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. IgG...
IgE; by activating eosinophils
opsonizes
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
B - T - and NK cells

2. 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
Complement activation (active in both)
pathogenesis
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

3. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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!

4. What is recomb beta interferon used for?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
MS
When you select for which MHC it will have; take out the lymphs that self react
IgM

5. What lymph node drains the sigmoid colon?
Its main effect is a defect in Ab opsonization for killing
Inferior mesenteric
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
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

6. Name 5 ways Antibody diversity is generated?
S. aureus - E. Coli - aspergillus
No because no peptide fragment!
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
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

7. what cell surface marker is used for NK cells as it is unique to them?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
CD56
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti IF

8. A lymph node is a ________ lymphoid organ.
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
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
secondary
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

9. What links the adaptive and innate immunity?
IgA
Complement activation (active in both)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

10. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Celiac
Tetanus - Botulinum - HBV - Rabies
Cross link
IL 4

11. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
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)
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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
Cross link

12. What are the main symptoms of T cell immunodeficiencies?
delayed!
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Edema and necrosis in that region
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

13. So antibodies are the effectors for the humoral response. List some of their functions.
Anti TSh receptor
TLR ad nuclear receptors
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Its main effect is a defect in Ab opsonization for killing

14. What does granulysin do?
Anti Ach receptor
IgAs in mothers breast milk!
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Give a vaccine with a peptide comp from it that the cell mediated immunity otherwise cant get to! like h.influenzae vaccine. then class switching and memory response can occur

15. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Inferior mesenteric
Activate macrophages
IgM and IgA

16. What bugs can actually infect the lymph node itself?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
2 heavy chains and two light chains
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
Its main effect is a defect in Ab opsonization for killing

17. What is the receptor for EBV? On what cells is that located?
IL 4 - 5 - 10 - 6
CD21 on B cells (although there is T cell lymphocytosis in EBV)
In the germinal center of secondary follicles (In the paler center)
Viral neutralization of igM and IgG!

18. What is the defect in hyper IgM syndrome? What are the lab results?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
TGF beta and IL 10
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

19. What do mature naive B lymphocytes express?
S. aureus - E. Coli - aspergillus
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
IgM and IgD
Axillary

20. which B and T cell disorder presents with specifically low IgM?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Wiskott Aldrich syndrome
False! B cell class switching requires a second signal
Antidesmoglein

21. what prevents NK cells from killing normal cells if their default is to kill?
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
MHC class molecules bind to KIRS or CD94 to prevent killing
DM type I and RA
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

22. Leukocyte adhesion defect presents with...
neutrophilia!
Para aortic
MS
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

23. 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).
Wiskott Aldrich syndrome
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!
CRP - C3b - IgM
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

24. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
IgAs in mothers breast milk!
TNF alpha and IL1
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

25. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Bind FcG for antibody dependent cellular cytotoxicity
Fc
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
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)

26. What cytokines to Th2 secrete?
Lymphocytes
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Antidote for digoxin intoxication
IL 4 - 5 - 10 - 6

27. What is anergy? why does this occur?
All MHC 1/CD8
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Anti Jo -1

28. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Steroid responsive nephrotic syndrome
RNA segment reassortment
...

29. Which MHC presents intracellular peptides? how so?
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
MHC I; from RER with help of the B2 microglobulin
Anti Jo -1
Severe pyogenic infections early in life

30. How is the antigen loaded onto a MHC II?
Edema and necrosis in that region
IL 5
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
Paracortex

31. Which diseases are associated with DR4?
Th cells fail to produce interferon gamma; a lot of IgE
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
By transcytosis
DM type I and RA

32. What are the autoantibodies for polymyositis and dermatomyositis?
Superficial inguinal
Anti Jo -1
Yes
IL 5

33. What does IL 10 do? who is secreted by?
Alternative splicing of mRNA
Antidesmoglein
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 :(
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

34. What is the pathology seen in chronic transplant rejection?
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Type IV

35. What is the pathology of acute transplant rejection? is it reversible?
Increases expression of MHC I and MHC II and also activates NK cells
Delayed type hypersensitivity
Immunosuppression after kidney transplantation
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

36. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Hereditary angioedema; PNH
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

37. What is the white pulp of the spleen?
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anti SS- A (anti RO) and Anti SS- B

38. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
T cell activation; no with CD 4 or CD 8
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

39. Only the _______ contribute to the Fc region
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
heavy chains
Yes
Liver! (they are proteins circulating in the blood)

40. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

41. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Alternative splicing of mRNA
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 :(
Histamine; post capillary venules - vasodilation
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

42. which antibodies can bind complement?
IgM and IgG
2 heavy chains and two light chains
Macrophages - Dendritic cells - B cells
IL 5

43. What is digoxin immune Fab used for?
MHC I; from RER with help of the B2 microglobulin
Antidote for digoxin intoxication
IL 3; supports growth and differentiation of bone marrow stem cells
Antihistone

44. What are the autoantibodies for sjorgens syndrome?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Anti SS- A (anti RO) and Anti SS- B
CD56

45. Which disease is associated with HLA A3?
Lymphocytes
MHC II - B7
Hemochromatosis
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

46. How do you test for chronic granulomatous disease?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
SP infections
Negative nitroblue tetrazolium reduction test

47. What lymph node drains the scrotum?
Superficial inguinal
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

48. How is the thymus organized? what happens in each section?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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
IgE
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

49. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
pentamer
Thrombocytopenia
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

50. What is the main cytokine that activates eosinophils?
Viral neutralization of igM and IgG!
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
IL 5