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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
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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 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
Activates Th1 helper cells; Macrophages
Anti glutamate carboxylase and anti insulin
Its a serine protease that activates apoptosis; NK and CD8

2. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Anti topoisomerase
MS
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Receiving preformed Antibodies

3. What are the two signals required for T cells? what happens after?
Basophils! THey want IG E class switch!
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Superficial inguinal
In the germinal center of secondary follicles (In the paler center)

4. Which disease is associated with HLA A3?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Edema and necrosis in that region
Hemochromatosis
IgG

5. What does IL 10 do? who is secreted by?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
MS - hay fever - SLE - goodpastures
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Secretory component

6. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Complement activation (active in both)
Tetanus - Botulinum - HBV - Rabies
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

7. What links the adaptive and innate immunity?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Steroid responsive nephrotic syndrome
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
Complement activation (active in both)

8. What are the autoantibodies for Celiac disease?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Immunosuppression after kidney transplantation
IgG
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

9. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Bind FcG for antibody dependent cellular cytotoxicity
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Superficial inguinal

10. which antibody activate mast cells - basophils - and eosinophils?
IgE
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Cells that stil have weird parts of their membrane that macrophages usually bite off

11. The secondary follicles have __________; primary follicles are dense
pale central germinal centers
Bind FcG for antibody dependent cellular cytotoxicity
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
Immunosuppression after kidney transplantation

12. What do multimeric antibodies require for assembly?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Basophils! THey want IG E class switch!
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
A j chain

13. What lymph node drains the lateral side of the dorsum of the foot?
Macrophages - Dendritic cells - B cells
Popliteal
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
heavy chains

14. which interleukin receptor is required for NK development? activation?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Severe pyogenic infections early in life
IL 15; IL 12 - interferon Beta and interferon alpha
Axillary

15. what ensure that a memory response is generated?
Remove encapsulated bacateria
If there is class switching and plasma cell production (that is when memory cells are produced)
heavy chains
Paracortex; viral infection

16. What is the main function of IL 12? other than macrophages who else can release IL 12?
...
Type IV
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

17. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Paracortex; viral infection
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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

18. what cytokine does basophils secrete?
IL 4
encapsulated
IgM and IgD
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

19. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Paracortex; viral infection
CRP - C3b - IgM

20. What cytokines are released by Th1 cells?
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Interferon gamma and IL 2
Cyclosporine - OKT3

21. What is the common variable immunodeficiency ? How is it different from Brutons?
Para aortic
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T 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

22. what cell surface marker is used for NK cells as it is unique to them?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
IgM and IgG
CD56
lowest concentration

23. which of the hypersensitivity reactions is not Ab mediated?
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!
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Type IV
2 heavy chains and two light chains

24. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Anti alpha subunit 3 of collagen on type IV bm
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
secondary
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

25. what mediates the type II hypersensitivity? What are the two different methods?
CRP - C3b - IgM
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Paracortex
Antibody mediated cytotoxicity; either complement dependent or complement independent

26. What are the cell surface proteins for Macrophages? which two are for opsonins?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
IgG
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
...

27. What is three common causes of severe combined immunodef? What is the result of all three?
Local infection/inflammation; infection of the ln itself; metastasis
MS - hay fever - SLE - goodpastures
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

28. What is the main cytokine that activates eosinophils?
Anti smooth muscle
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
IL 5

29. 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)
SP infections
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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

30. What are the two signals required for B cell class switching? Which is the second signal?
Antihistone
acute phase reactants
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

31. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
CRP - C3b - IgM
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
MHC II - B7
Histamine; post capillary venules - vasodilation

32. what secretes IL 4?
Basophils! THey want IG E class switch!
not Ab mediated
DM type I and RA
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

33. What are the autoantibodies for type I diabetes mellitus?
Superficial inguinal
Anti glutamate carboxylase and anti insulin
Antidote for digoxin intoxication
Liver! (they are proteins circulating in the blood)

34. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
pathogenesis
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Fab portion
Superior mesenteric

35. Name two endogenous pyrogens
IL 1 and IL 6
Anti topoisomerase
Antibody mediated cytotoxicity; either complement dependent or complement independent
Its a serine protease that activates apoptosis; NK and CD8

36. What are MHC's necessary for? By themselves?
TGF beta and IL 10
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
heavy chains
T cell activation; no with CD 4 or CD 8

37. Which diseases are associated with DR4?
IgM and IgG
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
DM type I and RA
Local infection/inflammation; infection of the ln itself; metastasis

38. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Histamine; post capillary venules - vasodilation
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

39. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
DM type I and RA
IgG
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

40. Complements are...
Immunoflourescent staining of tissue biopsies
Antidesmoglein
Anti SS- A (anti RO) and Anti SS- B
acute phase reactants

41. What are the main symptoms of T cell immunodeficiencies?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Its main effect is a defect in Ab opsonization for killing
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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

42. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Cyclosporine - OKT3
lowest concentration

43. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
pale central germinal centers
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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

44. ________ regulate the cell mediated response.
Humoral
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
IgE

45. What cytokines to Th2 secrete?
Antimicrosomal and antithyroglobulin
Its main effect is a defect in Ab opsonization for killing
CRP - C3b - IgM
IL 4 - 5 - 10 - 6

46. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
heavy chains
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

47. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Antibody mediated cytotoxicity; either complement dependent or complement independent
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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

48. what cell surface proteins are on all APCs?
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
type four
MHC II - B7
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

49. Describe the complement independent Type II hypersenstivity reaction. Give an example.
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
active complement pathway
encapsulated

50. What is the main function of IL 8?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Delayed type hypersensitivity
A chemotactic factor for neutrophils
Antidote for digoxin intoxication