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 the major functions of Antibodies?
pathogenesis
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
IgM and IgA

2. The MALT/GALT are not...
Steroid responsive nephrotic syndrome
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
All MHC 1/CD8
encapsulated

3. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Influenza; antigenic shift; antigenic drift
acute phase reactants
Not thymus - BM

4. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
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
RNA segment reassortment
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
mesenchymal

5. What does interferon gamma do to be antiviral?
DM type I and RA
Previous transfusion; pregnant woman whose fetus had paternal antigens
Increases expression of MHC I and MHC II and also activates NK cells
CRP - C3b - IgM

6. which interleukin receptor is required for NK development? activation?
IL 15; IL 12 - interferon Beta and interferon alpha
isotype
Anti U1 RNP (ribonucleoprotein)
IgM and IgA

7. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
MS - hay fever - SLE - goodpastures
Previous transfusion; pregnant woman whose fetus had paternal antigens
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

8. What is the pathogenesis of acute transplant rejection? When does it occur?
The igA found in breast milk
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IL 5
Yes

9. Which disease is associated with DR3?
Edema and necrosis in that region
acute phase reactants
Anti topoisomerase
DM type I

10. are Th cells involved in trapping of antigens of endotoxin/LPS?
No because no peptide fragment!
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgM

11. In thymic development - What is the positive selection? negative selections?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
When you select for which MHC it will have; take out the lymphs that self react
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

12. What does granulysin do?
Anti Jo -1
Daclizumab; prevent ACUTE rejection of renal transplant
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

13. In general What are T cells good for?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Anti viral and anti tumor
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

14. What does Interferon alpha and beta do? how?
type four
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

15. What bugs can actually infect the lymph node itself?
In the germinal center of secondary follicles (In the paler center)
Activates cytotoxic CD 8 T cells as second signal
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

16. How is the thymus organized? what happens in each section?
IgG
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

17. What is the presentation of common variable immunodef? and What are the labs?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
MS
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

18. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
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
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
IL 1 and IL 6

19. How do you test for chronic granulomatous disease?
Its a serine protease that activates apoptosis; NK and CD8
Humoral
Negative nitroblue tetrazolium reduction test
...

20. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
Anti SS- A (anti RO) and Anti SS- B
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

21. Describe the complement independent Type II hypersenstivity reaction. Give an example.
By transcytosis
Anti smooth muscle
Popliteal
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

22. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Hemochromatosis
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

23. What is the main function of interferons?
Delayed type hypersensitivity
IgE; by activating eosinophils
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Interferon gamma; Th1

24. What does it mean if there are igM in the serum at birth?
Superficial inguinal
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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

25. what cell surface marker is used for NK cells as it is unique to them?
CD56
Fc
A j chain
type four

26. What is a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
IgAs in mothers breast milk!
Graves
CRP - C3b - IgM

27. What are the function of B cells?
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
Hemochromatosis
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

28. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
CRP - C3b - IgM
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
IgM and IgG

29. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
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
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
pale central germinal centers

30. 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
IgAs in mothers breast milk!
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
2 heavy chains and two light chains

31. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
...
RNA segment reassortment
IL 4 - 5 - 10 - 6

32. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
Increases expression of MHC I and MHC II and also activates NK cells
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
IgA

33. What does IL 5 do?
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
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
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

34. What are the autoantibodies for myasthenia gravis?
IgM and IgD
except hyperacute
Anti Ach receptor
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

35. What are the autoantibodies for autoimmune hepatitis?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Anti smooth muscle
except hyperacute

36. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
B - T - and NK cells
If there is class switching and plasma cell production (that is when memory cells are produced)

37. What cytokines to Th2 secrete?
TNF alpha and IL1
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
IL 4 - 5 - 10 - 6
Paracortex; viral infection

38. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
IL 1 and IL 6
Anemias (esp due to renal failure)

39. which antibody is involved in the primary response or immediate response to an antigen?
lowest concentration
CRP - C3b - IgM
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
IgM

40. Describe the capsular structure of a lymph node; What are the functions of the LN?
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
Yes
Previous transfusion; pregnant woman whose fetus had paternal antigens
Activate macrophages

41. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Celiac
Chronic granulomatous disease
RNA segment reassortment

42. What are the autoantibodies for graves?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Anti TSh receptor
IgM
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

43. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
S. aureus - E. Coli - aspergillus
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
not Ab mediated

44. 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)
Anti alpha subunit 3 of collagen on type IV bm
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
Inferior mesenteric

45. is IgM an opsonizer?
encapsulated
Negative!
lowest concentration
Cross link

46. in which immunodef order do you see a lot of pus? no pus?
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

47. What are the autoantibodies for Celiac disease?
TLR ad nuclear receptors
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

48. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
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
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Remove encapsulated bacateria
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

49. What is the mechanism for sirolimus? what else it known as?
Activates Th1 helper cells; Macrophages
Recom IL 11; thrombocytopenia
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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

50. What are the autoantibodies for sjorgens syndrome?
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anti viral and anti tumor
Anti SS- A (anti RO) and Anti SS- B