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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?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
IgG
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
Anti TSh receptor

2. What is immune complex disease? give an example.
Superficial inguinal
MHC I; from RER with help of the B2 microglobulin
Antimicrosomal and antithyroglobulin
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

3. What does it mean if there are igM in the serum at birth?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Bind FcG for antibody dependent cellular cytotoxicity
Antimicrosomal and antithyroglobulin
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

4. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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
Negative nitroblue tetrazolium reduction test
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

5. Name 5 ways Antibody diversity is generated?
DM type I
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

6. What are the main Cell surface proteins on T cells?
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
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
2 heavy chains and two light chains

7. IgG...
Anti alpha subunit 3 of collagen on type IV bm
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
opsonizes
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

8. which cells have more complete tolerance - B or T cells?
Anti glutamate carboxylase and anti insulin
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the
T
Activates cytotoxic CD 8 T cells as second signal

9. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
neutrophilia!
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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 :(

10. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Immunoflourescent staining of tissue biopsies
Rheumatic arthritis
mesenchymal
All MHC 1/CD8

11. What is recomb alpha interferon used for?
Superficial inguinal
RNA segment reassortment
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

12. What is an example of a parasite showing antigenic variation?
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
DM type I and RA
Immunosuppression after kidney transplantation

13. other than C3a - what other complement acts as an anaphyloxin?
C5a
Immunoflourescent staining of tissue biopsies
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
B - T - and NK cells

14. What is the marginal zone of the spleen? what happens there?
Activate macrophages
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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

15. What is the clinical use of Muromonab?
Anti Ach receptor
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
delayed!
Immunosuppression after kidney transplantation

16. How do you test for type III hypersensitivity?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Immunoflourescent staining of tissue biopsies
T cell dysfunction

17. From where do cytokines come from?
Macrophages - Dendritic cells - B cells
Lymphocytes
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
IgM and IgD

18. Give three examples of bacteria that use antigenic variation and how.
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 TSh receptor
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

19. which antibodies can bind complement?
Histamine; post capillary venules - vasodilation
IgM 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
except hyperacute

20. what ensure that a memory response is generated?
If there is class switching and plasma cell production (that is when memory cells are produced)
Graves
IgM
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

21. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
Activates cytotoxic CD 8 T cells as second signal
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
IgM

22. Which disease is associated with DR3?
DM type I
Fab portion
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

23. What is recomb gamma interferon used for?
Chronic granulomatous disease
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

24. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Superficial inguinal
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

25. What is the clinical use for azathioprine?
...
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
T cell dysfunction

26. Leukocyte adhesion defect presents with...
Previous transfusion; pregnant woman whose fetus had paternal antigens
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
neutrophilia!
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

27. What lymph node drains the lateral side of the dorsum of the foot?
Paracortex
Pernicious Anemia and Hashimotos
type four
Popliteal

28. What is the white pulp of the spleen?
Cytokine IL 10 secreted by Th2
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
No because no peptide fragment!
Sinusitis - otitis media - pneumonia

29. How fast does it occur?
The patient could become cyanotic in the OR!
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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!
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

30. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
...
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
cannot cross placenta

31. which type of immunity is slow but long lasting? as opposed to...
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Active; passive - fast but short half life (3 weeks!)
heavy chains

32. 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
RNA segment reassortment
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Thrombocytopenia

33. What are the mediators that mast cells release?
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!
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
IL 5
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

34. How do you test for chronic granulomatous disease?
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
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
Negative nitroblue tetrazolium reduction test
Paracortex; viral infection

35. What lymph node drains the scrotum?
Basophils! THey want IG E class switch!
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Superficial inguinal
Severe pyogenic infections early in life

36. which interleukin receptor is required for NK development? activation?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
IL 15; IL 12 - interferon Beta and interferon alpha
Inferior mesenteric

37. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
CD56
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

38. Give an example of someone who could get hyperacute transplant rejection.
Anti TSh receptor
2 heavy chains and two light chains
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
Previous transfusion; pregnant woman whose fetus had paternal antigens

39. The ______ in the BM are DN - the DP are in the cortex of thymus
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
T cell precursor
Thrombocytopenia

40. What happens in a deficiency of C3?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Active; passive - fast but short half life (3 weeks!)
Interferon gamma; Th1
Severe pyogenic infections early in life

41. describe the classic complement pathway.
pathogenesis
TLR ad nuclear receptors
Carbohydrate
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

42. What is the pathology in hyperacute transplant rejection?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
2 heavy chains and two light chains
Superficial inguinal

43. what cell surface marker is used for NK cells as it is unique to them?
CD56
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
TLR ad nuclear receptors
Increases expression of MHC I and MHC II and also activates NK cells

44. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Anemias (esp due to renal failure)
The igA found in breast milk
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 :(

45. What are the autoantibodies for graves?
Daclizumab; prevent ACUTE rejection of renal transplant
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Anti TSh receptor
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

46. what secretes IL 4?
Basophils! THey want IG E class switch!
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Popliteal
mesenchymal

47. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
...
Complement activation (active in both)
DM type I and RA
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

48. which of the transplant rejections is antibody mediated? why does it occur?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
2 heavy chains and two light chains
opsonizes
A - B - C; all the D's

49. What are the main cell surface proteins on B cells?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Steroid responsive nephrotic syndrome
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 :(
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

50. What is oprelevkin? and What is it used for?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Recom IL 11; thrombocytopenia
IgM and IgD
Interferon gamma and IL 2

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USMLE Step 1 Immunology

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