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

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2. What are the function of B cells?
Immunosuppression after kidney transplantation
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
If there is class switching and plasma cell production (that is when memory cells are produced)

3. What is the receptor for EBV? On what cells is that located?
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
Lymphocytes
Type IV
CD21 on B cells (although there is T cell lymphocytosis in EBV)

4. What does interferon gamma do? What two type of cells does it attack mostly?
Carbohydrate
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

5. 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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

6. T/F B cells do not require a second signal
delayed!
dimer
IgAs in mothers breast milk!
False! B cell class switching requires a second signal

7. What are the labs in brutons agammaglobulinemia?
delayed!
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
dimer
IL 1 and IL 6

8. What is the clinical use for azathioprine?
...
IL 3; supports growth and differentiation of bone marrow stem cells
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Glycoproteins; HLA

9. which of the hypersensitivity reactions is not Ab mediated?
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
Type IV
Hemochromatosis
opsonizes

10. Name the three opsonins
Histamine; post capillary venules - vasodilation
Cyclosporine - OKT3
CRP - C3b - IgM
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

11. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Anti glutamate carboxylase and anti insulin
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

12. are Th cells involved in trapping of antigens of endotoxin/LPS?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
No because no peptide fragment!
Antihistone

13. is IgM an opsonizer?
secondary
CD56
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
Negative!

14. What does IgA pick up from epithelial cells before being secreted?
T cell dysfunction
Anti mitochondrial
Secretory component
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

15. Name two endogenous pyrogens
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
IL 1 and IL 6

16. 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)?
Alternative splicing of mRNA
IgM
Not thymus - BM
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

17. What is the general structure of an Ab?
Alternative splicing of mRNA
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
TLR ad nuclear receptors
2 heavy chains and two light chains

18. How do you test for chronic granulomatous disease?
CD56
Barrel hoop basement membrane fenestrations
Negative nitroblue tetrazolium reduction test
Acts as second signal on B cells to induce class switching to IgE and IgG

19. What lymph node drains the thigh?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Superficial inguinal
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
In the germinal center of secondary follicles (In the paler center)

20. What is the presentation of scid? treatment?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
cannot cross placenta
No because no peptide fragment!

21. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Anti IF
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

22. What is anergy? why does this occur?
MHC I - CD16 - CD56
Anti alpha subunit 3 of collagen on type IV bm
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

23. what happens in a deficiency of C1 esterase inhibitor? DAF?
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!
Hereditary angioedema; PNH
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Antibody mediated cytotoxicity; either complement dependent or complement independent

24. What cytokines are released by Th1 cells?
Anti glutamate carboxylase and anti insulin
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Interferon gamma and IL 2
...

25. what ensure that a memory response is generated?
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Severe pyogenic infections early in life
If there is class switching and plasma cell production (that is when memory cells are produced)

26. What type of side chains are found on Fc region of an antibody?
pathogenesis
False! B cell class switching requires a second signal
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Carbohydrate

27. Leukocyte adhesion defect presents with...
S. aureus - E. Coli - aspergillus
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
neutrophilia!

28. What are four results of a splenectomy?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Th2; Th1
TLR ad nuclear receptors
Axillary

29. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
DM type I and RA
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

30. The idiotype; the Fc portion determines the...
A - B - C; all the D's
Anti Jo -1
Yes
isotype

31. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
T cell precursor
Lymphocytes

32. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
Antidote for digoxin intoxication
Fab portion
...

33. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
active complement pathway
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
TNF alpha and IL1
Antimicrosomal and antithyroglobulin

34. Which helper T cells' development is induced by IL 4? IL 12?
Th2; Th1
Axillary
Cross link
not Ab mediated

35. 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
T cell activation; no with CD 4 or CD 8
Acts as second signal on B cells to induce class switching to IgE and IgG
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

36. where are complements produced?
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
Anti topoisomerase
Liver! (they are proteins circulating in the blood)
Immunosuppression after kidney transplantation

37. What is the pathology of acute transplant rejection? is it reversible?
Interferon gamma; Th1
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Macrophages - Dendritic cells - B cells
Negative nitroblue tetrazolium reduction test

38. Which disease is associated withB B27?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
When you select for which MHC it will have; take out the lymphs that self react
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

39. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Recom IL 11; thrombocytopenia
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Its main effect is a defect in Ab opsonization for killing

40. What are the main Cell surface proteins on T cells?
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
Inferior mesenteric
Anti viral and anti tumor
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

41. describe the pathogenesis of delayed type IV hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Fab portion
Th cells fail to produce interferon gamma; a lot of IgE

42. What does granulysin do?
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Celiac
Rheumatic arthritis

43. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
IL 1 and IL 6
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Acts as second signal on B cells to induce class switching to IgE and IgG

44. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
pathogenesis
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

45. What are the main symptoms of T cell immunodeficiencies?
Hereditary angioedema; PNH
encapsulated
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
MHC I; from RER with help of the B2 microglobulin

46. What is the main function of IL 12? other than macrophages who else can release IL 12?
IgM
Anti U1 RNP (ribonucleoprotein)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Fab portion

47. Which cytokines do Th2 release and For what?
In the germinal center of secondary follicles (In the paler center)
Graves
Kill them because they have CD16 on them that recognize the FcG portion
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

48. What is the treatment of acute transplant rejection?
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
Negative nitroblue tetrazolium reduction test
Cyclosporine - OKT3
Sinusitis - otitis media - pneumonia

49. Which antibodies can be multimeric?
A j chain
IgM and IgA
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

50. Give an example of someone who could get hyperacute transplant rejection.
Previous transfusion; pregnant woman whose fetus had paternal antigens
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!
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
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

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USMLE Step 1 Immunology

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