Test your basic knowledge |

USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can study here.
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 three types of APCs?
Negative!
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
Macrophages - Dendritic cells - B cells
Yes

2. What is the most common selective Ig deficiency? What is the presentation?
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
DM type I and RA

3. What does granzyme do? who secretes it?
Its a serine protease that activates apoptosis; NK and CD8
IL 1 and IL 6
active complement pathway
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

4. What is the defect in hyper IgM syndrome? What are the lab results?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Anti SS- A (anti RO) and Anti SS- B
A - B - C; all the D's

5. What is muromonab - CD3 (OKT3)
MS
Previous transfusion; pregnant woman whose fetus had paternal antigens
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IgG

6. How fast does it occur?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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
The patient could become cyanotic in the OR!
except hyperacute

7. What is digoxin immune Fab used for?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Antidote for digoxin intoxication
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Popliteal

8. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
The igA found in breast milk
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

9. where do somatic hypermutation and class switching occur?
acute phase reactants
In the germinal center of secondary follicles (In the paler center)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Popliteal

10. How does complement link innate and adaptive?
Complement activation (active in both)
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
...
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

11. What is the general structure of an Ab?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
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
2 heavy chains and two light chains

12. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
not Ab mediated
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

13. What are C1 - C2 - C3 - C4 important for?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Viral neutralization of igM and IgG!
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
MHC I; from RER with help of the B2 microglobulin

14. What does IL 5 do?
Thrombocytopenia
Anti smooth muscle
Histamine; post capillary venules - vasodilation
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

15. What lymph node drains the breast?
Axillary
IgA
IgG
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a

16. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Internal iliac
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
Cross link
Superficial inguinal

17. which of the hypersensitivity reactions is not Ab mediated?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Type IV
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
SP infections

18. What are the autoantibodies for pernicious anemia?
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
Anti IF
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Type IV

19. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
A - B - C; all the D's
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
pathogenesis

20. What are the autoantibodies for systemic sclerosis?
Pernicious Anemia and Hashimotos
Anti topoisomerase
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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

21. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
pathogenesis
Complement activation (active in both)
Its main effect is a defect in Ab opsonization for killing
Severe pyogenic infections early in life

22. Other than stimulating fever - what else does IL 6 do?
Stimulate the liver to release acute phase reactants
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
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

23. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Bind FcG for antibody dependent cellular cytotoxicity
No because no peptide fragment!
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Type IV

24. other than eat and bite RBCs what else do Macrophages of spleen do>
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Remove encapsulated bacateria
Antihistone
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

25. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Interferon gamma and IL 2
TNF alpha and IL1
C5a
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

26. From where do cytokines come from?
Bind FcG for antibody dependent cellular cytotoxicity
Lymphocytes
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
IL 4

27. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
type four
DM type I

28. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
C5a
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Antihistone
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

29. What links the adaptive and innate immunity?
Complement activation (active in both)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
...
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

30. Type Iv hypersensitivity is...
T cell activation; no with CD 4 or CD 8
delayed!
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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

31. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
SP infections
Previous transfusion; pregnant woman whose fetus had paternal antigens
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

32. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Sinusitis - otitis media - pneumonia
Hereditary angioedema; PNH
...
Influenza; antigenic shift; antigenic drift

33. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
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
Stimulate the liver to release acute phase reactants
2 heavy chains and two light chains
Daclizumab; prevent ACUTE rejection of renal transplant

34. What is the most common example of passive immunity?
IgAs in mothers breast milk!
Acts as second signal on B cells to induce class switching to IgE and IgG
The patient could become cyanotic in the OR!
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

35. What is the clinical use of Muromonab?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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
Immunosuppression after kidney transplantation
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 are the three immune privileged sites? why are they called that? what happens after infection in these areas?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Its main effect is a defect in Ab opsonization for killing
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
CRP - C3b - IgM

37. what happens in a deficiency of C1 esterase inhibitor? DAF?
Hereditary angioedema; PNH
Active; passive - fast but short half life (3 weeks!)
Tetanus - Botulinum - HBV - Rabies
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

38. What happens in a secondary follicle?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
False! B cell class switching requires a second signal
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

39. What does Interferon alpha and beta do? how?
neutrophilia!
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!
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

40. which antibodies can bind complement?
IgM and IgG
A chemotactic factor for neutrophils
Fab portion
MS

41. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
...
Carbohydrate
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
A chemotactic factor for neutrophils

42. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
IL 4 - 5 - 10 - 6
not Ab mediated
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

43. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
IL 4 - 5 - 10 - 6
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
TNF alpha and IL1

44. What lymph node drains the anal canal (below the pectinate line)?
Superficial inguinal
type four
C5a
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

45. What are some catalase positive organisms?
Anti mitochondrial
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
Receiving preformed Antibodies
S. aureus - E. Coli - aspergillus

46. What are the autoantibodies for sjorgens syndrome?
IgM and IgA
SP infections
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Anti SS- A (anti RO) and Anti SS- B

47. What is filgrastim and sargramostim? and What is it used for?
RNA segment reassortment
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
isotype
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

48. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
lowest concentration
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Axillary

49. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
CRP - C3b - IgM
Alternative splicing of mRNA
Anti Ach receptor
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

50. Which is the most abundant antibody in blood?
Histamine; post capillary venules - vasodilation
MHC I; from RER with help of the B2 microglobulin
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
IgG