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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.

This is a study tool. The 3 wrong answers for each question are randomly chosen from answers to other questions. So, you might find at times the answers obvious, but you will see it re-enforces your understanding as you take the test each time.

1. From where do cytokines come from?
S. aureus - E. Coli - aspergillus
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Lymphocytes
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway

2. What are target cells?
Macrophages - Dendritic cells - B cells
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

3. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Bind FcG for antibody dependent cellular cytotoxicity
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

4. Which is the main antibody that provides passive immunity to infants?
IgG
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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
Inferior mesenteric

5. What is hereditary angioedema? What are the C3 levels?
Interferon gamma; Th1
Graves
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

6. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Hereditary angioedema; PNH
Activates Th1 helper cells; Macrophages
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

7. What is the pathogenesis of a candida skin test?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
not Ab mediated
Delayed type hypersensitivity

8. What are the two signals to kill for NK cells?
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
Its main effect is a defect in Ab opsonization for killing
Anti U1 RNP (ribonucleoprotein)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

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?
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
IgG
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

10. what mediates the type II hypersensitivity? What are the two different methods?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Lymphocytes
Antibody mediated cytotoxicity; either complement dependent or complement independent
Edema and necrosis in that region

11. What is passive immunity?
Th cells fail to produce interferon gamma; a lot of IgE
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
IgE; by activating eosinophils
Receiving preformed Antibodies

12. What is digoxin immune Fab used for?
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
Antidote for digoxin intoxication
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
acute phase reactants

13. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
opsonizes
Cross link
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
pathogenesis

14. What are the three types of APCs?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
T cell activation; no with CD 4 or CD 8
secondary
Macrophages - Dendritic cells - B cells

15. 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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
When you select for which MHC it will have; take out the lymphs that self react

16. can igG cross the placenta?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Yes
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

17. What is thrombopoietin used for?
The igA found in breast milk
Thrombocytopenia
Interferon gamma and IL 2
Superficial inguinal

18. What are four results of a splenectomy?
Paracortex
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
IL 4
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

19. The secondary follicles have __________; primary follicles are dense
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
pale central germinal centers
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

20. what characterizes an arthus reaction?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
IgE
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Edema and necrosis in that region

21. Type Iv hypersensitivity is...
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
Antidote for digoxin intoxication
delayed!
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

22. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Activate macrophages
Its a serine protease that activates apoptosis; NK and CD8
Influenza; antigenic shift; antigenic drift
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

23. what prevents NK cells from killing normal cells if their default is to kill?
Anti Ach receptor
S. aureus - E. Coli - aspergillus
MHC class molecules bind to KIRS or CD94 to prevent killing
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

24. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
not Ab mediated
Paracortex; viral infection
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

25. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Negative selection
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Antidesmoglein

26. What is recomb beta interferon used for?
...
MS
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

27. Which is the most abundant antibody in blood?
Its a serine protease that activates apoptosis; NK and CD8
IgG
Th cells fail to produce interferon gamma; a lot of IgE
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

28. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Anti SS- A (anti RO) and Anti SS- B
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

29. What cytokines are released by Th1 cells?
Interferon gamma and IL 2
Paracortex
Daclizumab; prevent ACUTE rejection of renal transplant
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

30. 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)
T cell dysfunction
Barrel hoop basement membrane fenestrations
MS

31. The MALT/GALT are not...
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
encapsulated
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

32. what cell surface marker is used for NK cells as it is unique to them?
CD56
RNA segment reassortment
Cells that stil have weird parts of their membrane that macrophages usually bite off
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

33. where are complements produced?
Liver! (they are proteins circulating in the blood)
cannot cross placenta
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Thrombocytopenia

34. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
except hyperacute
carboxy terminal
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

35. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
MHC I; from RER with help of the B2 microglobulin
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Tetanus - Botulinum - HBV - Rabies

36. What is the presentation of scid? treatment?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
By transcytosis
2 heavy chains and two light chains
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

37. What lymph node drains the testes?
Para aortic
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Negative selection
IL 3; supports growth and differentiation of bone marrow stem cells

38. What type of side chains are found on Fc region of an antibody?
IL 3; supports growth and differentiation of bone marrow stem cells
Carbohydrate
Severe pyogenic infections early in life
Yes

39. What are the two signals required for T cells? what happens after?
MS
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!
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

40. What lymph node drains the rectum (above the pectinate line)?
Internal iliac
Antidesmoglein
Pernicious Anemia and Hashimotos
A chemotactic factor for neutrophils

41. What does granulysin do?
mesenchymal
Anti Jo -1
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

42. What is the pathogenesis of a hypersensitivity reaction?
Antidote for digoxin intoxication
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
Negative selection
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

43. What are the autoantibodies for wegeners granulomatosis?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Lymphocytes
Celiac

44. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

45. which antibodies prevent antigens from binding mucosal surfaces?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
The igA found in breast milk
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
IgA

46. What is three common causes of severe combined immunodef? What is the result of all three?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Its a serine protease that activates apoptosis; NK and CD8
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Para aortic

47. What are the main symptoms of T cell immunodeficiencies?
Its main effect is a defect in Ab opsonization for killing
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Its a serine protease that activates apoptosis; NK and CD8

48. What lymph node drains the duodenum - jejunum?
Anti SS- A (anti RO) and Anti SS- B
Superior mesenteric
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

49. What are the main cell surface proteins on B cells?
except hyperacute
Anti TSh receptor
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

50. The pathogenesis of contact dermatitis is ________ hypersensitivity
Stimulate the liver to release acute phase reactants
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
type four
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