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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 does IL 4 do?
Acts as second signal on B cells to induce class switching to IgE and IgG
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Tetanus - Botulinum - HBV - Rabies
Cells that stil have weird parts of their membrane that macrophages usually bite off

2. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
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
SP infections
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

3. Describe the complement independent Type II hypersenstivity reaction. Give an example.
IgG
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Anti glutamate carboxylase and anti insulin
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

4. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
pathogenesis
Influenza; antigenic shift; antigenic drift
Fc
pentamer

5. What lymph node drains the anal canal (below the pectinate line)?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Superficial inguinal
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
IL 15; IL 12 - interferon Beta and interferon alpha

6. What is the main function of interferons?
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
Popliteal
Its main effect is a defect in Ab opsonization for killing
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

7. What lymph node drains the thigh?
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
Superficial inguinal
Antibody mediated cytotoxicity; either complement dependent or complement independent
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

8. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Antidesmoglein
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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

9. What is the most common example of passive immunity?
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
IgAs in mothers breast milk!
CRP - C3b - IgM
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

10. How fast does it occur?
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 :(
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
The patient could become cyanotic in the OR!
Active; passive - fast but short half life (3 weeks!)

11. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Alternative splicing of mRNA
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

12. 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
IgG
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
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

13. What are the main Cell surface proteins on T cells?
In the germinal center of secondary follicles (In the paler center)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
2 heavy chains and two light chains
lowest concentration

14. What are howell jolly bodies?
TLR ad nuclear receptors
TNF alpha and IL1
Its main effect is a defect in Ab opsonization for killing
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

15. ________ regulate the cell mediated response.
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 :(
Humoral
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

16. What kinds of receptors activate innate immunity?
...
In the germinal center of secondary follicles (In the paler center)
TLR ad nuclear receptors
Chronic granulomatous disease

17. How is sirolimus different from tacrolimus?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

18. T/F B cells do not require a second signal
IgG
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
False! B cell class switching requires a second signal
IL 4 - 5 - 10 - 6

19. Give an example of someone who could get hyperacute transplant rejection.
neutrophilia!
Not thymus - BM
Previous transfusion; pregnant woman whose fetus had paternal antigens
Anti U1 RNP (ribonucleoprotein)

20. What is the general structure of an Ab?
...
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
IgG
2 heavy chains and two light chains

21. The lymphocytes are ________ origin
IgE
mesenchymal
MS
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

22. What do multimeric antibodies require for assembly?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Fab portion
neutrophilia!
A j chain

23. What happens in a secondary follicle?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Recom IL 11; thrombocytopenia
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

24. What are C1 - C2 - C3 - C4 important for?
active complement pathway
Activates Th1 helper cells; Macrophages
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
Viral neutralization of igM and IgG!

25. What is the presentation of hyperIgM syndrome?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Severe pyogenic infections early in life
The igA found in breast milk

26. What are target cells?
Wiskott Aldrich syndrome
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
Superior mesenteric

27. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Histamine; post capillary venules - vasodilation
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
Influenza; antigenic shift; antigenic drift

28. which of the hypersensitivity reactions is not Ab mediated?
IgG
Type IV
Negative!
Immunosuppression after kidney transplantation

29. How do you test for chronic granulomatous disease?
Active; passive - fast but short half life (3 weeks!)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Inferior mesenteric
Negative nitroblue tetrazolium reduction test

30. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
TGF beta and IL 10
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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

31. What is a factor that is a predictor for a bad transplantation?
Viral neutralization of igM and IgG!
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
MS - hay fever - SLE - goodpastures
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

32. What happens in a deficiency of C3?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Macrophages - Dendritic cells - B cells
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Anti topoisomerase

33. What bugs can actually infect the lymph node itself?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Daclizumab; prevent ACUTE rejection of renal transplant
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

34. What lymph node drains the stomach?
Antidote for digoxin intoxication
Celiac
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

35. What does granulysin do?
CD56
T cell dysfunction
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

36. 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
Cells that stil have weird parts of their membrane that macrophages usually bite off
Bind FcG for antibody dependent cellular cytotoxicity
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

37. What is the pathogenesis of a hypersensitivity reaction?
Celiac
IgA
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
Cytokine IL 10 secreted by Th2

38. What is a type I hypersensitivity reaction? What is atopic?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Cytokine IL 10 secreted by Th2
carboxy terminal

39. is IgM an opsonizer?
Negative!
IL 4
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

40. 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
IgE
Activate macrophages
Negative selection

41. can igG cross the placenta?
Yes
Type IV
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Immunosuppression after kidney transplantation

42. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
NK cells
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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

43. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Anti topoisomerase
pathogenesis
heavy chains
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

44. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Previous transfusion; pregnant woman whose fetus had paternal antigens
T cell activation; no with CD 4 or CD 8
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
acute phase reactants

45. What is colostrum?
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
The igA found in breast milk

46. Other than stimulating fever - what else does IL 6 do?
Stimulate the liver to release acute phase reactants
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Para aortic
...

47. What is passive immunity?
Tetanus - Botulinum - HBV - Rabies
MHC class molecules bind to KIRS or CD94 to prevent killing
Receiving preformed Antibodies
Lymphocytes

48. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
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
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
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

49. What are the autoantibodies for myasthenia gravis?
DM type I and RA
Rheumatic arthritis
Anti Ach receptor
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

50. What is the main function of IL 12? other than macrophages who else can release IL 12?
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Negative!
TLR ad nuclear receptors