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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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1. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Paracortex; viral infection
opsonizes

2. In general What are T cells good for?
Thrombocytopenia
Internal iliac
IgG
Anti viral and anti tumor

3. Which diseases are associated with DR4?
DM type I and RA
No because no peptide fragment!
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
A j chain

4. What is the main cytokine released by T cells? What does it do
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Histamine; post capillary venules - vasodilation
Edema and necrosis in that region
IL 3; supports growth and differentiation of bone marrow stem cells

5. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Activates Th1 helper cells; Macrophages
T cell dysfunction
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
mesenchymal

6. What are the major functions of Antibodies?
Receiving preformed Antibodies
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
IL 15; IL 12 - interferon Beta and interferon alpha
IL 3; supports growth and differentiation of bone marrow stem cells

7. What are the main symptoms of T cell immunodeficiencies?
Secretory component
Cyclosporine - OKT3
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

8. So antibodies are the effectors for the humoral response. List some of their functions.
Stimulate the liver to release acute phase reactants
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti

9. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
type four
Paracortex; viral infection
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

10. Describe the capsular structure of a lymph node; What are the functions of the LN?
Fc
Paracortex; viral infection
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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

11. which antibodies can bind complement?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
IgM and IgG
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

12. Which MHC presents intracellular peptides? how so?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Th2; Th1
S. aureus - E. Coli - aspergillus
MHC I; from RER with help of the B2 microglobulin

13. What are the mediators that mast cells release?
acute phase reactants
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

14. What does interferon gamma do to be antiviral?
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
Increases expression of MHC I and MHC II and also activates NK cells
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
IgE; by activating eosinophils

15. Leukocyte adhesion defect presents with...
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
neutrophilia!
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
TLR ad nuclear receptors

16. what cell surface marker is used for NK cells as it is unique to them?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
CD56
IL 3; supports growth and differentiation of bone marrow stem cells
C5a

17. What are the autoantibodies for systemic sclerosis?
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Anti topoisomerase
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

18. which antibody activate mast cells - basophils - and eosinophils?
Cyclosporine - OKT3
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
T cell activation; no with CD 4 or CD 8
IgE

19. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
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
IgM and IgD
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

20. hat is the presentation of Jobs syndrome or Hyper IgE?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
mesenchymal
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

21. How does complement link innate and adaptive?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Secretory component

22. What is three common causes of severe combined immunodef? What is the result of all three?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Macrophages - Dendritic cells - B cells
If there is class switching and plasma cell production (that is when memory cells are produced)

23. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
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
Basophils! THey want IG E class switch!
TNF alpha and IL1
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

24. What lymph node drains the lateral side of the dorsum of the foot?
Anti alpha subunit 3 of collagen on type IV bm
Cross link
MS
Popliteal

25. Which HLA's are included in MHC I? MHC II?

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26. Type Iv hypersensitivity is...
heavy chains
IgA
delayed!
A - B - C; all the D's

27. What does interferon gamma do? What two type of cells does it attack mostly?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Activate macrophages
Viral neutralization of igM and IgG!
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

28. T/F B cells do not require a second signal
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
False! B cell class switching requires a second signal
heavy chains
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

29. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Hemochromatosis
Barrel hoop basement membrane fenestrations
TNF alpha and IL1
C5a

30. What are the main symptoms of B cell immunodeficiencies?
Immunosuppression after kidney transplantation
Anti Ach receptor
SP infections
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

31. What are the three types of APCs?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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!
Macrophages - Dendritic cells - B cells
Activates cytotoxic CD 8 T cells as second signal

32. IgE has the ___________ in the serum
lowest concentration
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
T cell dysfunction
Wiskott Aldrich syndrome

33. What is the general structure of an Ab?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
2 heavy chains and two light chains
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
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

34. what cytokine does basophils secrete?
IL 4
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
type four
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

35. What are the labs in brutons agammaglobulinemia?
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
T cell dysfunction
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Anti mitochondrial

36. What are the two signals required for Th1 cells? what happens after then activated?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Negative nitroblue tetrazolium reduction test
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
TGF beta and IL 10

37. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
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
2 heavy chains and two light chains
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

38. What is passive immunity?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Receiving preformed Antibodies
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

39. where do NK cells develop?
TLR ad nuclear receptors
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
active complement pathway
Not thymus - BM

40. Which disease is associated with DR7?
Interferon gamma and IL 2
neutrophilia!
Steroid responsive nephrotic syndrome
Axillary

41. 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
IgG
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
Viral neutralization of igM and IgG!

42. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
IL 5
All MHC 1/CD8
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Pernicious Anemia and Hashimotos

43. For which toxins are preformed antibodies (passive) given?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
The patient could become cyanotic in the OR!
Tetanus - Botulinum - HBV - Rabies
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

44. what prevents NK cells from killing normal cells if their default is to kill?
MHC class molecules bind to KIRS or CD94 to prevent killing
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Histamine; post capillary venules - vasodilation
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

45. What is the white pulp of the spleen?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Active; passive - fast but short half life (3 weeks!)

46. Give an example of someone who could get hyperacute transplant rejection.
A chemotactic factor for neutrophils
Previous transfusion; pregnant woman whose fetus had paternal antigens
Hereditary angioedema; PNH
Type IV

47. What are howell jolly bodies?
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
dimer
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Viral neutralization of igM and IgG!

48. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
NK cells
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
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

49. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
MHC II - B7
Interferon gamma and IL 2

50. What is the presentation of hyperIgM syndrome?
Axillary
Negative!
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Severe pyogenic infections early in life