Test your basic knowledge |

USMLE Step 1 Immunology

Subjects : 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. give an example of how influenza does a major antigenic shift.
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
RNA segment reassortment
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

2. What are the autoantibodies for polymyositis and dermatomyositis?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
Anti Jo -1

3. which cytokine inhibits TH2 cells? secreted by who?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Interferon gamma; Th1
Liver! (they are proteins circulating in the blood)

4. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
Antihistone

5. What does interferon gamma do? What two type of cells does it attack mostly?
IL 3; supports growth and differentiation of bone marrow stem cells
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
...

6. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
isotype
If there is class switching and plasma cell production (that is when memory cells are produced)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

7. What is the toxicity of azathioprine?
...
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

8. What does it mean if there are igM in the serum at birth?
not Ab mediated
IgG
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

9. What lymph node drains the anal canal (below the pectinate line)?
IgG
Antihistone
Superficial inguinal
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

10. What is the main function of IL 8?
Viral neutralization of igM and IgG!
...
A chemotactic factor for neutrophils
The patient could become cyanotic in the OR!

11. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
carboxy terminal
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Complement activation (active in both)

12. describe the pathogenesis of delayed type IV hypersensitivity
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
The igA found in breast milk
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Macrophages - Dendritic cells - B cells

13. is IgM an opsonizer?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
...
pathogenesis
Negative!

14. What are the cell surface proteins for Macrophages? which two are for opsonins?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Anti viral and anti tumor

15. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Tetanus - Botulinum - HBV - Rabies

16. what cytokine does basophils secrete?
Interferon gamma; Th1
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
IL 4

17. what prevents NK cells from killing normal cells if their default is to kill?
MHC class molecules bind to KIRS or CD94 to prevent killing
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
Cyclosporine - OKT3
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

18. What is a factor that is a predictor for a bad transplantation?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
IgG

19. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
isotype
Cyclosporine - OKT3
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
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

20. What is the common variable immunodeficiency ? How is it different from Brutons?
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

21. What is the marginal zone of the spleen? what happens there?
Antihistone
Inferior mesenteric
TLR ad nuclear receptors
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

22. The two heavy chains of an antibody contribute to the...
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Cytokine IL 10 secreted by Th2
Fab portion
Paracortex

23. IgE has the ___________ in the serum
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
lowest concentration
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Antibody mediated cytotoxicity; either complement dependent or complement independent

24. What is the clinical use of Muromonab?
IL 4
Immunosuppression after kidney transplantation
Th cells fail to produce interferon gamma; a lot of IgE
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

25. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Hereditary angioedema; PNH
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II

26. What are the three types of lymphocytes?
encapsulated
B - T - and NK cells
Negative selection
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

27. What are the main symptoms of B cell immunodeficiencies?
Severe pyogenic infections early in life
SP infections
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

28. What is an example of a parasite showing antigenic variation?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
isotype
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a

29. The MALT/GALT are not...
type four
dimer
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
encapsulated

30. which antibodies prevent antigens from binding mucosal surfaces?
IgA
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
Internal iliac
Negative nitroblue tetrazolium reduction test

31. what secretes IL 4?
IgE; by activating eosinophils
Basophils! THey want IG E class switch!
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
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

32. Which HLA's are included in MHC I? MHC II?

Warning: Invalid argument supplied for foreach() in /var/www/html/basicversity.com/show_quiz.php on line 183

33. Type Iv hypersensitivity is...
delayed!
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
Activates cytotoxic CD 8 T cells as second signal
Anti topoisomerase

34. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Superficial inguinal
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
type four
...

35. What is digoxin immune Fab used for?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
mesenchymal
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Antidote for digoxin intoxication

36. What are target cells?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Cells that stil have weird parts of their membrane that macrophages usually bite off
False! B cell class switching requires a second signal
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

37. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
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
MS - hay fever - SLE - goodpastures
Superior mesenteric

38. What is epo used for?
Anemias (esp due to renal failure)
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

39. What is the mechanism for sirolimus? what else it known as?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Hereditary angioedema; PNH
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
Anti viral and anti tumor

40. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
secondary
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

41. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Alternative splicing of mRNA
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IgE

42. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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 :(
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a

43. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
MHC I - CD16 - CD56
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
MS
A recomb cytokine of IL 2; RCC and metastatic melanoma

44. So antibodies are the effectors for the humoral response. List some of their functions.
Anti smooth muscle
Rheumatic arthritis
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

45. What is the late phase reaction of anaphylaxis allergy? what mediates it?
pale central germinal centers
except hyperacute
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)
TLR ad nuclear receptors

46. What is the cause of thymic aplasia? What is its presentation? What are the labs?
DM type I
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
False! B cell class switching requires a second signal
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a

47. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Activates Th1 helper cells; Macrophages
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

48. What lymph node drains the breast?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Previous transfusion; pregnant woman whose fetus had paternal antigens
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Axillary

49. Name 5 ways Antibody diversity is generated?
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
heavy chains
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

50. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
except hyperacute
All MHC 1/CD8
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)