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Test your basic knowledge |
USMLE Step 1 Immunology
Start Test
Study First
Subjects
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health-sciences
,
usmle-step-1
Instructions:
Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can
study here
.
Match each statement with the correct term.
Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.
This is a study tool. The 3 wrong answers for each question are randomly chosen from answers to other questions. So, you might find at times the answers obvious, but you will see it re-enforces your understanding as you take the test each time.
1. IgE has the ___________ in the serum
mesenchymal
Hereditary angioedema; PNH
IL 4 - 5 - 10 - 6
lowest concentration
2. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Daclizumab; prevent ACUTE rejection of renal transplant
Thrombocytopenia
Th2; Th1
Paracortex; viral infection
3. Type IV hypersensitivity is i...
not Ab mediated
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IgAs in mothers breast milk!
4. what characterizes an arthus reaction?
active complement pathway
Edema and necrosis in that region
All MHC 1/CD8
Anti viral and anti tumor
5. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
IL 4 - 5 - 10 - 6
not Ab mediated
Give a vaccine with a peptide comp from it that the cell mediated immunity otherwise cant get to! like h.influenzae vaccine. then class switching and memory response can occur
Th cells fail to produce interferon gamma; a lot of IgE
6. So antibodies are the effectors for the humoral response. List some of their functions.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Fab portion
Paracortex
CD21 on B cells (although there is T cell lymphocytosis in EBV)
7. what secretes IL 4?
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
CD56
Basophils! THey want IG E class switch!
8. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
MHC class molecules bind to KIRS or CD94 to prevent killing
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
9. What can cause a lymph node enlargement?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Local infection/inflammation; infection of the ln itself; metastasis
When you select for which MHC it will have; take out the lymphs that self react
Humoral
10. What happens in a deficiency of C3?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Anti topoisomerase
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
11. Other than stimulating fever - what else does IL 6 do?
Stimulate the liver to release acute phase reactants
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
MHC class molecules bind to KIRS or CD94 to prevent killing
12. The secondary follicles have __________; primary follicles are dense
Type IV
Severe pyogenic infections early in life
pale central germinal centers
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti
13. What is the common variable immunodeficiency ? How is it different from Brutons?
Carbohydrate
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
Cross link
IgM and IgG
14. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
neutrophilia!
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
Paracortex
15. what cytokine does basophils secrete?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
IL 4
Chronic granulomatous disease
MHC II - B7
16. What are C1 - C2 - C3 - C4 important for?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Viral neutralization of igM and IgG!
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
IL 4 - 5 - 10 - 6
17. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Sinusitis - otitis media - pneumonia
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
18. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
Para aortic
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Bind FcG for antibody dependent cellular cytotoxicity
19. What is recomb gamma interferon used for?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Chronic granulomatous disease
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
20. What are the autoantibodies for graves?
Anti TSh receptor
T cell dysfunction
Bind FcG for antibody dependent cellular cytotoxicity
Activate macrophages
21. What is serum sickness? give an example.
Anti topoisomerase
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
Liver! (they are proteins circulating in the blood)
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
22. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
The patient could become cyanotic in the OR!
Lymphocytes
Sinusitis - otitis media - pneumonia
23. What are the autoantibodies for wegeners granulomatosis?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Brain - eyes - placenta/fetus - testicles; because they can have an antigen in there and not get attacked by immune system because dont have contact with immune system via blood and lymph; if an infection occurs such that trauma results in exposure t
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
24. The ______ in the BM are DN - the DP are in the cortex of thymus
T cell precursor
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
heavy chains
IgG
25. What is the treatment of acute transplant rejection?
Cyclosporine - OKT3
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti
pathogenesis
26. What lymph node drains the duodenum - jejunum?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Superior mesenteric
27. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
carboxy terminal
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
28. What is the pathogenesis of a hypersensitivity reaction?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
encapsulated
29. What does CD16 on NK cells do?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
Superficial inguinal
Bind FcG for antibody dependent cellular cytotoxicity
30. What are the main cell surface proteins on B cells?
Stimulate the liver to release acute phase reactants
All MHC 1/CD8
Secretory component
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
31. What is digoxin immune Fab used for?
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig
Antidote for digoxin intoxication
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton
32. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Alternative splicing of mRNA
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep
33. __________ are a part of the innate system.
NK cells
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
34. The two heavy chains of an antibody contribute to the...
Fab portion
Glycoproteins; HLA
2 heavy chains and two light chains
Negative nitroblue tetrazolium reduction test
35. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
DM type I
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Cells that stil have weird parts of their membrane that macrophages usually bite off
36. What are the cell surface proteins for Macrophages? which two are for opsonins?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
MHC I - CD16 - CD56
37. What does granzyme do? who secretes it?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Its a serine protease that activates apoptosis; NK and CD8
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Basophils! THey want IG E class switch!
38. How do you test for type III hypersensitivity?
Antidesmoglein
Immunoflourescent staining of tissue biopsies
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in
IgM and IgD
39. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Chronic granulomatous disease
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
40. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
Anti alpha subunit 3 of collagen on type IV bm
Local infection/inflammation; infection of the ln itself; metastasis
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
41. What lymph node drains the stomach?
Anti U1 RNP (ribonucleoprotein)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Celiac
Immunoflourescent staining of tissue biopsies
42. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
...
43. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig
Barrel hoop basement membrane fenestrations
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Thrombocytopenia
44. where do NK cells develop?
Anti Jo -1
Influenza; antigenic shift; antigenic drift
Not thymus - BM
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
45. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Negative!
Immunoflourescent staining of tissue biopsies
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
cannot cross placenta
46. Which MHC presents intracellular peptides? how so?
In the germinal center of secondary follicles (In the paler center)
dimer
IL 3; supports growth and differentiation of bone marrow stem cells
MHC I; from RER with help of the B2 microglobulin
47. IgM can exist as a _______ also
IgG
pentamer
Th2; Th1
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
48. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway
Rheumatic arthritis
Negative nitroblue tetrazolium reduction test
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
49. Name 5 ways Antibody diversity is generated?
pentamer
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
50. what cell surface marker is used for NK cells as it is unique to them?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
MS
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
CD56