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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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1. in which immunodef order do you see a lot of pus? no pus?
Anti alpha subunit 3 of collagen on type IV bm
Anemias (esp due to renal failure)
Yes
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

2. What does it mean if there are igM in the serum at birth?
IgG
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
T cell precursor
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

3. Complements are...
acute phase reactants
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
IL 1 and IL 6
By transcytosis

4. What is the main function of TNF alpha? How does it do this?
...
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

5. What is digoxin immune Fab used for?
Anti glutamate carboxylase and anti insulin
Antidote for digoxin intoxication
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Its a serine protease that activates apoptosis; NK and CD8

6. What is the main cytokine that activates eosinophils?
Antihistone
S. aureus - E. Coli - aspergillus
Fc
IL 5

7. What are the two signals required for T cells? what happens after?
...
Anti viral and anti tumor
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

8. What is the pathogenesis of acute transplant rejection? When does it occur?
...
DM type I
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)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

9. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
TLR ad nuclear receptors
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

10. are Th cells involved in trapping of antigens of endotoxin/LPS?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Inferior mesenteric
Carbohydrate
No because no peptide fragment!

11. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
IgAs in mothers breast milk!
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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

12. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Its main effect is a defect in Ab opsonization for killing
Cells that stil have weird parts of their membrane that macrophages usually bite off
Superficial inguinal
Anti SS- A (anti RO) and Anti SS- B

13. What are superantigens? give two examples.
Negative selection
Anti Ach receptor
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

14. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
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
Anti IF
dimer
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

15. What is recomb beta interferon used for?
Delayed type hypersensitivity
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
MS
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

16. What does IgA pick up from epithelial cells before being secreted?
NK cells
Secretory component
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
T

17. Describe the capsular structure of a lymph node; What are the functions of the LN?
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
encapsulated
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
MS

18. What are the autoantibodies for autoimmune hepatitis?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
A chemotactic factor for neutrophils
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Anti smooth muscle

19. What is the clinical use of Muromonab?
Immunosuppression after kidney transplantation
Graves
NK cells
acute phase reactants

20. What are MHC's necessary for? By themselves?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
acute phase reactants
T cell activation; no with CD 4 or CD 8

21. What is the presentation of Brutons agammaglobulinemia?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Interferon gamma and IL 2
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

22. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Stimulate the liver to release acute phase reactants
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Rheumatic arthritis
mesenchymal

23. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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 :(
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
Thrombocytopenia

24. what secretes IL 4?
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Basophils! THey want IG E class switch!
...

25. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Edema and necrosis in that region
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
The patient could become cyanotic in the OR!

26. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Interferon gamma; Th1
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
B - T - and NK cells
active complement pathway

27. Which disease is associated with HLA A3?
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
Hemochromatosis
pathogenesis
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

28. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

29. What is the general structure of an Ab?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
2 heavy chains and two light chains
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Humoral

30. What do multimeric antibodies require for assembly?
Local infection/inflammation; infection of the ln itself; metastasis
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
A j chain
Th cells fail to produce interferon gamma; a lot of IgE

31. Which is the most abundant antibody in blood?
IgG
DM type I and RA
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Superficial inguinal

32. What is the white pulp of the spleen?
Wiskott Aldrich syndrome
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
If there is class switching and plasma cell production (that is when memory cells are produced)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

33. The secondary follicles have __________; primary follicles are dense
pale central germinal centers
delayed!
Anti viral and anti tumor
Delayed type hypersensitivity

34. What are C1 - C2 - C3 - C4 important for?
TLR ad nuclear receptors
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Viral neutralization of igM and IgG!

35. In thymic development - What is the positive selection? negative selections?
When you select for which MHC it will have; take out the lymphs that self react
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
Alternative splicing of mRNA
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

36. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Antibody mediated cytotoxicity; either complement dependent or complement independent
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
TNF alpha and IL1

37. What is the common variable immunodeficiency ? How is it different from Brutons?
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Thrombocytopenia

38. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
IgG
CRP - C3b - IgM

39. What links the adaptive and innate immunity?
Complement activation (active in both)
B - T - and NK cells
Recom IL 11; thrombocytopenia
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

40. What are the autoantibodies for Celiac disease?
Th cells fail to produce interferon gamma; a lot of IgE
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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

41. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Type IV
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!
Glycoproteins; HLA
A - B - C; all the D's

42. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
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
neutrophilia!
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Alternative splicing of mRNA

43. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
...
Anti topoisomerase
2 heavy chains and two light chains
TLR ad nuclear receptors

44. 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
IgE
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
CD56

45. The pathogenesis of contact dermatitis is ________ hypersensitivity
Lymphocytes
type four
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

46. What lymph node drains the scrotum?
Anti viral and anti tumor
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
Superficial inguinal
Anti glutamate carboxylase and anti insulin

47. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

48. what prevents NK cells from killing normal cells if their default is to kill?
Complement activation (active in both)
MHC class molecules bind to KIRS or CD94 to prevent killing
IgG
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

49. Other than stimulating fever - what else does IL 6 do?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Yes
Stimulate the liver to release acute phase reactants
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

50. What are the autoantibodies for graves?
Anti SS- A (anti RO) and Anti SS- B
Anti TSh receptor
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
Negative!

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USMLE Step 1 Immunology

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