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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. What are the autoantibodies for graves?
Antimicrosomal and antithyroglobulin
The patient could become cyanotic in the OR!
Anti TSh receptor
Interferon gamma and IL 2

2. which cytokine inhibits TH2 cells? secreted by who?
DM type I and RA
Antidote for digoxin intoxication
Acts as second signal on B cells to induce class switching to IgE and IgG
Interferon gamma; Th1

3. How does igA cross the epithelium?
By transcytosis
Wiskott Aldrich syndrome
Paracortex
acute phase reactants

4. Which antibodies can be multimeric?
IgM and IgA
Axillary
Wiskott Aldrich syndrome
Anti smooth muscle

5. What is a factor that is a predictor for a bad transplantation?
dimer
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Severe pyogenic infections early in life

6. which of the transplant rejections is antibody mediated? why does it occur?
Its main effect is a defect in Ab opsonization for killing
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
IL 15; IL 12 - interferon Beta and interferon alpha

7. What is a type I hypersensitivity reaction? What is atopic?
T
Popliteal
A j chain
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

8. What are the symptoms of serum sickness?
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Para aortic
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

9. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
MHC I - CD16 - CD56
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
lowest concentration

10. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
In the germinal center of secondary follicles (In the paler center)
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
Paracortex
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

11. What is serum sickness? give an example.
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
Th cells fail to produce interferon gamma; a lot of IgE
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
Lymphocytes

12. What are C1 - C2 - C3 - C4 important for?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Severe pyogenic infections early in life
Viral neutralization of igM and IgG!
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

13. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
TGF beta and IL 10
Superficial inguinal
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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

14. What is recomb gamma interferon used for?
Cells that stil have weird parts of their membrane that macrophages usually bite off
pathogenesis
type four
Chronic granulomatous disease

15. IgE has the ___________ in the serum
lowest concentration
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
A chemotactic factor for neutrophils

16. What are the main Cell surface proteins on T cells?
Antimicrosomal and antithyroglobulin
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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
RNA segment reassortment

17. What are some sinopulmonary infections?
A chemotactic factor for neutrophils
Sinusitis - otitis media - pneumonia
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Secretory component

18. what will NK cells do to cells covered in IgG Ab? why?
Kill them because they have CD16 on them that recognize the FcG portion
S. aureus - E. Coli - aspergillus
opsonizes
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

19. What are the cell surface proteins on NK cells?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
MHC I - CD16 - CD56
Liver! (they are proteins circulating in the blood)
secondary

20. where are complements produced?
Liver! (they are proteins circulating in the blood)
Activates Th1 helper cells; Macrophages
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

21. describe the pathogenesis of delayed type IV hypersensitivity
Anti Jo -1
TGF beta and IL 10
IgA
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

22. What is the treatment of acute transplant rejection?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
When you select for which MHC it will have; take out the lymphs that self react
Cyclosporine - OKT3
Antimicrosomal and antithyroglobulin

23. Which disease is associated with DR7?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
SP infections
Steroid responsive nephrotic syndrome

24. What are the autoantibodies for drug induced lupus?
Superficial inguinal
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Antihistone
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

25. Name the three opsonins
CRP - C3b - IgM
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

26. What links the adaptive and innate immunity?
Activates cytotoxic CD 8 T cells as second signal
Complement activation (active in both)
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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

27. when can graft versus host disease? What is the result?
Paracortex
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
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
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

28. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
CD56
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Anti alpha subunit 3 of collagen on type IV bm

29. What is oprelevkin? and What is it used for?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Recom IL 11; thrombocytopenia
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

30. What do multimeric antibodies require for assembly?
Tetanus - Botulinum - HBV - Rabies
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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
A j chain

31. What lymph node drains the scrotum?
IgM and IgG
IgAs in mothers breast milk!
Superficial inguinal
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

32. IgM can exist as a _______ also
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
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
CD56
pentamer

33. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
mesenchymal
secondary
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

34. What are the autoantibodies for other vasculitides?
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

35. What are four results of a splenectomy?
Type IV
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Barrel hoop basement membrane fenestrations
Rheumatic arthritis

36. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
IgG
Stimulate the liver to release acute phase reactants
Daclizumab; prevent ACUTE rejection of renal transplant

37. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
IgG
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

38. What are the cell surface proteins for Macrophages? which two are for opsonins?
Type IV
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Fc
Hemochromatosis

39. The MALT/GALT are not...
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgM and IgG
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
encapsulated

40. What happens in a secondary follicle?
Th cells fail to produce interferon gamma; a lot of IgE
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
IgAs in mothers breast milk!
Complement activation (active in both)

41. What is the pathogenesis of a candida skin test?
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
Delayed type hypersensitivity
Axillary
NK cells

42. 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).
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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!
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
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

43. what characterizes an arthus reaction?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Antidote for digoxin intoxication
Edema and necrosis in that region
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

44. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
Anti alpha subunit 3 of collagen on type IV bm
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
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
dimer

45. What does granzyme do? who secretes it?
Its a serine protease that activates apoptosis; NK and CD8
Anti Ach receptor
...
Graves

46. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

47. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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

48. describe the classic complement pathway.
Negative nitroblue tetrazolium reduction test
Para aortic
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Recom IL 11; thrombocytopenia

49. What lymph node drains the breast?
Barrel hoop basement membrane fenestrations
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Anti smooth muscle
Axillary

50. what mediates the type II hypersensitivity? What are the two different methods?
Antibody mediated cytotoxicity; either complement dependent or complement independent
mesenchymal
...
Interferon gamma and IL 2