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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 happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

2. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
DM type I and RA

3. What is the main function of IL 8?
A chemotactic factor for neutrophils
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anti Ach receptor

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

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5. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Kill them because they have CD16 on them that recognize the FcG portion
Steroid responsive nephrotic syndrome
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

6. which type of immunity is slow but long lasting? as opposed 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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Active; passive - fast but short half life (3 weeks!)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

7. Describe the Mannose Lectin pathway
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
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

8. What are the autoantibodies for drug induced lupus?
Recom IL 11; thrombocytopenia
Antihistone
Active; passive - fast but short half life (3 weeks!)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

9. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Anti mitochondrial
Activates Th1 helper cells; Macrophages

10. What are the autoantibodies for other vasculitides?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
IgM and IgD
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

11. What is immune complex disease? give an example.
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

12. What is a type I hypersensitivity reaction? What is atopic?
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Cytokine IL 10 secreted by Th2
T cell activation; no with CD 4 or CD 8

13. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
IL 5
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

14. What lymph node drains the stomach?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
In the germinal center of secondary follicles (In the paler center)
Celiac
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in

15. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
T cell precursor
Cross link
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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!

16. Which helper T cells' development is induced by IL 4? IL 12?
Type IV
A - B - C; all the D's
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
Th2; Th1

17. What are the main Cell surface proteins on T cells?
Local infection/inflammation; infection of the ln itself; metastasis
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Axillary

18. 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!
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
IgE; by activating eosinophils
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 :(

19. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
dimer
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Th cells fail to produce interferon gamma; a lot of IgE

20. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
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
except hyperacute
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Th cells fail to produce interferon gamma; a lot of IgE

21. 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)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
pentamer
MHC class molecules bind to KIRS or CD94 to prevent killing

22. 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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

23. 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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Anti Jo -1

24. How does igA cross the epithelium?
Th cells fail to produce interferon gamma; a lot of IgE
TGF beta and IL 10
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
By transcytosis

25. what bacteria are a splenectomy patient most susceptible to? why?
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
MS - hay fever - SLE - goodpastures
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
active complement pathway

26. what mediates the type II hypersensitivity? What are the two different methods?
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
Antibody mediated cytotoxicity; either complement dependent or complement independent
Yes
Para aortic

27. What is filgrastim and sargramostim? and What is it used for?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
The patient could become cyanotic in the OR!
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

28. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Active; passive - fast but short half life (3 weeks!)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

29. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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

30. How fast does it occur?
Steroid responsive nephrotic syndrome
The patient could become cyanotic in the OR!
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

31. Describe the capsular structure of a lymph node; What are the functions of the LN?
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
Local infection/inflammation; infection of the ln itself; metastasis
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

32. What is the toxicity of azathioprine?
heavy chains
except hyperacute
Increases expression of MHC I and MHC II and also activates NK cells
...

33. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Influenza; antigenic shift; antigenic drift
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Antidesmoglein

34. What can cause a lymph node enlargement?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Sinusitis - otitis media - pneumonia
Local infection/inflammation; infection of the ln itself; metastasis
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

35. what characterizes an arthus reaction?
Edema and necrosis in that region
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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

36. Which antibody mediates immunity to worms? how?
Anti glutamate carboxylase and anti insulin
Lymphocytes
IgE; by activating eosinophils
Increases expression of MHC I and MHC II and also activates NK cells

37. what prevents NK cells from killing normal cells if their default is to kill?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
MHC class molecules bind to KIRS or CD94 to prevent killing

38. The MALT/GALT are not...
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Superior mesenteric
encapsulated
Axillary

39. What happens in a deficiency of C3?
Liver! (they are proteins circulating in the blood)
T cell activation; no with CD 4 or CD 8
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
cannot cross placenta

40. Name the three opsonins
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in
CRP - C3b - IgM
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Axillary

41. What is serum sickness? give an example.
IgE; by activating eosinophils
CD56
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
Antidesmoglein

42. What are C1 - C2 - C3 - C4 important for?
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
IgM and IgG
Anti glutamate carboxylase and anti insulin
Viral neutralization of igM and IgG!

43. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Severe pyogenic infections early in life
Barrel hoop basement membrane fenestrations
Histamine; post capillary venules - vasodilation
Antidesmoglein

44. What cytokines are released by Th1 cells?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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
Interferon gamma and IL 2
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

45. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Antihistone
Stimulate the liver to release acute phase reactants
Rheumatic arthritis
dimer

46. What does IL 2 do?
C5a
Activates cytotoxic CD 8 T cells as second signal
Barrel hoop basement membrane fenestrations
In the germinal center of secondary follicles (In the paler center)

47. What are the two signals to kill for NK cells?
Delayed type hypersensitivity
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)
SP infections

48. What do multimeric antibodies require for assembly?
Complement activation (active in both)
A j chain
Macrophages - Dendritic cells - B cells
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

49. What are the autoantibodies for autoimmune hepatitis?
Delayed type hypersensitivity
S. aureus - E. Coli - aspergillus
Steroid responsive nephrotic syndrome
Anti smooth muscle

50. Which are the only two antiinflammatory cytokines?
Its main effect is a defect in Ab opsonization for killing
Viral neutralization of igM and IgG!
TGF beta and IL 10
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)