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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
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1. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
IL 5
IgM and IgD

2. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
Anti Jo -1
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Yes

3. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
All MHC 1/CD8
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

4. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
When you select for which MHC it will have; take out the lymphs that self react
Cytokine IL 10 secreted by Th2
carboxy terminal

5. which antibodies can bind complement?
opsonizes
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
Local infection/inflammation; infection of the ln itself; metastasis
IgM and IgG

6. What do multimeric antibodies require for assembly?
Inferior mesenteric
A j chain
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

7. Describe complement dependent Type II hypersensitivity. Give an example.
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
T cell dysfunction
TLR ad nuclear receptors
isotype

8. What does IL 4 do?
Anti SS- A (anti RO) and Anti SS- B
Acts as second signal on B cells to induce class switching to IgE and IgG
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
Sinusitis - otitis media - pneumonia

9. What is the receptor for EBV? On what cells is that located?
Humoral
Th cells fail to produce interferon gamma; a lot of IgE
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

10. What are the main symptoms of T cell immunodeficiencies?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IgM and IgA

11. What is thrombopoietin used for?
C5a
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
TNF alpha and IL1
Thrombocytopenia

12. What is the common variable immunodeficiency ? How is it different from Brutons?
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Acts as second signal on B cells to induce class switching to IgE and IgG
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

13. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Negative!
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

14. Which is the main antibody in the delayed or secondary response to an antigen?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
IgG
Anemias (esp due to renal failure)
Antimicrosomal and antithyroglobulin

15. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Yes
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
Negative nitroblue tetrazolium reduction test

16. What are the main Cell surface proteins on T cells?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Not thymus - BM

17. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

18. What is three common causes of severe combined immunodef? What is the result of all three?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Activate macrophages
mesenchymal
pentamer

19. So antibodies are the effectors for the humoral response. List some of their functions.
The patient could become cyanotic in the OR!
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
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

20. How is the antigen loaded onto a MHC II?
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
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
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

21. what prevents NK cells from killing normal cells if their default is to kill?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IgM and IgD
MHC class molecules bind to KIRS or CD94 to prevent killing
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

22. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
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
Not thymus - BM

23. other than C3a - what other complement acts as an anaphyloxin?
Previous transfusion; pregnant woman whose fetus had paternal antigens
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
C5a
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

24. Which helper T cells' development is induced by IL 4? IL 12?
type four
Th2; Th1
Activates cytotoxic CD 8 T cells as second signal
MS - hay fever - SLE - goodpastures

25. What is the main cytokine released by T cells? What does it do
Popliteal
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
IL 3; supports growth and differentiation of bone marrow stem cells
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

26. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Its main effect is a defect in Ab opsonization for killing
cannot cross placenta
secondary

27. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
T cell precursor
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

28. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Anti IF
IL 4
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

29. is IgM an opsonizer?
Negative!
...
Anti Ach receptor
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

30. What lymph node drains the lateral side of the dorsum of the foot?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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
Popliteal
Activate macrophages

31. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Tetanus - Botulinum - HBV - Rabies
secondary
except hyperacute

32. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Macrophages - Dendritic cells - B cells
Histamine; post capillary venules - vasodilation
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
IgE

33. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
False! B cell class switching requires a second signal
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

34. What are superantigens? give two examples.
Basophils! THey want IG E class switch!
Remove encapsulated bacateria
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

35. The lymphocytes are ________ origin
Its a serine protease that activates apoptosis; NK and CD8
mesenchymal
Anti glutamate carboxylase and anti insulin
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

36. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Influenza; antigenic shift; antigenic drift
Thrombocytopenia
DM type I
A chemotactic factor for neutrophils

37. which cells have more complete tolerance - B or T cells?
T
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
MS - hay fever - SLE - goodpastures
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

38. Which HLA's are included in MHC I? MHC II?
A - B - C; all the D's
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Paracortex; viral infection
IgM

39. What are some catalase positive organisms?
IgM
S. aureus - E. Coli - aspergillus
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
MHC class molecules bind to KIRS or CD94 to prevent killing

40. What are the autoantibodies for systemic sclerosis?
IgE
IgA
Anti topoisomerase
Axillary

41. what happens in a deficiency of C1 esterase inhibitor? DAF?
Its a serine protease that activates apoptosis; NK and CD8
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
Kill them because they have CD16 on them that recognize the FcG portion
Hereditary angioedema; PNH

42. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
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
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Cytokine IL 10 secreted by Th2

43. What are the autoantibodies for other vasculitides?
IgG
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

44. What is the most common example of passive immunity?
IgAs in mothers breast milk!
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
isotype
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

45. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
lowest concentration
Immunoflourescent staining of tissue biopsies

46. Other than stimulating fever - what else does IL 6 do?
Daclizumab; prevent ACUTE rejection of renal transplant
Cross link
Stimulate the liver to release acute phase reactants
MHC class molecules bind to KIRS or CD94 to prevent killing

47. What does granzyme do? who secretes it?
Activates cytotoxic CD 8 T cells as second signal
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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

48. Which is the main antibody that provides passive immunity to infants?
IL 3; supports growth and differentiation of bone marrow stem cells
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
carboxy terminal
IgG

49. What lymph node drains the stomach?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Celiac
Its main effect is a defect in Ab opsonization for killing
MHC I; from RER with help of the B2 microglobulin

50. What lymph node drains the breast?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Axillary
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
...

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