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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 cell surface proteins on NK cells?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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
MHC I - CD16 - CD56
RNA segment reassortment

2. Only the _______ contribute to the Fc region
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
T cell precursor
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
heavy chains

3. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
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
Acts as second signal on B cells to induce class switching to IgE and IgG
Cross link
Anti U1 RNP (ribonucleoprotein)

4. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Influenza; antigenic shift; antigenic drift
Cytokine IL 10 secreted by Th2
secondary
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

5. What are the cell surface proteins for Macrophages? which two are for opsonins?
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
TGF beta and IL 10
Its main effect is a defect in Ab opsonization for killing
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

6. What is filgrastim and sargramostim? and What is it used for?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Superficial inguinal

7. what cytokine does basophils secrete?
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
IL 4
MHC II - B7
Anti IF

8. What are the main cell surface proteins on B cells?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
...
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

9. What is the main function of IL 12? other than macrophages who else can release IL 12?
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
DM type I
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

10. Which is the main antibody in the delayed or secondary response to an antigen?
IgG
encapsulated
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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

11. What are the autoantibodies for Celiac disease?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
isotype
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Anti SS- A (anti RO) and Anti SS- B

12. What is the presentation of scid? treatment?
IgM and IgD
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
Anti IF
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

13. Which helper T cells' development is induced by IL 4? IL 12?
Th2; Th1
secondary
IL 3; supports growth and differentiation of bone marrow stem cells
2 heavy chains and two light chains

14. The ______ in the BM are DN - the DP are in the cortex of thymus
T cell precursor
Antidesmoglein
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Edema and necrosis in that region

15. What is the presentation of hyperIgM syndrome?
Hereditary angioedema; PNH
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Anti Jo -1
Severe pyogenic infections early in life

16. What links the adaptive and innate immunity?
Antidote for digoxin intoxication
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
Complement activation (active in both)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

17. What cytokines are released by Th1 cells?
Para aortic
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Interferon gamma and IL 2
Active; passive - fast but short half life (3 weeks!)

18. What type of fenestrations are found in the red pulp of the spleen?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Paracortex
Type IV
Barrel hoop basement membrane fenestrations

19. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
False! B cell class switching requires a second signal
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Superficial inguinal

20. What are the function of B cells?
Active; passive - fast but short half life (3 weeks!)
Cytokine IL 10 secreted by Th2
RNA segment reassortment
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

21. Type Iv hypersensitivity is...
Stimulate the liver to release acute phase reactants
neutrophilia!
Celiac
delayed!

22. What does granzyme do? who secretes it?
Paracortex; viral infection
Its a serine protease that activates apoptosis; NK and CD8
If there is class switching and plasma cell production (that is when memory cells are produced)
When you select for which MHC it will have; take out the lymphs that self react

23. when can graft versus host disease? What is the result?
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)
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
IgA
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

24. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
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
Recom IL 11; thrombocytopenia
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

25. What is the treatment of acute transplant rejection?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Superficial inguinal
Cyclosporine - OKT3

26. What is anergy? why does this occur?
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

27. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Para aortic
Anti Ach receptor
...
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

28. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Wiskott Aldrich syndrome
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
...

29. What does interferon gamma do to be antiviral?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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
Increases expression of MHC I and MHC II and also activates 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

30. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Histamine; post capillary venules - vasodilation
MS - hay fever - SLE - goodpastures
MHC I - CD16 - CD56
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

31. What are the autoantibodies for drug induced lupus?
Hereditary angioedema; PNH
Antihistone
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

32. What are the two signals required for B cell class switching? Which is the second signal?
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
dimer
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

33. How fast does it occur?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
Th cells fail to produce interferon gamma; a lot of IgE
The patient could become cyanotic in the OR!

34. What happens in a deficiency of C3?
Cyclosporine - OKT3
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
TGF beta and IL 10

35. What lymph node drains the breast?
Axillary
Superficial inguinal
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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

36. which type of immunity is slow but long lasting? as opposed to...
Anti mitochondrial
Kill them because they have CD16 on them that recognize the FcG portion
Active; passive - fast but short half life (3 weeks!)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

37. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

38. The secondary follicles have __________; primary follicles are dense
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
IL 3; supports growth and differentiation of bone marrow stem cells
pale central germinal centers
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

39. describe the pathogenesis of delayed type IV hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
IL 15; IL 12 - interferon Beta and interferon alpha
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Type IV

40. Leukocyte adhesion defect presents with...
neutrophilia!
Cells that stil have weird parts of their membrane that macrophages usually bite off
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Negative!

41. What are the three types of APCs?
Anti SS- A (anti RO) and Anti SS- B
CRP - C3b - IgM
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Macrophages - Dendritic cells - B cells

42. What are the autoantibodies for graves?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
TGF beta and IL 10
Anti TSh receptor
Superficial inguinal

43. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
IL 4
Cross link
T cell precursor
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

44. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Receiving preformed Antibodies
2 heavy chains and two light chains

45. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Secretory component
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

46. What are the main symptoms of B cell immunodeficiencies?
When you select for which MHC it will have; take out the lymphs that self react
SP infections
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

47. What are superantigens? give two examples.
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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
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
Immunosuppression after kidney transplantation

48. What bugs can actually infect the lymph node itself?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
2 heavy chains and two light chains
Celiac
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

49. What does granulysin do?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
IgM
not Ab mediated
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

50. what secretes IL 4?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
Basophils! THey want IG E class switch!