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. Complements are...
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
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 :(
acute phase reactants
IgM

2. Describe complement dependent Type II hypersensitivity. Give an example.
IL 1 and IL 6
Wiskott Aldrich syndrome
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

3. Which is the main antibody in the delayed or secondary response to an antigen?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
If there is class switching and plasma cell production (that is when memory cells are produced)
IgG

4. Describe the complement independent Type II hypersenstivity reaction. Give an example.
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
In the germinal center of secondary follicles (In the paler center)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
carboxy terminal

5. IgM can fix complement but...
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Anti Jo -1
cannot cross placenta
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

6. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
...
Rheumatic arthritis
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Negative selection

7. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Delayed type hypersensitivity

8. What do mature naive B lymphocytes express?
Thrombocytopenia
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)
IgM and IgD
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

9. What are the autoantibodies for goodpastures syndrome?
IgE; by activating eosinophils
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Anti alpha subunit 3 of collagen on type IV bm

10. which B and T cell disorder presents with specifically low IgM?
No because no peptide fragment!
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Wiskott Aldrich syndrome
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

11. Monomer in circulation - ___ when secreted
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Its a serine protease that activates apoptosis; NK and CD8
dimer
C5a

12. Describe the capsular structure of a lymph node; What are the functions of the LN?
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
Celiac
Barrel hoop basement membrane fenestrations
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 :(

13. what will NK cells do to cells covered in IgG Ab? why?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Kill them because they have CD16 on them that recognize the FcG portion
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
By transcytosis

14. what ensure that a memory response is generated?
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
If there is class switching and plasma cell production (that is when memory cells are produced)
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Delayed type hypersensitivity

15. are Th cells involved in trapping of antigens of endotoxin/LPS?
B - T - and NK cells
No because no peptide fragment!
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

16. where do NK cells develop?
Not thymus - BM
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

17. What is immune complex disease? give an example.
Influenza; antigenic shift; antigenic drift
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Activates Th1 helper cells; Macrophages

18. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
Anti smooth muscle
Fab portion
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

19. What is the main function of interferons?
Activate macrophages
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Cyclosporine - OKT3
IgM and IgA

20. What is the pathology of acute transplant rejection? is it reversible?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Anti alpha subunit 3 of collagen on type IV bm
not Ab mediated
IgAs in mothers breast milk!

21. The alternative pathway is the only constutively...
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
active complement pathway
A j chain
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

22. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Superficial inguinal
Activates Th1 helper cells; Macrophages
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
If there is class switching and plasma cell production (that is when memory cells are produced)

23. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Activate macrophages

24. what cytokine does basophils secrete?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
IL 4
Anti Jo -1
heavy chains

25. What is the marginal zone of the spleen? what happens there?
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
IL 5
Negative!
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

26. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Th2; Th1
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Cross link
Anti IF

27. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
By transcytosis
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

28. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
T cell precursor
Not thymus - BM
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
active complement pathway

29. what secretes IL 4?
Activates Th1 helper cells; Macrophages
Basophils! THey want IG E class switch!
Immunoflourescent staining of tissue biopsies
Paracortex

30. What lymph node drains the thigh?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
neutrophilia!
Superficial inguinal

31. 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
TNF alpha and IL1
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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

32. Describe the Mannose Lectin pathway
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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 BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

33. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Anti Jo -1
Daclizumab; prevent ACUTE rejection of renal transplant
Local infection/inflammation; infection of the ln itself; metastasis
Inferior mesenteric

34. give an example of how influenza does a major antigenic shift.
Macrophages - Dendritic cells - B cells
Para aortic
RNA segment reassortment
Secretory component

35. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
MS
dimer
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

36. How is the antigen loaded onto a MHC II?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Local infection/inflammation; infection of the ln itself; metastasis
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
Steroid responsive nephrotic syndrome

37. what prevents NK cells from killing normal cells if their default is to kill?
MHC class molecules bind to KIRS or CD94 to prevent killing
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Receiving preformed Antibodies
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

38. The idiotype; the Fc portion determines the...
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Liver! (they are proteins circulating in the blood)
Anti smooth muscle
isotype

39. What are the autoantibodies for hashimotos?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Antimicrosomal and antithyroglobulin
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

40. Which disease is associated with DR7?
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
Steroid responsive nephrotic syndrome
Antimicrosomal and antithyroglobulin
IgG

41. Type Iv hypersensitivity is...
Antidote for digoxin intoxication
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
delayed!
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

42. What are the T cell functions?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Anti glutamate carboxylase and anti insulin
Basophils! THey want IG E class switch!
Influenza; antigenic shift; antigenic drift

43. which cells have more complete tolerance - B or T cells?
Humoral
T
IgE
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

44. Which are the only two antiinflammatory cytokines?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
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
TGF beta and IL 10
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

45. Which diseases are associated with DR5?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
neutrophilia!
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Pernicious Anemia and Hashimotos

46. What is Aldesleukin? What is it used for
Interferon gamma; Th1
A recomb cytokine of IL 2; RCC and metastatic melanoma
mesenchymal
Acts as second signal on B cells to induce class switching to IgE and IgG

47. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
T cell dysfunction
Negative nitroblue tetrazolium reduction test
Anemias (esp due to renal failure)
Alternative splicing of mRNA

48. The secondary follicles have __________; primary follicles are dense
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
DM type I
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
pale central germinal centers

49. How is i Th1 helper cell inhibited?
Cytokine IL 10 secreted by Th2
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Interferon gamma; Th1
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

50. Which is the main antibody that provides passive immunity to infants?
Local infection/inflammation; infection of the ln itself; metastasis
IgG
Anti SS- A (anti RO) and Anti SS- B
IL 1 and IL 6