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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. IgG...
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
opsonizes
2 heavy chains and two light chains
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

2. What does granulysin do?
Anemias (esp due to renal failure)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Fab portion

3. What are the cell surface proteins on NK cells?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Paracortex; viral infection
MHC I - CD16 - CD56
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

4. The MALT/GALT are not...
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
encapsulated

5. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
...
Wiskott Aldrich syndrome
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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

6. in which immunodef order do you see a lot of pus? no pus?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Complement activation (active in both)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

7. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IgE; by activating eosinophils
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

8. What is the clinical use for azathioprine?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
...
Paracortex; viral infection
Stimulate the liver to release acute phase reactants

9. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Immunosuppression after kidney transplantation
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

10. Type Iv hypersensitivity is...
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
delayed!
Anti IF
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

11. What are the autoantibodies for pemphigus bulgaris?
T cell activation; no with CD 4 or CD 8
Antidesmoglein
SP infections
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

12. What is the pathology seen in chronic transplant rejection?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
S. aureus - E. Coli - aspergillus
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

13. What is anergy? why does this occur?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Its main effect is a defect in Ab opsonization for killing
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

14. What are superantigens? give two examples.
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
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

15. What is a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Wiskott Aldrich syndrome
...
MHC I; from RER with help of the B2 microglobulin

16. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
cannot cross placenta
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
S. aureus - E. Coli - aspergillus

17. hat is the presentation of Jobs syndrome or Hyper IgE?
pathogenesis
Chronic granulomatous disease
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

18. What are the autoantibodies for goodpastures syndrome?
type four
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anti alpha subunit 3 of collagen on type IV bm

19. Describe the Mannose Lectin pathway
Carbohydrate
Immunosuppression after kidney transplantation
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

20. What is the general structure of an Ab?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
2 heavy chains and two light chains
Graves
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

21. other than C3a - what other complement acts as an anaphyloxin?
All MHC 1/CD8
DM type I
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
C5a

22. Leukocyte adhesion defect presents with...
Not thymus - BM
Tetanus - Botulinum - HBV - Rabies
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
neutrophilia!

23. What are some sinopulmonary infections?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Kill them because they have CD16 on them that recognize the FcG portion
Sinusitis - otitis media - pneumonia
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

24. What are the autoantibodies for Celiac disease?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Recom IL 11; thrombocytopenia
IgG

25. How is the antigen loaded onto a MHC II?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

26. what secretes IL 4?
Antimicrosomal and antithyroglobulin
Acts as second signal on B cells to induce class switching to IgE and IgG
Basophils! THey want IG E class switch!
Th2; Th1

27. What are some catalase positive organisms?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Steroid responsive nephrotic syndrome
S. aureus - E. Coli - aspergillus
The patient could become cyanotic in the OR!

28. describe the classic complement pathway.
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Para aortic
Anti alpha subunit 3 of collagen on type IV bm

29. The ______ in the BM are DN - the DP are in the cortex of thymus
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
T cell precursor
type four

30. Name the three opsonins
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
CRP - C3b - IgM

31. For which toxins are preformed antibodies (passive) given?
Delayed type hypersensitivity
Antibody mediated cytotoxicity; either complement dependent or complement independent
Cytokine IL 10 secreted by Th2
Tetanus - Botulinum - HBV - Rabies

32. What lymph node drains the breast?
The igA found in breast milk
Axillary
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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

33. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
No because no peptide fragment!
Anti smooth muscle
Th cells fail to produce interferon gamma; a lot of IgE
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

34. Monomer in circulation - ___ when secreted
Edema and necrosis in that region
Delayed type hypersensitivity
dimer
carboxy terminal

35. what prevents NK cells from killing normal cells if their default is to kill?
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
Severe pyogenic infections early in life
Lymphocytes
MHC class molecules bind to KIRS or CD94 to prevent killing

36. What are four results of a splenectomy?
IgG
Hereditary angioedema; PNH
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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

37. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
pathogenesis
In the germinal center of secondary follicles (In the paler center)

38. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
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
Lymphocytes
Its main effect is a defect in Ab opsonization for killing
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

39. Which disease is associated with DR3?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
DM type I
Anti Jo -1
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

40. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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
Bind FcG for antibody dependent cellular cytotoxicity

41. What is the main function of IL 12? other than macrophages who else can release IL 12?
T cell activation; no with CD 4 or CD 8
Immunoflourescent staining of tissue biopsies
Superficial inguinal
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

42. what happens in a deficiency of C1 esterase inhibitor? DAF?
IL 4
Activates Th1 helper cells; Macrophages
Popliteal
Hereditary angioedema; PNH

43. What is the main function of IL 8?
Viral neutralization of igM and IgG!
A chemotactic factor for neutrophils
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

44. What is the autoantibody for SLE that is nonspecific? Specific?
isotype
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Its main effect is a defect in Ab opsonization for killing
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

45. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
No because no peptide fragment!
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
pathogenesis
T

46. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
NK cells
Interferon gamma and IL 2
Anti TSh receptor

47. 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?
Activates Th1 helper cells; Macrophages
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

48. ________ regulate the cell mediated response.
Humoral
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

49. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Macrophages - Dendritic cells - B cells
TNF alpha and IL1
Antibody mediated cytotoxicity; either complement dependent or complement independent

50. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Antihistone
pale central germinal centers