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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.
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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. How is the thymus organized? what happens in each section?
Anti IF
Antimicrosomal and antithyroglobulin
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
Hereditary angioedema; PNH

2. What does IL 4 do?
A - B - C; all the D's
Acts as second signal on B cells to induce class switching to IgE and IgG
Anti IF
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

3. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
pathogenesis
Lymphocytes
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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

4. The pathogenesis of contact dermatitis is ________ hypersensitivity
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
type four
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
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)

5. What are superantigens? give two examples.
Secretory component
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Recom IL 11; thrombocytopenia

6. Which is the most abundant antibody in blood?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Th2; Th1
IgG

7. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
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
IgG
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
Cross link

8. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
secondary
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

9. What is colostrum?
Active; passive - fast but short half life (3 weeks!)
The igA found in breast milk
IgG
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

10. What does interferon gamma do? What two type of cells does it attack mostly?
Its main effect is a defect in Ab opsonization for killing
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
cannot cross placenta

11. describe the classic complement pathway.
Superficial inguinal
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
DM type I and RA
IL 4 - 5 - 10 - 6

12. ________ regulate the cell mediated response.
Daclizumab; prevent ACUTE rejection of renal transplant
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
IgM and IgA
Humoral

13. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Acts as second signal on B cells to induce class switching to IgE and IgG
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Edema and necrosis in that region
A chemotactic factor for neutrophils

14. what cell surface marker is used for NK cells as it is unique to them?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
CD56
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

15. What is the defect in hyper IgM syndrome? What are the lab results?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Type IV

16. What are the cell surface proteins on NK cells?
RNA segment reassortment
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
MHC I - CD16 - CD56
...

17. What are the two signals required for Th1 cells? what happens after then activated?
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
Graves
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Delayed type hypersensitivity

18. What lymph node drains the stomach?
Fc
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Celiac
dimer

19. What lymph node drains the thigh?
IgM and IgD
Active; passive - fast but short half life (3 weeks!)
T cell activation; no with CD 4 or CD 8
Superficial inguinal

20. What links the adaptive and innate immunity?
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
The igA found in breast milk
Complement activation (active in both)
Yes

21. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Negative!
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

22. What is the general structure of an Ab?
Antidesmoglein
2 heavy chains and two light chains
Type IV
IL 5

23. A lymph node is a ________ lymphoid organ.
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Basophils! THey want IG E class switch!
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
secondary

24. What are the three types of APCs?
Acts as second signal on B cells to induce class switching to IgE and IgG
Macrophages - Dendritic cells - B cells
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
The patient could become cyanotic in the OR!

25. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Local infection/inflammation; infection of the ln itself; metastasis

26. What is hereditary angioedema? What are the C3 levels?
When you select for which MHC it will have; take out the lymphs that self react
IgM and IgD
DM type I
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

27. What is three common causes of severe combined immunodef? What is the result of all three?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
IgM and IgD
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
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 filgrastim and sargramostim? and What is it used for?
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
except hyperacute
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

29. Which MHC presents intracellular peptides? how so?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
MHC I; from RER with help of the B2 microglobulin
Interferon gamma and IL 2
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

30. which interleukin receptor is required for NK development? activation?
IL 15; IL 12 - interferon Beta and interferon alpha
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

31. The alternative pathway is the only constutively...
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
active complement pathway
S. aureus - E. Coli - aspergillus
dimer

32. which type of immunity is slow but long lasting? as opposed to...
IgM and IgA
Rheumatic arthritis
Active; passive - fast but short half life (3 weeks!)
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)

33. What does IL 2 do?
encapsulated
Activates cytotoxic CD 8 T cells as second signal
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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

34. what bacteria are a splenectomy patient most susceptible to? why?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

35. Name the three opsonins
If there is class switching and plasma cell production (that is when memory cells are produced)
acute phase reactants
CRP - C3b - IgM
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

36. What are the autoantibodies for sjorgens syndrome?
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti SS- A (anti RO) and Anti SS- B
The patient could become cyanotic in the OR!

37. What are the autoantibodies for systemic sclerosis?
A chemotactic factor for neutrophils
Anti topoisomerase
Th cells fail to produce interferon gamma; a lot of IgE
type four

38. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Axillary

39. Give an example of someone who could get hyperacute transplant rejection.
Histamine; post capillary venules - vasodilation
TNF alpha and IL1
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Previous transfusion; pregnant woman whose fetus had paternal antigens

40. What are the main cell surface proteins on B cells?
IgM and IgA
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Antidesmoglein

41. Which disease is associated with DR3?
DM type I
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Severe pyogenic infections early in life

42. What is thrombopoietin used for?
Interferon gamma; Th1
Activate macrophages
Cross link
Thrombocytopenia

43. Give three examples of bacteria that use antigenic variation and how.
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
...
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

44. What is recomb gamma interferon used for?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Chronic granulomatous disease
IgE

45. What are four results of a splenectomy?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Steroid responsive nephrotic syndrome
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

46. Which cytokines do Th2 release and For what?
Axillary
DM type I and RA
Its a serine protease that activates apoptosis; NK and CD8
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

47. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IgE; by activating eosinophils
IgG

48. what cell surface proteins are on all APCs?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Active; passive - fast but short half life (3 weeks!)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
MHC II - B7

49. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Negative selection
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

50. What are the autoantibodies for pernicious anemia?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Anti IF
NK cells
Anti viral and anti tumor