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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. when can graft versus host disease? What is the result?
MHC I; from RER with help of the B2 microglobulin
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
Lymphocytes
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

2. Which are the only two antiinflammatory cytokines?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
TGF beta and IL 10
DM type I
Viral neutralization of igM and IgG!

3. What is a factor that is a predictor for a bad transplantation?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Th cells fail to produce interferon gamma; a lot of IgE
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

4. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Carbohydrate
Celiac

5. Which is the most abundant antibody in blood?
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!
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
MS
IgG

6. What is the autoantibody for SLE that is nonspecific? Specific?
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
cannot cross placenta
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

7. What are the autoantibodies for drug induced lupus?
Activates Th1 helper cells; Macrophages
IgM and IgG
Sinusitis - otitis media - pneumonia
Antihistone

8. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Steroid responsive nephrotic syndrome
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

9. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
TLR ad nuclear receptors
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
Immunoflourescent staining of tissue biopsies
Lymphocytes

10. describe the pathogenesis of delayed type IV hypersensitivity
Inferior mesenteric
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
The patient could become cyanotic in the OR!
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

11. What are the autoantibodies for wegeners granulomatosis?
acute phase reactants
Para aortic
...
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

12. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Anti TSh receptor
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

13. ________ regulate the cell mediated response.
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
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
Humoral

14. What lymph node drains the duodenum - jejunum?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Superior mesenteric
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)
In the germinal center of secondary follicles (In the paler center)

15. How is the antigen loaded onto a MHC II?
Graves
Edema and necrosis in that region
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
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

16. what prevents NK cells from killing normal cells if their default is to kill?
Type IV
carboxy terminal
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
MHC class molecules bind to KIRS or CD94 to prevent killing

17. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Inferior mesenteric
Cyclosporine - OKT3
Rheumatic arthritis
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

18. Describe complement dependent Type II hypersensitivity. Give an example.
IL 3; supports growth and differentiation of bone marrow stem cells
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
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
encapsulated

19. 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
not Ab mediated
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Antihistone

20. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
Anti smooth muscle
IL 5
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

21. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
By transcytosis
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Paracortex; viral infection
Remove encapsulated bacateria

22. IgG...
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!
pentamer
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
opsonizes

23. Give an example of someone who could get hyperacute transplant rejection.
Antidote for digoxin intoxication
Previous transfusion; pregnant woman whose fetus had paternal antigens
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

24. So antibodies are the effectors for the humoral response. List some of their functions.
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Cytokine IL 10 secreted by Th2
Wiskott Aldrich syndrome

25. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
CD56
Barrel hoop basement membrane fenestrations

26. IgM can fix complement but...
Pernicious Anemia and Hashimotos
Graves
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
cannot cross placenta

27. What is the treatment of acute transplant rejection?
secondary
Basophils! THey want IG E class switch!
T
Cyclosporine - OKT3

28. where are complements produced?
carboxy terminal
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Liver! (they are proteins circulating in the blood)

29. what will NK cells do to cells covered in IgG Ab? why?
Steroid responsive nephrotic syndrome
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Kill them because they have CD16 on them that recognize the FcG portion
Its main effect is a defect in Ab opsonization for killing

30. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
Liver! (they are proteins circulating in the blood)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

31. What is the main function of interferons?
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!
Antimicrosomal and antithyroglobulin
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
IgM and IgG

32. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Basophils! THey want IG E class switch!
Increases expression of MHC I and MHC II and also activates NK cells
Cross link

33. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Pernicious Anemia and Hashimotos
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
Paracortex
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

34. What is the clinical use of Muromonab?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Immunosuppression after kidney transplantation
acute phase reactants
IgM and IgA

35. What type of fenestrations are found in the red pulp of the spleen?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
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
Barrel hoop basement membrane fenestrations
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

36. What is the presentation of Brutons agammaglobulinemia?
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
IgM and IgD
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

37. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
pathogenesis
T

38. What is oprelevkin? and What is it used for?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Cross link
Recom IL 11; thrombocytopenia
Severe pyogenic infections early in life

39. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
type four

40. in which immunodef order do you see a lot of pus? no pus?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Th cells fail to produce interferon gamma; a lot of IgE
Influenza; antigenic shift; antigenic drift

41. What is the marginal zone of the spleen? what happens there?
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
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
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
delayed!

42. How do you test for type III hypersensitivity?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Active; passive - fast but short half life (3 weeks!)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Immunoflourescent staining of tissue biopsies

43. To what portion of the Antibody do the complements bind?
Thrombocytopenia
Anti smooth muscle
False! B cell class switching requires a second signal
Fc

44. What is filgrastim and sargramostim? and What is it used for?
T
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Superior mesenteric
neutrophilia!

45. What are the autoantibodies for pemphigus bulgaris?
Antidesmoglein
Antibody mediated cytotoxicity; either complement dependent or complement independent
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 Ach receptor

46. What does it mean if there are igM in the serum at birth?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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
type four
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

47. What is recomb gamma interferon used for?
CRP - C3b - IgM
Chronic granulomatous disease
A j chain
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

48. 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
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
T cell activation; no with CD 4 or CD 8
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. Which disease is associated with DR3?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
DM type I
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

50. other than eat and bite RBCs what else do Macrophages of spleen do>
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Remove encapsulated bacateria
Humoral
mesenchymal

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USMLE Step 1 Immunology

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