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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Barrel hoop basement membrane fenestrations
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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
Type IV

2. What does interferon gamma do? What two type of cells does it attack mostly?
Antidesmoglein
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Anti topoisomerase
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

3. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
No because no peptide fragment!
S. aureus - E. Coli - aspergillus
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

4. What type of fenestrations are found in the red pulp of the spleen?
Activate macrophages
Barrel hoop basement membrane fenestrations
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
A chemotactic factor for neutrophils

5. which cytokine inhibits TH2 cells? secreted by who?
Cross link
Interferon gamma; Th1
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

6. What lymph node drains the lateral side of the dorsum of the foot?
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
Popliteal
Active; passive - fast but short half life (3 weeks!)
T

7. Complements are...
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
acute phase reactants
By transcytosis

8. what results in symptoms of shock in an acute hemolytic transfusion reaction?
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
TNF alpha and IL1

9. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Fab portion
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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
A recomb cytokine of IL 2; RCC and metastatic melanoma

10. What lymph node drains the testes?
MHC I - CD16 - CD56
Para aortic
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
IL 4

11. What is the presentation of scid? treatment?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
pale central germinal centers
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

12. To what portion of the Antibody do the complements bind?
IL 5
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
Fc

13. What is the pathology in hyperacute transplant rejection?
Interferon gamma and IL 2
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Anti TSh receptor
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

14. The ______ in the BM are DN - the DP are in the cortex of thymus
NK cells
Immunosuppression after kidney transplantation
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
T cell precursor

15. What is the main function of IL 8?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
A chemotactic factor for neutrophils
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

16. What is the most common selective Ig deficiency? What is the presentation?
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
not Ab mediated
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

17. where do somatic hypermutation and class switching occur?
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
In the germinal center of secondary follicles (In the paler center)
IgAs in mothers breast milk!
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

18. 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).
Anti SS- A (anti RO) and Anti SS- B
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!
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

19. which cells have more complete tolerance - B or T cells?
T
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

20. What is the marginal zone of the spleen? what happens there?
IL 1 and IL 6
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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

21. What lymph node drains the anal canal (below the pectinate line)?
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
Superficial inguinal
IL 1 and IL 6
Macrophages - Dendritic cells - B cells

22. What is the common variable immunodeficiency ? How is it different from Brutons?
Anti IF
Celiac
IgE; by activating eosinophils
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

23. which antibody is involved in the primary response or immediate response to an antigen?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Anti alpha subunit 3 of collagen on type IV bm
IgM
Chronic granulomatous disease

24. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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
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)
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
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

25. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Antihistone
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

26. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Superficial inguinal
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

27. can igG cross the placenta?
delayed!
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
active complement pathway
Yes

28. What are the autoantibodies for myasthenia gravis?
Not thymus - BM
Anti Ach receptor
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

29. 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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Basophils! THey want IG E class switch!
Secretory component

30. what cell surface marker is used for NK cells as it is unique to them?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
IL 4 - 5 - 10 - 6
CD56
RNA segment reassortment

31. What are the main symptoms of T cell immunodeficiencies?
Cross link
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!
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Acts as second signal on B cells to induce class switching to IgE and IgG

32. What are the two signals to kill for NK cells?
Liver! (they are proteins circulating in the blood)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Negative!
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

33. What is the autoantibody for SLE that is nonspecific? Specific?
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Anti alpha subunit 3 of collagen on type IV bm
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

34. What are the three types of lymphocytes?
B - T - and NK cells
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

35. Which diseases are associated with DR4?
RNA segment reassortment
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
DM type I and RA

36. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Remove encapsulated bacateria
dimer
Secretory component

37. Which is the main antibody in the delayed or secondary response to an antigen?
IL 4 - 5 - 10 - 6
IgG
Complement activation (active in both)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

38. What are howell jolly bodies?
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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

39. What are the two signals required for T cells? what happens after?
opsonizes
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

40. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
carboxy terminal
IgM
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
NK cells

41. The lymphocytes are ________ origin
Antihistone
Remove encapsulated bacateria
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
mesenchymal

42. which B and T cell disorder presents with specifically low IgM?
Axillary
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Wiskott Aldrich syndrome
Local infection/inflammation; infection of the ln itself; metastasis

43. What are the three types of APCs?
When you select for which MHC it will have; take out the lymphs that self react
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
Macrophages - Dendritic cells - B cells
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

44. What are the autoantibodies for pernicious anemia?
opsonizes
Anti IF
isotype
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!

45. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
pale central germinal centers
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
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

46. What is the pathogenesis of a hypersensitivity reaction?
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
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
not Ab mediated
Paracortex

47. What is serum sickness? give an example.
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

48. What is an example of a parasite showing antigenic variation?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
IgA
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
not Ab mediated

49. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Fc
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
mesenchymal
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

50. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Bind FcG for antibody dependent cellular cytotoxicity
except hyperacute
Acts as second signal on B cells to induce class switching to IgE and IgG
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

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USMLE Step 1 Immunology

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