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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. what cell surface marker is used for NK cells as it is unique to them?
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
Anti glutamate carboxylase and anti insulin
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
CD56

2. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Acts as second signal on B cells to induce class switching to IgE and IgG
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

3. What lymph node drains the anal canal (below the pectinate line)?
2 heavy chains and two light chains
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Liver! (they are proteins circulating in the blood)
Superficial inguinal

4. Which antibody mediates immunity to worms? how?
When you select for which MHC it will have; take out the lymphs that self react
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
IgE; by activating eosinophils
Antidesmoglein

5. What is a factor that is a predictor for a bad transplantation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
delayed!
Negative selection

6. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
Macrophages - Dendritic cells - B cells
Remove encapsulated bacateria

7. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
IgE; by activating eosinophils
Anti smooth muscle
T cell activation; no with CD 4 or CD 8
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

8. How is the thymus organized? what happens in each section?
Influenza; antigenic shift; antigenic drift
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

9. In general What are T cells good for?
NK cells
IgM and IgA
Anti viral and anti tumor
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

10. What is digoxin immune Fab used for?
Hereditary angioedema; PNH
By transcytosis
Antidote for digoxin intoxication
Anti topoisomerase

11. What is filgrastim and sargramostim? and What is it used for?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Basophils! THey want IG E class switch!
Anti topoisomerase
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

12. which antibodies can bind complement?
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
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
IgM and IgG
Cells that stil have weird parts of their membrane that macrophages usually bite off

13. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
The igA found in breast milk
Fab portion

14. Describe the Mannose Lectin pathway
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
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!
Activates Th1 helper cells; Macrophages
acute phase reactants

15. What is the common variable immunodeficiency ? How is it different from Brutons?
Anti mitochondrial
Fab portion
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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

16. What are the main symptoms of T cell immunodeficiencies?
The patient could become cyanotic in the OR!
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Antihistone
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

17. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Cyclosporine - OKT3

18. What is the toxicity of muromonab?
Receiving preformed Antibodies
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
IgM and IgD
The patient could become cyanotic in the OR!

19. where do somatic hypermutation and class switching occur?
MS - hay fever - SLE - goodpastures
In the germinal center of secondary follicles (In the paler center)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

20. What is a type I hypersensitivity reaction? What is atopic?
TNF alpha and IL1
Glycoproteins; HLA
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

21. What are the main cell surface proteins on B cells?
Increases expression of MHC I and MHC II and also activates NK cells
The patient could become cyanotic in the OR!
NK cells
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

22. is IgM an opsonizer?
Chronic granulomatous disease
Negative!
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
TGF beta and IL 10

23. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
Chronic granulomatous disease
IL 1 and IL 6
Histamine; post capillary venules - vasodilation

24. What are the autoantibodies for Celiac disease?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Influenza; antigenic shift; antigenic drift

25. which of the transplant rejections is antibody mediated? why does it occur?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Negative nitroblue tetrazolium reduction test
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
carboxy terminal

26. What is hereditary angioedema? What are the C3 levels?
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
except hyperacute
The igA found in breast milk
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

27. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
not Ab mediated
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
pathogenesis

28. What is the main cytokine that activates eosinophils?
IL 5
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

29. Type Iv hypersensitivity is...
delayed!
mesenchymal
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

30. What are the two signals required for B cell class switching? Which is the second signal?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Fc
Activates Th1 helper cells; Macrophages
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

31. From where do cytokines come from?
Rheumatic arthritis
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
Lymphocytes
T cell dysfunction

32. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
MHC II - B7
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

33. 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)?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
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
Viral neutralization of igM and IgG!

34. which of the hypersensitivity reactions is not Ab mediated?
Type IV
CD56
Active; passive - fast but short half life (3 weeks!)
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

35. What are some sinopulmonary infections?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Sinusitis - otitis media - pneumonia

36. What are superantigens? give two examples.
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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

37. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Lymphocytes
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
C5a

38. Type IV hypersensitivity is i...
not Ab mediated
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
IgA
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

39. what will NK cells do to cells covered in IgG Ab? why?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
The patient could become cyanotic in the OR!
Kill them because they have CD16 on them that recognize the FcG portion
Cross link

40. How do you test for chronic granulomatous disease?
Anti smooth muscle
Pernicious Anemia and Hashimotos
IgG
Negative nitroblue tetrazolium reduction test

41. are Th cells involved in trapping of antigens of endotoxin/LPS?
Fc
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
No because no peptide fragment!
Cross link

42. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
Activate macrophages

43. What does IL 5 do?
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
Its main effect is a defect in Ab opsonization for killing
IgM and IgA
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

44. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IgE
Thrombocytopenia
IgE; by activating eosinophils

45. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
MHC I; from RER with help of the B2 microglobulin
neutrophilia!
Histamine; post capillary venules - vasodilation
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

46. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Daclizumab; prevent ACUTE rejection of renal transplant
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

47. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
IgE
Glycoproteins; HLA
pentamer
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

48. IgM can fix complement but...
Viral neutralization of igM and IgG!
cannot cross placenta
Liver! (they are proteins circulating in the blood)
S. aureus - E. Coli - aspergillus

49. Give three examples of bacteria that use antigenic variation and how.
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Anti glutamate carboxylase and anti insulin
carboxy terminal

50. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
Its a serine protease that activates apoptosis; NK and CD8
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

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USMLE Step 1 Immunology

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