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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. The Fc region is found on the...
Pernicious Anemia and Hashimotos
IL 15; IL 12 - interferon Beta and interferon alpha
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
carboxy terminal

2. other than C3a - what other complement acts as an anaphyloxin?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Antidote for digoxin intoxication
C5a
Axillary

3. What are the autoantibodies for sjorgens syndrome?
carboxy terminal
Anti SS- A (anti RO) and Anti SS- B
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
IL 5

4. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Paracortex; viral infection
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

5. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
SP infections
2 heavy chains and two light chains

6. What cytokines to Th2 secrete?
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
IL 4 - 5 - 10 - 6
Interferon gamma and IL 2
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

7. How is the thymus organized? what happens in each section?
Cytokine IL 10 secreted by Th2
MS
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
cannot cross placenta

8. What are the main symptoms of T cell immunodeficiencies?
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
carboxy terminal
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

9. which antibodies prevent antigens from binding mucosal surfaces?
Local infection/inflammation; infection of the ln itself; metastasis
IgA
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)
pale central germinal centers

10. What kinds of receptors activate innate immunity?
pale central germinal centers
Negative selection
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
TLR ad nuclear receptors

11. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
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
active complement pathway
Superficial inguinal
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

12. How does igA cross the epithelium?
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
A recomb cytokine of IL 2; RCC and metastatic melanoma
By transcytosis
Rheumatic arthritis

13. What are the three types of APCs?
Macrophages - Dendritic cells - B cells
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
S. aureus - E. Coli - aspergillus

14. What cytokines are released by Th1 cells?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
S. aureus - E. Coli - aspergillus
Interferon gamma and IL 2

15. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

16. How do you test for type III hypersensitivity?
Viral neutralization of igM and IgG!
Immunoflourescent staining of tissue biopsies
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Macrophages - Dendritic cells - B cells

17. What bugs can actually infect the lymph node itself?
Thrombocytopenia
Cytokine IL 10 secreted by Th2
Yes
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

18. 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
Anti topoisomerase
Anti smooth muscle
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

19. is IgM an opsonizer?
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
Negative!

20. What are the main Cell surface proteins on T cells?
Immunosuppression after kidney transplantation
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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

21. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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

22. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Negative selection
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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
Superficial inguinal

23. Only the _______ contribute to the Fc region
heavy chains
Antidesmoglein
Negative nitroblue tetrazolium reduction test
IgG

24. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
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
Hereditary angioedema; PNH

25. Leukocyte adhesion defect presents with...
neutrophilia!
IL 1 and IL 6
Complement activation (active in both)
Interferon gamma; Th1

26. What portion of the lymph node is not well developed in DiGeorge Syndrome?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
dimer
Paracortex
Negative!

27. What is the main cytokine that activates eosinophils?
Previous transfusion; pregnant woman whose fetus had paternal antigens
IL 5
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)

28. Monomer in circulation - ___ when secreted
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
carboxy terminal
dimer
C5a

29. What is the presentation of hyperIgM syndrome?
Hemochromatosis
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Severe pyogenic infections early in life
IgG

30. The lymphocytes are ________ origin
mesenchymal
IgM and IgG
Para aortic
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

31. what cell surface marker is used for NK cells as it is unique to them?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
pentamer
CD56
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

32. Which disease is associated with B8?
Graves
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
The igA found in breast milk

33. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Pernicious Anemia and Hashimotos
Not thymus - BM

34. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
SP infections
...
Lymphocytes
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

35. What are the PALS?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T 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
IgM and IgD
encapsulated

36. What lymph node drains the scrotum?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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
mesenchymal
Superficial inguinal

37. Which cytokines do Th2 release and For what?
Axillary
MS
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

38. How is sirolimus different from tacrolimus?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
pentamer
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
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

39. How do you test for chronic granulomatous disease?
except hyperacute
Cells that stil have weird parts of their membrane that macrophages usually bite off
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Negative nitroblue tetrazolium reduction test

40. other than eat and bite RBCs what else do Macrophages of spleen do>
T cell precursor
Remove encapsulated bacateria
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Wiskott Aldrich syndrome

41. Name the three opsonins
CRP - C3b - IgM
T cell activation; no with CD 4 or CD 8
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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

42. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Antimicrosomal and antithyroglobulin
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
Superior mesenteric
Bind FcG for antibody dependent cellular cytotoxicity

43. what ensure that a memory response is generated?
If there is class switching and plasma cell production (that is when memory cells are produced)
IgE; by activating eosinophils
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
IgA

44. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Type IV
Lymphocytes
TNF alpha and IL1
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

45. __________ are a part of the innate system.
Macrophages - Dendritic cells - B cells
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
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
NK cells

46. What is the toxicity of muromonab?
Severe pyogenic infections early in life
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

47. What are target cells?
Anti U1 RNP (ribonucleoprotein)
Antidote for digoxin intoxication
Cells that stil have weird parts of their membrane that macrophages usually bite off
opsonizes

48. What does interferon gamma do? What two type of cells does it attack mostly?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Interferon gamma and IL 2
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

49. What is epo used for?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Anemias (esp due to renal failure)
Anti SS- A (anti RO) and Anti SS- B
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

50. What are the main symptoms of B cell immunodeficiencies?
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
SP infections
Glycoproteins; HLA
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