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. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Antidote for digoxin intoxication
acute phase reactants
Glycoproteins; HLA
Remove encapsulated bacateria

2. What are the autoantibodies for myasthenia gravis?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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
Th cells fail to produce interferon gamma; a lot of IgE
Anti Ach receptor

3. Type IV hypersensitivity is i...
Anti IF
MHC II - B7
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
not Ab mediated

4. What are the three types of APCs?
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
IgM and IgG
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Macrophages - Dendritic cells - B cells

5. What are the autoantibodies for hashimotos?
IgM and IgG
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
Antimicrosomal and antithyroglobulin
T cell precursor

6. Which MHC presents intracellular peptides? how so?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Antimicrosomal and antithyroglobulin
MHC I; from RER with help of the B2 microglobulin
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

7. Which disease is associated with HLA A3?
IL 3; supports growth and differentiation of bone marrow stem cells
2 heavy chains and two light chains
Hemochromatosis
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

8. what cell surface proteins are on all APCs?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
MHC II - B7
The igA found in breast milk

9. 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
Yes
pentamer
No because no peptide fragment!

10. What are C1 - C2 - C3 - C4 important for?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Viral neutralization of igM and IgG!
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

11. Which disease is associated withB B27?
T cell dysfunction
...
Axillary
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

12. What is the pathogenesis of a hypersensitivity reaction?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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
Superficial inguinal
Antidesmoglein

13. What does Interferon alpha and beta do? how?
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
carboxy terminal

14. In general What are T cells good for?
Anti smooth muscle
Anti viral and anti tumor
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

15. 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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
IgM and IgD
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

16. What is the main function of interferons?
MHC II - B7
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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
IgM and IgG

17. What lymph node drains the thigh?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Superficial inguinal
False! B cell class switching requires a second signal
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

18. What does interferon gamma do to be antiviral?
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
Anti alpha subunit 3 of collagen on type IV bm
Increases expression of MHC I and MHC II and also activates NK cells
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

19. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
...
MS
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Active; passive - fast but short half life (3 weeks!)

20. What is the autoantibody for SLE that is nonspecific? Specific?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IL 3; supports growth and differentiation of bone marrow stem cells
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Antidote for digoxin intoxication

21. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
Severe pyogenic infections early in life
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

22. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
Complement activation (active in both)
The patient could become cyanotic in the OR!

23. What does IL 4 do?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Stimulate the liver to release acute phase reactants
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 :(
Acts as second signal on B cells to induce class switching to IgE and IgG

24. For which toxins are preformed antibodies (passive) given?
Stimulate the liver to release acute phase reactants
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Tetanus - Botulinum - HBV - Rabies

25. What is the main function of TNF alpha? How does it do this?
Negative selection
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
IgM and IgA
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

26. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Superficial inguinal
Rheumatic arthritis
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

27. Describe the Mannose Lectin pathway
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 :(
Edema and necrosis in that region
Negative!
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

28. What type of side chains are found on Fc region of an antibody?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Carbohydrate
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
Chronic granulomatous disease

29. Which antibody mediates immunity to worms? how?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
IgE; by activating eosinophils
opsonizes

30. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
MHC I; from RER with help of the B2 microglobulin
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

31. What is the white pulp of the spleen?
False! B cell class switching requires a second signal
Anti Ach receptor
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

32. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Cross link
MS
Local infection/inflammation; infection of the ln itself; metastasis

33. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Its main effect is a defect in Ab opsonization for killing
pentamer
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

34. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
lowest concentration
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
All MHC 1/CD8
isotype

35. What is the late phase reaction of anaphylaxis allergy? what mediates it?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
When you select for which MHC it will have; take out the lymphs that self react
Secretory component
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)

36. Monomer in circulation - ___ when secreted
dimer
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 :(
Secretory component
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

37. What is hereditary angioedema? What are the C3 levels?
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
The igA found in breast milk
Barrel hoop basement membrane fenestrations

38. Which disease is associated with B8?
By transcytosis
TLR ad nuclear receptors
Graves
except hyperacute

39. What is the mechanism for sirolimus? what else it known as?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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
MHC I - CD16 - CD56
mesenchymal

40. IgE has the ___________ in the serum
lowest concentration
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Liver! (they are proteins circulating in the blood)
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!

41. What are the function of B cells?
IgM and IgG
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Activates cytotoxic CD 8 T cells as second signal
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

42. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
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
IgM
B - T - and NK cells
Activate macrophages

43. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Fc
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

44. To what portion of the Antibody do the complements bind?
Interferon gamma and IL 2
Daclizumab; prevent ACUTE rejection of renal transplant
Fc
Remove encapsulated bacateria

45. which type of immunity is slow but long lasting? as opposed to...
Active; passive - fast but short half life (3 weeks!)
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
Edema and necrosis in that region
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

46. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
mesenchymal
Anti mitochondrial
Th cells fail to produce interferon gamma; a lot of IgE

47. IgM can exist as a _______ also
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
pentamer
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
heavy chains

48. What are the cell surface proteins for Macrophages? which two are for opsonins?
Anti TSh receptor
Antihistone
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Its a serine protease that activates apoptosis; NK and CD8

49. what ensure that a memory response is generated?
acute phase reactants
If there is class switching and plasma cell production (that is when memory cells are produced)
IL 5
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

50. What is recomb beta interferon used for?
MS
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
acute phase reactants