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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.
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 cell surface proteins on NK cells?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Activates cytotoxic CD 8 T cells as second signal
MHC I - CD16 - CD56
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

2. T/F B cells do not require a second signal
Superficial inguinal
False! B cell class switching requires a second signal
Antimicrosomal and antithyroglobulin
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

3. Which cytokines do Th2 release and For what?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Severe pyogenic infections early in life
Kill them because they have CD16 on them that recognize the FcG portion

4. What is the toxicity of azathioprine?
Viral neutralization of igM and IgG!
...
IgG
IgE; by activating eosinophils

5. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
IgG
Paracortex; viral infection
Stimulate the liver to release acute phase reactants
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

6. What are the major functions of Antibodies?
neutrophilia!
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Superior mesenteric
Macrophages - Dendritic cells - B cells

7. Which is the most abundant antibody in blood?
IgM
Receiving preformed Antibodies
IgG
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

8. Which is the main antibody in the delayed or secondary response to an antigen?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
IgG
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
pale central germinal centers

9. What are the autoantibodies for other vasculitides?
Antidote for digoxin intoxication
Rheumatic arthritis
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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

10. What is a type I hypersensitivity reaction? What is atopic?
A - B - C; all the D's
IL 4 - 5 - 10 - 6
T
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

11. What is serum sickness? give an example.
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
Not thymus - BM
All MHC 1/CD8
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

12. can igG cross the placenta?
Yes
T
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Liver! (they are proteins circulating in the blood)

13. Complements are...
acute phase reactants
MHC I - CD16 - CD56
The igA found in breast milk
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

14. From where do cytokines come from?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Lymphocytes
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

15. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Type IV
lowest concentration
The patient could become cyanotic in the OR!
Alternative splicing of mRNA

16. What are the symptoms of serum sickness?
Th cells fail to produce interferon gamma; a lot of IgE
Steroid responsive nephrotic syndrome
Histamine; post capillary venules - vasodilation
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

17. what mediates the type II hypersensitivity? What are the two different methods?
Internal iliac
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Antibody mediated cytotoxicity; either complement dependent or complement independent
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

18. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
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
Activate macrophages
MHC II - B7
delayed!

19. Which antibodies can be multimeric?
IgM and IgA
Macrophages - Dendritic cells - B cells
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
IL 4 - 5 - 10 - 6

20. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
If there is class switching and plasma cell production (that is when memory cells are produced)
Fab portion
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
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

21. Monomer in circulation - ___ when secreted
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
delayed!
Sinusitis - otitis media - pneumonia
dimer

22. What does granulysin do?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Anti IF
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

23. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Histamine; post capillary venules - vasodilation
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

24. In general What are T cells good for?
Anti viral and anti tumor
Steroid responsive nephrotic syndrome
Severe pyogenic infections early in life
cannot cross placenta

25. What is the clinical use for azathioprine?
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
...
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Fab portion

26. IgM can fix complement but...
cannot cross placenta
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
delayed!
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

27. What is colostrum?
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
The igA found in breast milk
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
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

28. What is oprelevkin? and What is it used for?
Carbohydrate
Recom IL 11; thrombocytopenia
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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

29. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
MHC class molecules bind to KIRS or CD94 to prevent killing
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

30. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Its main effect is a defect in Ab opsonization for killing
T cell activation; no with CD 4 or CD 8
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

31. The secondary follicles have __________; primary follicles are dense
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
pale central germinal centers

32. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Complement activation (active in both)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Remove encapsulated bacateria
Receiving preformed Antibodies

33. What is the toxicity of muromonab?
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Paracortex; viral infection

34. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
C5a
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

35. which of the transplant rejections is antibody mediated? why does it occur?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Alternative splicing of mRNA
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

36. What are the autoantibodies for goodpastures syndrome?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Anti alpha subunit 3 of collagen on type IV bm
By transcytosis

37. The idiotype; the Fc portion determines the...
IgG
...
isotype
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

38. What is the main function of IL 8?
A chemotactic factor for neutrophils
IL 1 and IL 6
Barrel hoop basement membrane fenestrations
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

39. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Anti SS- A (anti RO) and Anti SS- B
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
pathogenesis
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

40. 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
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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 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

41. What is the clinical use of Muromonab?
Immunosuppression after kidney transplantation
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)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Axillary

42. Which is the main antibody that provides passive immunity to infants?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Remove encapsulated bacateria
IgG
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

43. What is the common variable immunodeficiency ? How is it different from Brutons?
Anti glutamate carboxylase and anti insulin
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
Cytokine IL 10 secreted by Th2
IgE; by activating eosinophils

44. Which disease is associated with DR3?
All MHC 1/CD8
DM type I
Cytokine IL 10 secreted by Th2
Anemias (esp due to renal failure)

45. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Viral neutralization of igM and IgG!
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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

46. What is the most common selective Ig deficiency? What is the presentation?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Its a serine protease that activates apoptosis; NK and CD8
T cell precursor

47. What is Aldesleukin? What is it used for
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
A recomb cytokine of IL 2; RCC and metastatic melanoma

48. What lymph node drains the duodenum - jejunum?
IL 1 and IL 6
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
Superior mesenteric
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

49. which interleukin receptor is required for NK development? activation?
T cell activation; no with CD 4 or CD 8
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
If there is class switching and plasma cell production (that is when memory cells are produced)
IL 15; IL 12 - interferon Beta and interferon alpha

50. What do multimeric antibodies require for assembly?
pathogenesis
Anti topoisomerase
Superior mesenteric
A j chain