates NK (together with IL12)
8
Q
Leukotriene B4 and IL-8 function and origin:
A
IL8 is made by macrophages and epithelial cells
LTB4 comes from the mb phospholipids of macrophages, neutrophils, mast cells that break and start the arachidonic acid cascade
Chemotactic, call neutrophils to go to the antigen site. Neutrophils come before (B4)
9
Q
IL2 function and origin:
A
Made by T helper 1
Increases proliferation of lymphocytes: CD4, CD8 and NKs! and monocytes. Aldeskeukin in tto of renal cell ca. and melanoma
Induce secretion of INF gamma, abundant in granulomatous diseases
10
Q
Tissue damage that leads to abscess formation is due to:
A
Lysosomal enzymes released by neutrophils and macrophages
11
Q
Type 4 hypersensitivity is mediated by:
A
T helper 1 (activated by IL12 through T-bet)
T helper 17 (activated by IL23 through ROR gamma T)
It is delayed
12
Q
IL5 function and origin:
A
Made by T helper 2 and mast cells
Helps eosinophils (type 1 hypersensitivity, atopic disorders as asthma)
Helps TGF beta to class switch to IgA
13
Q
IL12 function and origin:
A
Made by macrophages and B cells
Promotes differentiation of T helper cells into T helper 1 (important in granuloma and psoriasis)
Activates natural killer cells (together with INF-gamma)
With IL2 activates CD8+ cytotoxic T cells
14
Q
IL10 function and origin:
A
Made by T helper 2 and Tregs
Shuts down T helper 1: ↓IL2, INFγ, MHC2, dendritic cells and macrophages
15
Q
TGF-beta function and origin:
A
Made by platelets, macrophages, lymphocytes and mast cells
Tissue regeneration and repair, promotes differentiation of fibroblasts into myofibroblasts (fibroblast growth factor, active after burns and during scaring, contributes to keloids)
Activates class switching to IgA (also IL-5)
16
Q
Where is CD14 and what recognizes?
A
On all phagocytes (macrophages)
Recognizes lipopolysaccharide on gram - bacteria
17
Q
NF-kappaB function:
A
Activates synthesis of immune mediators when toll-like receptors are activated, is a transcription factor.
Secretes: IL1, TNF-alpha, IL6, IL8 and IL12
18
Q
PGE2 function:
A
Mediates pain and fever
Maintains the patency of the ductus arteriosus (we give alprostadil as a drug to maintain PDA that is actually PGE1)
19
Q
PGI2 function:
A
Also called prostacyclin, made by the endothelium
Inhibits platelet aggregation!!
Vasodilation
Opposite to TXA2
20
Q
Substances that attract neutrophils, important for migration:
A
Endogenous:
Leukotriene B4: +potent
IL8 (by macrophages, persistent acute inflammation)
C5a! the A!
Kallikrein! (SILK: C5a, IL8, LTB4, kallikrein)
Fibropeptides
5-HETE (leukotriene precursor)
Exogenous: Bacterial products (N-formyl methionyl peptides)
21
Q
What causes mast cell activation?
A
Trauma
C3a and C5a
Cross linking of IgE by antigen
22
Q
Mediators of vasodilation:
A
Histamine (also swelling)
PGs
Bradykinin (it dilates the arterioles but constricts the veins)
23
Q
Macrophages production of IL-1 and TNF-alpha causes:
A
Increases COX activity in the hypothalamus which increases PGE2 to cause fever.
TNF-alpha causes cachexia, insulin resistance and increases capillary permeability (leads to ARDS and shock in sepsis)
IL-1 activates osteoclasts
Think SYSTEMIC inflammation!!
Abundant in rheumatoid arthritis
24
Q
IL-1 function and origin:
A
Made by monocytes, macrophages, B cells, dendritic cells, endothelium…
Neutrophils rolling and adhesion (increases endothelial ICAMs)
Actives the hypothalamus for fever
Activates T helper, B cells and NK
25
Leukocyte adhesion deficiency; cause and presentation:
Defect in CD18 (beta 2 chain) of LFA-1 integrin
| Omphalitis, difficult wound healing, necrotic lesions, increased circulating neutrophils and no pus
26
Chediak-Higashi syndrome; cause and presentation:
```
Microtubule defect due to CHS1/LYST protein
Pyogenic infections (no phagolysosomes)
Neutropenia (no neutrophil division)
Giant granules in leukocytes
Defective platelets
Albinism
Peripheral neuropathy
So abnormal phagocytes, NK cells and cytotoxic T lymphocytes
```
27
Chronic granulomatous disease; cause and presentation:
NADPH oxidase defect (colorless/ yellow/ negative nitroblue tetrazolium test)
Catalase + infections: PLACES Pseudomona, Listeria, Aspergillus, mucor, Candida, cryptococcus, enterobacteriae as E. coli, S. aureus, burkholderia cepacia, serratia (osteomyelitis), nocardia
Tto: INF-gamma
28
CD4+ T cells recognize:
MHC class II (4*2=8)
29
CD8+ T cells recognize:
MHC class I (8*1=8)
30
Where is MHC II and which antigens carries?
Is on antigen presenting cells, carries extracellular antigens
31
Where is MHC I and which antigens carries?
Is on all nucleated cells and platelets, carries intracellular antigens
32
T cells flight:
T helper 1: intracellular
T helper 2: parasitic
T helper 17: extracellular bacteria and fungi
33
Causes of severe combined immunodeficiency:
IL-2 receptor defects (X-linked) 50%
JAK-STAT signaling deficit (recessive)
Adenosine deaminase deficiency (buildup of dATP that inhibits de novo deoxynucleotides synthesis) (recessive)
Rag mutations (recessive)
MHC II deficiency (CD4+ helper T cannot help maturation of B and T cells) (recessive)
34
Deficit and common infections in X-linked (Burton) agammaglobulina:
Btk deficiency: no B cells in blood, all Ig low, but a lot of immature preB in bone marrow
T cells are fine
They get bacterial, enterovirus and Giardia infections
Onset in kid
35
Main characteristics of common variable immunodeficiency:
B cells ok but all Ig low and decreasing
Increased risk of autoimmune disease and lymphoma
Onset at teens-20s
36
Pathophysiology of X-linked hyper-IgM sd:
```
The activation of naïve IgM is good but mutated CD40 LIGAND (CD154) on T cell so no class switching of B cell: you get a lot of IgM but not IgA, IgG and IgE (mucosal infections)
X-linked recessive (actually there is a rare CD40 deficiency that is AR)
```
Onset in kid
37
C5-C9 completament deficiency causes:
Neisseria (gonorrhoeae and meningitidis) infections
38
C1 inhibitor deficiency causes:
Edema of skin and mucosas (periorbital)
39
What type of hypersensitivity is lupus? what are it's key plasma findings?
Type 3, antigen-antibody complexes that activate complement
Low lymphocytes
Low C3 and C4
Mild thormbocytopenia
Increased gamma globulin production
40
Antibodies for lupus:
More specific:
Anti-dsDNA: prognostic and renal disease activity indicator; in 70%
Anti-Smith: pathognomonic but just in 30%
More sensitive: ANAs; in 95-100%
```
Others:
Antiphospholipid
Anti-ribonucleoprotein P (psychosis)
Anti-histones (drug induced HIP)
Anti-SSA (Ro) IgG that can cause heart block in the baby
Low early complement C1q, C4 and C2
```
41
Which is the most common renal damage in lupus? what is its imaging? Which is the most common pulmonary damage in lupus?
Renal:
Type 4: diffuse proliferative glomerulonephritis (type of nephritic sd.) also the most severe
LM: Wire looping
IF: granular; IgG and C3 deposition
EM: sub-ENDOthelial (capillary loops get thick making the wire loop)
Pulmonary:
Interstitial lung disease
42
Cause of nephrotic sd. in lupus and imaging:
Type 5: membranous glomerulonephritis
LM: silver stain, membrane thickening
IF: granular; IgG and C3 deposition
EM: spike and dome, sub-EPIthelial
43
What type of hypersensitivity is sjögren sd?
Type 4, lymphocyte (cell) mediated
44
Specific antibodies and histology for Sjögren sd:
ANA and anti-ribonucleoprotein! (SSA form mom to baby can cause congenital heart block)
Lymphocytic infiltrates often with germinal centers (periductal in focal lymphocytic sialadenitis!!)
45
Specific antibodies for limited sclerodermia:
Anti-Centromere
46
Specific antibodies for diffuse sclerodermia:
More specific: Anti-DNA topoisomerase 1 (anti-Scl-70 antibody)
Anti-RNA polymerase 3
47
Specific antibodies and clinic in mixed connective tissue disease:
U1 ribonucleoprotein: most specific
ANA and rheumatoid factor
Clinic is a mixtures of SLE, systemic sclerosis and polymyositis
48
TGF-alpha function:
Epithelial and fibroblast growth factor for wound healing
TGF-beta is also a fibroblast growth factor
49
Name 2 angiogenic growth factors? and 4 activators of fibroblasts?
Angiogenic:
VEGF
Fibroblast GF!!! FGF
Fibroblasts (trichrome, reticulin staining): in chrirrosis, nodular sclerosis, sclerodermia:
IL1
TGF-β (thanks goddess for fibrosis baby)
PDGF (important for the migration of smooth m. cells into in atherosclerosis)
FGF
50
Causes of eosinophilia:
Allergy, asthma (type I hypersensitivity)
Parasites
Hodgkin mixed cellularity (IL5)
Chung-Strauss
Chronic adrenal insufficiency
Myeloproliferative disorders (+ basophils in CML)
51
IL-6 function and origin:
Made by monocytes, macrophages, T helper 2 and bone marrow
Stimulates plasma cell growth and antibody production. It is high in mieloma multiple (but it is IL1 who causes the lytic lesions in MM)
Induces synthesis of acute phase reactants
Increases hepcidin that binds to ferroportin to trap iron in macrophages (ferritin increases) and decrease absorption
52
Important T lymphocyte marker:
CD3 (important for signal transduction)
Also CD2, CD4, CD8
53
Important B lymphocyte markers:
CD19, CD20 and CD21
Also CD40
54
Important macrophage markers:
CD14 (binds to TLR-4 in LPS of gram negative bacteria). Is in all phagocytes
CD16 (Fc receptor for Fc of IgG). On macrophages, NKs and neutrophils
Macrophages are tennagers
55
What is secreted by T helper 2 cells as in asthma (type 1 hypersensitivity), parasitic infection or lepromatous leprosy?
IL4 and IL13: IgE class switching
IL5:eosinophils and helps INF-beta to IgA class switching
IL10: shuts down T helper 1 and activates T helper 2
56
Functions of the three subtypes of CD4+ T cells:
T helper 1: intracellular; secrete INF-gamma and activate macrophages and IgG class switching (antibody-dependent)
T helper 2: parasitic; secrete IL5 to activate eosinophils and IgA class switching (with INF-beta), IL4 and 13 for IgE class switching (antibody-dependent)
T helper 17: bacteria and fungi; secrete IL17 and IL22 to call neutrophils and increase cell binding to contain infection
57
Live viral vaccines examples and what inmune response do they activate:
MMR (measles, mumps and rubella)
Varicella
Rotavirus
...
Activate both humoral (B cells) and cell mediated (T cells) responses
58
Killed viral vaccines examples and what inmune response do they activate:
Rest In Piece Always:
Rabies
Influenza
Polio
Hepatitis A
Activate just humoral (B cells) response because there is no peptide to present in MHC 2 to T cells so the B cell activation is T-independent: IgM
59
What type of hypersensitivity is poststreptococcal glomerulonephritis and imaging:
Type III, inmune complexes
LM: hyper-cellular
IF: lumpy-bumpy; granular starry sky; IgG, C3 and ¡¡IgM!! deposition
EM: sub-epithelial
60
What type of hypersensitivity is type I diabetes?
Type IV, beta cell destruction by T lymphocytes
61
Characteristics of hyperacute graft rejection:
Happens within min-hours
Due to preformed IgG ANTIBODIES (previous transplant, multiple pregnancies)
Antibodies activate COMPLEMENT causing fibrinoid necrosis, thrombosis and ischemia
Predominant neutrophils
62
Characteristics of accelerated graft rejection:
Happens within days
Due to previously sensitized T cells (memory)
Parenchymal damage and endothelialitis
63
Characteristics of acute graft rejection:
Happens within weeks-up to 1 year
Due to T cells and antibodies activated by MHC1 and 2 mismatch (nr celular and humoral immunity)
```
Celular:
Predominant lymphocytes
Endotheliitis, tubulitis
Patchy infiltrates if lung
Treat with cyclosporin, basilizumab...
```
Humoral: Do not choose it unless very obvious
Necrotizing vasculitis
Complement deposition, low Cd4
Treat with rituximab
DD in kidney:
Neutrophils and fever: pyelonephritis, prevent with TMP-SMX
Acute kidney failure with no inflammatory cells: cyclosporin toxicity, take cyclosporin out
64
Characteristics of chronic graft rejection:
Happens within months-years; gradually
Smooth m. proliferation, FIBROSIS!!!! and mononuclear infiltration
Heart: accelerated aterosclerosis
Lung: bronchiolitis obliterans (small airway obstruction)
Liver: vanishing bile duct sd. (loss of ducts)
Kidney: nephropathy with interstitial fibrosis, atrophy, vascular thickening and therefore luminal narrowing, can show basement membrane splitting
65
Cells affected by Chediak-Higashi sd:
Phagocytes
NK cells
Cytotoxic T lymphocytes
66
Treatment of chronic granulomatous disease:
INF-gamma
67
Examples of type 1 hypersensitivity:
```
Allergic rhinitis
Anaphylaxis
Food allergies
Wheal and flare: allergy test
Asthma
```
68
Examples of type 2 cytotoxic hypersensitivity:
```
Acute hemolytic anemia (as erythroblastosis fetalis)
Acute rheumatic fever
Goodpasture
Transfusion reaction!!! transtwosion
Autoimmune thrombocytopenic purpura
Pemphigoid
```
69
Examples of type 2 non-cytotoxic hypersensitivity:
Myasthenia
Graves
Type 2 DM
Pernicious anemia
70
Examples of type 3 hypersensitivity:
Vasculitis, nephritis, arthritis
```
SLE
Post strep glomerulonephritis
Arthus reaction!!! Arthree
Serum sickness
Polyarteritis nodosa
```
71
Examples of type 4 hypersensitivity:
```
Stevens-Johnson
Tuberculin test, intracellular organisms
Contact dermatitis (nickel, poison ivy)
Hashimoto
MS
Rheumatoid arthritis
Type 1 DM
Guilliam-Barré
Crohn
```
72
What does TLR-2 recognizes?
Peptidoglycan
73
What does TLR-4 recognizes?
LPS of gram negative
74
TLR that recognize extracellular targets:
TLR-1,2,4,5,6
75
TLR that recognize intracellular targets:
TLR-3,7,8 (DNA and RNA form viruses) 9 (intracellular/non-cleared bacteria)
76
Therapeutic functions of INF:
INF-alpha: hepatitis, hairy B cell leukemia, CML, kaposi sarcoma
INF-beta: MS
INF-gamma: chronic granulomatous disease
77
Major criteria for rheumatic fever:
J❤️NES:
```
Joint, arthritis
❤️ carditis
Nodules, subcutaneous
Erythema marginatum
Sydenham chorea
```
78
Cytokines overproduced in toxic shock sd:
INF-gamma and IL2 form T helper 1
IL1, TNF-alpha and IL6 form macrophages
79
Wiskott-Aldrich sd; cause and presentation:
WAS mutation so cells can’t recognize actin cytoskeleton
X linked
Thrombocytopenia: few small platelets causing purpura
Eczema
Immunodeficiency: low IgM high IgE and IgA
Increased risk of non-Hodgkin lymphoma
80
Selective IgA deficiency; cause and presentation:
Unknown. Most frequent
```
Low IgA and high IgE
Atopy
Giardia infections
Risk for blood transfusion reaction (IgE anti IgA antibodies→ anaphylaxis)
Can give false positive beta-hCG
```
Onset in 20-30s
81
IL-7 function and origin:
Made by marrow and thymus
Induces differentiation into lymphocytes (NK, T helper and T cytotoxic)
82
IL-3 function and origin:
Made by T helper and NK cells
Induces differentiation into myeloid precursors with GMCSF
83
Which part of the complement pathway is activated in the presence of inmune complexes?
Classical; activated when IgM and IgG bind to C1
C3b removes the immune complexes
84
Test used to determine HLA-1 expression for transplant:
Microcytotoxicity test
85
What is Arthus reaction and what type of hypersensitivity is it?
Swelling after a vaccine (protein inoculation for which there are pre-existing antibodies)
Type 3 (even if it is localized)
86
How does the body react to parasitic infection?
IL4 —> GATA3 —> T helper 2 —> IL4, IL13 —> Class switching to IgE —> mast cell degranulation, basophils and eosinophils (through IL5) attack
87
Name B cells immunodeficiencies:
Burton
Selective IgA deficiency
Common variable immunodeficiency
88
Name T cell immunodeficiencies:
Thymic aplasia
IL-12 deficiency
Job sd (AD hyper-IgE)
Chronic mucocutaneous candidiasis
89
Which Coombs is for the mom and which for the baby?
Direct for the baby. Antigen
| Indirect for the mom. Antibody
90
Splenectomy is a risk factor for which type of pathogens?
```
Encapsulated
Blood parasites (babesia)
```
91
Important Treg marker:
CD25
92
Important NK markers:
CD56
CD16
All NK markers have 6 on them
93
Name 3 important opsonins:
Fc portion of IgG
C3b
Collectins= mannose-binding lectin
C reactive protein
94
Deficiency associated with encapsulated infections:
Complement factor C3
| No spleen
95
Antibodies for antiphospholipid syndrome:
```
Lupus anticoagulant (long PTT)
Anticardiolipin (false VDRL)
Anti-beta2 glycoprotein 1
```
If you see a long PTT in someone with lupus think about antiphospholipid syndrome, they will actually be at risk of thrombosis not of bleeding!!
96
Type I hypersensitivity is mediated by:
```
T helper 2 (activated by IL4 through GATA 3)
IL4 and IL13 induce class switching to IgE
```
97
Cosignal needed to activate T cells and B cells:
B7(CD80/CD86)-CD28 (Antigen presenting - T cell): needed to activate T cells
B7 for T cells!
CD40 Ligand-CD40 (T cell - B cell): needed to activate B cells for class switching and memory Abs
98
Specific antibodies for polymyositis and dermatomyositis:
Anti-Jo-1 (tRNA synthase)
Anti-SRP (signal recognition particle)
Anti-Mi2 (helicase)
99
What does seroconversion mean?
Class-switching, you test for this with western blot to look for antibodies
100
Specific antibodies, HLAs and histology for Hashimoto:
Anti-thyroid peroxidase (antimicrosomal), hypo
Antithyroglobulin
DR3, DR5
Hürthle cells and germinal centers; lymphocytic infiltration!!!
Does not hurt vs de Queravain (Queravain=pain)
101
Specific antibodies, HLAs and histology for Graves:
Thyroid-stimulating immunoglobulin (TSI) also called Long-acting Thyroid Stimulator antibodies (LATS), hyper
DR3, B8
Crowded follicles and scalloped colloid
102
Specific antibodies and HLAs for Celiac disease:
IgA anti-tissue transglutaminase (enz that deaminates gliadin)
anti-endomysial
anti-deaminated gliadin peptide
DQ2, DQ8, DR3
103
Specific antibodies and HLAs for DM1:
Anti-glutamic acid decarboxylase (anti-GAD)
DR3, DR4, DR3/4, DQ (DR3+DM1=DR4)
DR2 is associated with less DM1!
104
Which immunodeficiencies are X-linked?
Burton agammaglobulina (no B cells)
Hyper-IgM (a lot of IgM but not the other Igs)
SCID due to IL-2 receptor defects (↓NK ↓T cells)
Wiskott-Aldrich (thrombocytopenia+ezema)
Chronic granulomatous disease (catalase +)
105
Which cytokines cause vascular leak, DIC, insulin resistance and cachexia? how can your treat it?
Insulin resistance and cachexia because it reduces utilization of FA (also IL-1 and INF-gamma); you can give megestrol acetate to stimulate appetite
Vascular leak leads to septic shock and ARDS
Hypercoagulability because it kills tumors by causing coagulation and necrosis; hypercoagulability can lead to DIC
106
Specific antibodies and histology for primary biliary cholangitis:
Anti-mitochondrial
| Lymphocytic inflammation of the bile ducts+granulomas
107
Specific antibodies and HLAs for rheumatoid arthritis:
```
More specific: Alpha-cyclin citrullinated peptide (alpha-CCP)
Rheumatoid factor (IgM against the Fc portion of IgG). Big one eats the small one!
```
DR4!!!
108
Difference between papain, pepsin and monoclonal antibodies:
Papain: can bind to antigen but cannot cross-link (agglutinate) or activate complement. Fab + Fcx2
Pepsin: can bind to antigen and cross-link (agglutinate) because of the F(ab')2. Fc is digested so it cannot activate complement. F(ab')2 + digested Fc
Monoclonals can cross-link (agglutinate = precipitate)
109
IL-11 function:
Helps megakaryocytes to differentiate into platelets
Oprelvekin is IL-11 for myelosuppression due to QT
110
Substances secreted by mast cells and basophils:
Basophils: heparin, histamine and leukotrienes
Mast cells: heparin, histamine, eosinophil chemotactic factor and tryptase
111
Specific antibodies for pemphigus vulgaris:
Pemphigus: Ab against DESMOsomal DESMOsglein 1 and 3 (a cadherin)
Pemphigoid: BPAg1 and 2 Ab against hemidesmosomal dystonin
112
Specific antibodies for autoimmune hepatitis? What is the pathology?
Anti smooth muscle antibodies
Hypergammaglobulinemia
Micro: portal and periportal lymphocytic and plasma cell infiltration
113
What is the main mediator of cirrhosis?
TGF-β secreted by stellate cells
114
What are the consequences of a defect in TAP1?
TAP are transporter associated with antigen processing proteins, if they do not work you cannot load peptides in MHC class 1!!! so you will have ↓CD8 and nr CD4 as in bare lymphocyte sd type 1
115
Name positive and negative acute phase reactants:
```
Positive: More FFiSH in the C
FIBRINOGEN
Ferritin
Serum Amyloid A
Hepcidin
CRP
```
Alos ceruloplasmin, haptoglobin, vWF, complement, erythrocyte sedimentation rate
Negative:
ALBUMIN, prealbumin (transthyretin)
transferrin
PROCALCITONIN is + in BACTERIAL infections and - in viral!!!
116
Immunologic changes with age:
↓ NAIVE B and T cells: ↓ memory to NEW antigens
Phagocytosis and antigen presentation: ↓ memory to NEW antigens
Immune response to previously exposed antigens is intact because old memory cells remain ok bur can be some ↓ in preformed antibodies as ↓ IgM ABO antibody synthesis ↓ response to transfussions
↓ ability of neutrophils to cause apoptosis: delayed healing
↑ marrow fat and ↓ mass ↓ cell diversity and response to cytokines ↓ capacity of making new RBCs
117
Factor 12 Hageman function:
Coagulation and fibrinolysis activation (makes and breaks cloths, DIC)
Complement activation
Kinin cascade activation that ↑bradykinin
118
Which cells express CD4 on their surface?
Same ones attacked by HIV:
T helper cells (HIV uses CXCR4 and CCR5 as coreceptors)
Macrophages (HIV uses CCR5 as coreceptor, it hides in macrophages) and langerhans
Dendritic cells
R5 viruses use CCR5 and X4 viruses use CXCR4 so cannot infect macrophages
R5 is the one that is typically transmitted then mutates to X4 and progresses in the body
119
IL important in psoriasis:
IL12
| IL23
120
IL important in rheumatoid arthritis:
IL1 (fx ↓ by anakinra)
TNF-alpha (fx ↓ by adalimumab, etanercept)
Choose them when you don't know!
121
Receptors needed for margination (endothelium ↔ leukocyte):
Selectins (E,P -prefromed 1st to show up-) ↔ Sialyl Lewis
122
Receptors needed for adhesion (endothelium ↔ leukocyte):
ICAM-1 ↔ Integrin 18 β2 (CD11=LFA-1=Mac-1)
| VCAM-1 ↔ Integrin VLA-4
123
Receptors needed for diapedesis (endothelium ↔ leukocyte):
PECAM-1 (CD31) ↔ PECAM-1 (CD31)
Vascular marker
If the Passport (Pecam) matches you can go in
124
Which diseases are associated with HLA-B8 and DR3?
Addison and graves
B8 is associated with Addison, myasthenia and graves (don't Be late8 Dr. ADDISON or you will send MY patient to the GRAVE)
125
Which particle is associated with signal transduction in T helper cells?
CD3: signal transduction!! in both helper and cytotoxic T cells
CD4 and CD8 are to interact with MHCs
126
Define inmune privilege and give an example:
Inmune privileged organs (eyes and testes) are separate form the rest of the body and have some self antigens. After trauma they can release their antigens and this will cause an T cell response against those organs called sympathetic ophthalmia.
Even if the trauma is unilateral (for example one eye) the inmune response is bilateral (in both eyes).
127
DD. between lepromatous and tuberculoid leprosy:
Forget about the clinical signs
Tuberculoid: positive lepromin, induration! Th1, M1
Lepromatous: acid fast bacilli on lesions negative lepromin! Th2, M2
128
Large ovoid cells with eccentric nuclei refer to:
Plasma cells
129
Function of epidermal growth factor, fibroblast growth factor and platelet derived growth factor:
EGF: growth by TK, expressed by tumor cells
FGF: angiogenesis FA!
PDGF: fibroblasts and vascular remodeling
130
Why don't we need the thymus in adults?
Because the lymphocytes that mature in the thymus are long lived
131
How do you differentiate between drug side effect, acute rejection or infection as cause of a complication after transplant rejection?
Renal hypoperfusion, HT, tubular vacuolization!!!, no inflammatory cells: drug
Lymphocytes, tubulitis: acute rejection
Neutrophils (PMNs): infection
132
How do you make a conjugate vaccine?
Polysaccharide conjugated with protein fragment (to induce T dependent immune response)
Polysaccharide is a starch not a protein
133
What do CCR5 and CXCR-4 stand for? What is their fuction
CD4 is the HIV receptor CCR5 and CXCR-4 are the coreceptors
CCR5: Cysteine-cysteine chemokine receptor 5, also known as CD195 (Maraviroc is a chemokine receptor antagonist)
CXCR-4: C-X-C chemokine receptor type 4, also known as fusin or CD184
They are CHEMOKINE receptors and act as CORECEPTORS, they allow the conformation change in pg120 to show gp41 for FUSION (enfuvirtide blocks gp41)
134
What is the mechanism of Hep B vacccine? and the mechanism of the flu shoot?
Hep B vaccine: it is recombined HBsAg that allows the body to make anti-HBs antibodies so they IMPAIR VIRION ENTRY into hepatocytes
Flu vaccine: Stimulates the formation of neutralizing antibodies against hemagglutinin so they IMPAIR VIRION ENTRY into cells
135
Name two markers or mast cell activation:
Histamine
| Tryptase
136
What is the function of the peyer patches?
Place of presentation of antigens to the B cells
137
In which infections can you use passive immunization?
Tetanus, botulism, hep B, varicella and rabies
138
What is high at the early and late stage of an allergic reaction?
Early: mast cells
Late: eosinophils
Mast cells degranulate, producing histamine which attracts eosinophils. The early stage of an allergic reaction is mast cell mediated, but the late stage (including mucus production) is mediated by eosinophils
139
How would you explain that a recombinant or live vaccine does not generate IgG on certain healthy people?
MHCs of those individuals cannot recognize the polypeptides presented, this is possible because MHCs do not undergo somatic hypermutation
140
Specific HLA for narcolepsy:
DQB1
| tto: sodium oxybate, modafinil, amphetamines
141
What is CD95 and where is missing?
CD95 (Fas) receptors are death receptors that activate the extrinsic pathway of apoptosis
They are missing in autoimmune lymphoproliferative syndrome (autoimmunity)
