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 is recomb gamma interferon used for?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Chronic granulomatous disease
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
heavy chains

2. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
carboxy terminal
Anti SS- A (anti RO) and Anti SS- B
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

3. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Receiving preformed Antibodies
cannot cross placenta
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
NK cells

4. What are the cell surface proteins for Macrophages? which two are for opsonins?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

5. What is immune complex disease? give an example.
Negative!
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
TGF beta and IL 10
IgM and IgD

6. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
carboxy terminal
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

7. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Histamine; post capillary venules - vasodilation
Para aortic
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

8. What are MHC's necessary for? By themselves?
Anti topoisomerase
T cell activation; no with CD 4 or CD 8
IgM and IgG
Interferon gamma and IL 2

9. What lymph node drains the stomach?
Celiac
TGF beta and IL 10
pentamer
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)

10. In general What are T cells good for?
IL 4 - 5 - 10 - 6
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
delayed!
Anti viral and anti tumor

11. What kinds of receptors activate innate immunity?
Anti SS- A (anti RO) and Anti SS- B
TLR ad nuclear receptors
Superior mesenteric
Secretory component

12. What does IgA pick up from epithelial cells before being secreted?
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
Secretory component
A - B - C; all the D's
IgM and IgA

13. What is the receptor for EBV? On what cells is that located?
Activate macrophages
Carbohydrate
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Inferior mesenteric

14. What are some catalase positive organisms?
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
IgAs in mothers breast milk!
Anti U1 RNP (ribonucleoprotein)
S. aureus - E. Coli - aspergillus

15. what results in symptoms of shock in an acute hemolytic transfusion reaction?
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
T cell dysfunction
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

16. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Paracortex; viral infection

17. What does it mean if there are igM in the serum at birth?
Histamine; post capillary venules - vasodilation
TGF beta and IL 10
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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

18. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Anti mitochondrial
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

19. when can graft versus host disease? What is the result?
MHC class molecules bind to KIRS or CD94 to prevent killing
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
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

20. What is recomb beta interferon used for?
MS
Fab portion
Cross link
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

21. Which disease is associated with HLA A3?
Hemochromatosis
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Receiving preformed Antibodies
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

22. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
IgAs in mothers breast milk!
Anti U1 RNP (ribonucleoprotein)

23. What are the main cell surface proteins on B cells?
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
MS

24. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
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
...
opsonizes

25. What are some sinopulmonary infections?
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
Tetanus - Botulinum - HBV - Rabies
isotype
Sinusitis - otitis media - pneumonia

26. IgM can fix complement but...
cannot cross placenta
Anti U1 RNP (ribonucleoprotein)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Superficial inguinal

27. What lymph node drains the sigmoid colon?
Humoral
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
Negative selection
Inferior mesenteric

28. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Liver! (they are proteins circulating in the blood)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
CD56

29. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
IL 3; supports growth and differentiation of bone marrow stem cells
...

30. The idiotype; the Fc portion determines the...
isotype
A j chain
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
neutrophilia!

31. Which diseases are associated with DR5?
TLR ad nuclear receptors
Antidesmoglein
Superficial inguinal
Pernicious Anemia and Hashimotos

32. What links the adaptive and innate immunity?
Activates Th1 helper cells; Macrophages
Complement activation (active in both)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
A recomb cytokine of IL 2; RCC and metastatic melanoma

33. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
IgG
Antidote for digoxin intoxication
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
CD21 on B cells (although there is T cell lymphocytosis in EBV)

34. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Influenza; antigenic shift; antigenic drift
Glycoproteins; HLA
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

35. what prevents NK cells from killing normal cells if their default is to kill?
IL 4 - 5 - 10 - 6
MHC class molecules bind to KIRS or CD94 to prevent killing
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Wiskott Aldrich syndrome

36. In thymic development - What is the positive selection? negative selections?
If there is class switching and plasma cell production (that is when memory cells are produced)
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
Anti topoisomerase
When you select for which MHC it will have; take out the lymphs that self react

37. where do somatic hypermutation and class switching occur?
Stimulate the liver to release acute phase reactants
In the germinal center of secondary follicles (In the paler center)
dimer
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

38. 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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
type four
Th2; Th1

39. What lymph node drains the breast?
Complement activation (active in both)
Activates cytotoxic CD 8 T cells as second signal
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Axillary

40. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Antimicrosomal and antithyroglobulin
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Activates Th1 helper cells; Macrophages
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

41. What cytokines to Th2 secrete?
Interferon gamma and IL 2
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
IL 4 - 5 - 10 - 6
Interferon gamma; Th1

42. What is the cause of thymic aplasia? What is its presentation? What are the labs?
mesenchymal
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 II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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

43. Describe the capsular structure of a lymph node; What are the functions of the LN?
Cyclosporine - OKT3
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

44. What is the toxicity of azathioprine?
Interferon gamma; Th1
...
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

45. Leukocyte adhesion defect presents with...
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Negative!
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
neutrophilia!

46. can igG cross the placenta?
IgE; by activating eosinophils
TGF beta and IL 10
Wiskott Aldrich syndrome
Yes

47. What are the major functions of Antibodies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

48. What is the pathogenesis of a candida skin test?
Barrel hoop basement membrane fenestrations
TLR ad nuclear receptors
Delayed type hypersensitivity
Antidesmoglein

49. What lymph node drains the scrotum?
IgG
Superficial inguinal
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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

50. What is Aldesleukin? What is it used for
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
A recomb cytokine of IL 2; RCC and metastatic melanoma
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Secretory component