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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. hat is the presentation of Jobs syndrome or Hyper IgE?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
IgA
MHC I; from RER with help of the B2 microglobulin

2. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
acute phase reactants
Axillary
Stimulate the liver to release acute phase reactants
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

3. What is the pathology in hyperacute transplant rejection?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
2 heavy chains and two light chains
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
acute phase reactants

4. What does IL 2 do?
Activates cytotoxic CD 8 T cells as second signal
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)
lowest concentration
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

5. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Anti viral and anti tumor
mesenchymal

6. What does IgA pick up from epithelial cells before being secreted?
Secretory component
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
opsonizes
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

7. What is a factor that is a predictor for a bad transplantation?
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
Alternative splicing of mRNA
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

8. when can graft versus host disease? What is the result?
Cross link
Celiac
All MHC 1/CD8
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

9. What is three common causes of severe combined immunodef? What is the result of all three?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Active; passive - fast but short half life (3 weeks!)

10. What is the presentation of Brutons agammaglobulinemia?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
All MHC 1/CD8
isotype
Active; passive - fast but short half life (3 weeks!)

11. what prevents NK cells from killing normal cells if their default is to kill?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
MHC class molecules bind to KIRS or CD94 to prevent killing
Edema and necrosis in that region

12. How does igA cross the epithelium?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
By transcytosis
Cells that stil have weird parts of their membrane that macrophages usually bite off
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

13. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Immunoflourescent staining of tissue biopsies
not Ab mediated
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

14. Which is the most abundant antibody in blood?
Fab portion
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
Glycoproteins; HLA
IgG

15. What is the pathogenesis of a hypersensitivity reaction?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
TNF alpha and IL1
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
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

16. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

17. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
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
Thrombocytopenia
Paracortex; viral infection
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

18. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
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!
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
lowest concentration

19. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Anti alpha subunit 3 of collagen on type IV bm
Yes
Recom IL 11; thrombocytopenia
Th cells fail to produce interferon gamma; a lot of IgE

20. what ensure that a memory response is generated?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
T cell dysfunction
If there is class switching and plasma cell production (that is when memory cells are produced)
CD21 on B cells (although there is T cell lymphocytosis in EBV)

21. what happens in a deficiency of C1 esterase inhibitor? DAF?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Carbohydrate
Hereditary angioedema; PNH
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

22. which cells have more complete tolerance - B or T cells?
IgM and IgG
T cell activation; no with CD 4 or CD 8
Celiac
T

23. What lymph node drains the scrotum?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Superficial inguinal
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
2 heavy chains and two light chains

24. What is recomb beta interferon used for?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
cannot cross placenta
MS
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

25. which of the hypersensitivity reactions is not Ab mediated?
Immunosuppression after kidney transplantation
Type IV
Cytokine IL 10 secreted by Th2
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

26. What are superantigens? give two examples.
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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
Celiac

27. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Macrophages - Dendritic cells - B cells
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

28. Type Iv hypersensitivity is...
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
delayed!

29. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Popliteal
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Its a serine protease that activates apoptosis; NK and CD8
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

30. What is the main cytokine released by T cells? What does it do
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IL 3; supports growth and differentiation of bone marrow stem cells
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

31. What are target cells?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Activate macrophages
Anti alpha subunit 3 of collagen on type IV bm
Cells that stil have weird parts of their membrane that macrophages usually bite off

32. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
Superior mesenteric
Anti alpha subunit 3 of collagen on type IV bm
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

33. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
Antihistone
...
Superficial inguinal

34. Monomer in circulation - ___ when secreted
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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
dimer
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

35. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
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
A recomb cytokine of IL 2; RCC and metastatic melanoma
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

36. __________ are a part of the innate system.
NK cells
Hemochromatosis
Humoral
IgM and IgG

37. What is the main function of TNF alpha? How does it do this?
Active; passive - fast but short half life (3 weeks!)
type four
SP infections
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

38. What is digoxin immune Fab used for?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Antidote for digoxin intoxication
Receiving preformed Antibodies
Anti mitochondrial

39. what cytokine does basophils secrete?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
IL 4
IL 5
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

40. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Graves
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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

41. How is i Th1 helper cell inhibited?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Cytokine IL 10 secreted by Th2
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Lymphocytes

42. To what disease do the autoantibodies to IgG (rheumatoid factor)?
DM type I
In the germinal center of secondary follicles (In the paler center)
IgM and IgA
Rheumatic arthritis

43. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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 :(
Activate macrophages

44. where are complements produced?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Steroid responsive nephrotic syndrome
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Liver! (they are proteins circulating in the blood)

45. What are the T cell functions?
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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 :(

46. What are the autoantibodies for drug induced lupus?
delayed!
IgM
Antihistone
Axillary

47. What lymph node drains the stomach?
mesenchymal
IgG
Daclizumab; prevent ACUTE rejection of renal transplant
Celiac

48. what cell surface marker is used for NK cells as it is unique to them?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
CD56
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
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

49. What is the main cytokine that activates eosinophils?
IL 5
Sinusitis - otitis media - pneumonia
Anti alpha subunit 3 of collagen on type IV bm
mesenchymal

50. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
RNA segment reassortment
Not thymus - BM
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs