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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.
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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 immune privileged sites? why are they called that? what happens after infection in these areas?
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
When you select for which MHC it will have; take out the lymphs that self react
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

2. What lymph node drains the sigmoid colon?
encapsulated
A - B - C; all the D's
Inferior mesenteric
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

3. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Th cells fail to produce interferon gamma; a lot of IgE
Cross link
Superior mesenteric

4. What is the mechanism for sirolimus? what else it known as?
Acts as second signal on B cells to induce class switching to IgE and IgG
Negative!
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
Antidote for digoxin intoxication

5. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
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

6. What portion of the lymph node is not well developed in DiGeorge Syndrome?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Celiac
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Paracortex

7. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
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
Rheumatic arthritis
Para aortic
Secretory component

8. Which is the most abundant antibody in blood?
IgG
A chemotactic factor for neutrophils
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

9. What are the autoantibodies for Celiac disease?
Anti Ach receptor
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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

10. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
T cell dysfunction
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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

11. What is chronic mucocutaneous candidiasis d/t?
Barrel hoop basement membrane fenestrations
T cell dysfunction
Negative selection
DM type I

12. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Hereditary angioedema; PNH
Antibody mediated cytotoxicity; either complement dependent or complement independent
Activate macrophages
RNA segment reassortment

13. What are the autoantibodies for pernicious anemia?
Anti IF
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anti TSh receptor
Anti glutamate carboxylase and anti insulin

14. Which helper T cells' development is induced by IL 4? IL 12?
Not thymus - BM
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Th2; Th1

15. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
...
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

16. What are C1 - C2 - C3 - C4 important for?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Viral neutralization of igM and IgG!
active complement pathway

17. What does granzyme do? who secretes it?
Its a serine protease that activates apoptosis; NK and CD8
Wiskott Aldrich syndrome
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
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

18. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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
The igA found in breast milk
isotype

19. What type of side chains are found on Fc region of an antibody?
Histamine; post capillary venules - vasodilation
mesenchymal
Carbohydrate
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

20. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
IL 15; IL 12 - interferon Beta and interferon alpha
carboxy terminal
Activates cytotoxic CD 8 T cells as second signal
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

21. What are the two signals to kill for NK cells?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Antihistone
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
neutrophilia!

22. What are four results of a splenectomy?
The patient could become cyanotic in the OR!
Para aortic
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)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

23. How is the antigen loaded onto a MHC II?
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
...
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
lowest concentration

24. What is immune complex disease? give an example.
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Immunoflourescent staining of tissue biopsies
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

25. What happens in a deficiency of C3?
IgG
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

26. What are the T cell functions?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
MHC II - B7
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Internal iliac

27. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Active; passive - fast but short half life (3 weeks!)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
MHC II - B7

28. what secretes IL 4?
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Basophils! THey want IG E class switch!

29. How is i Th1 helper cell inhibited?
MHC class molecules bind to KIRS or CD94 to prevent killing
Cyclosporine - OKT3
Cytokine IL 10 secreted by Th2
A - B - C; all the D's

30. What is the common variable immunodeficiency ? How is it different from Brutons?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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
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)
MS - hay fever - SLE - goodpastures

31. What does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Th2; Th1
Anti alpha subunit 3 of collagen on type IV bm
Bind FcG for antibody dependent cellular cytotoxicity

32. How do you test for chronic granulomatous disease?
Lymphocytes
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Negative nitroblue tetrazolium reduction test
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

33. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Recom IL 11; thrombocytopenia
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

34. What is hereditary angioedema? What are the C3 levels?
acute phase reactants
cannot cross placenta
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
Anti smooth muscle

35. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
Type IV

36. What is a factor that is a predictor for a bad transplantation?
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
B - T - and NK cells
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

37. What does it mean if there are igM in the serum at birth?
Histamine; post capillary venules - vasodilation
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Steroid responsive nephrotic syndrome
IgE; by activating eosinophils

38. What is the presentation of common variable immunodef? and What are the labs?
T cell precursor
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
MS
Activate macrophages

39. What are the autoantibodies for wegeners granulomatosis?
TGF beta and IL 10
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

40. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
Edema and necrosis in that region
The patient could become cyanotic in the OR!
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

41. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Paracortex; viral infection
Tetanus - Botulinum - HBV - Rabies
The patient could become cyanotic in the OR!
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

42. Complements are...
Glycoproteins; HLA
acute phase reactants
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Paracortex

43. What are the three types of APCs?
Macrophages - Dendritic cells - B cells
Superficial inguinal
Daclizumab; prevent ACUTE rejection of renal transplant
Secretory component

44. give an example of how influenza does a major antigenic shift.
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
RNA segment reassortment
If there is class switching and plasma cell production (that is when memory cells are produced)

45. What is the pathogenesis of a hypersensitivity reaction?
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
Wiskott Aldrich syndrome
...

46. What is recomb gamma interferon used for?
IgM and IgD
Remove encapsulated bacateria
Chronic granulomatous disease
pentamer

47. What lymph node drains the lateral side of the dorsum of the foot?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Sinusitis - otitis media - pneumonia
acute phase reactants
Popliteal

48. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
A - B - C; all the D's
In the germinal center of secondary follicles (In the paler center)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

49. What are the symptoms of serum sickness?
Lymphocytes
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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)

50. What is the receptor for EBV? On what cells is that located?
active complement pathway
mesenchymal
Para aortic
CD21 on B cells (although there is T cell lymphocytosis in EBV)