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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 cell surface proteins are on all APCs?
IL 15; IL 12 - interferon Beta and interferon alpha
MHC II - B7
Activate macrophages
pathogenesis

2. Describe complement dependent Type II hypersensitivity. Give an example.
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
A j chain

3. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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 :(

4. Name the three opsonins
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
CRP - C3b - IgM
TGF beta and IL 10
Kill them because they have CD16 on them that recognize the FcG portion

5. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
neutrophilia!
MS - hay fever - SLE - goodpastures
Anti IF

6. is IgM an opsonizer?
Superficial inguinal
Negative!
T cell precursor
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

7. other than eat and bite RBCs what else do Macrophages of spleen do>
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Remove encapsulated bacateria
Liver! (they are proteins circulating in the blood)
Hereditary angioedema; PNH

8. What is the main function of IL 12? other than macrophages who else can release IL 12?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

9. Name two endogenous pyrogens
Recom IL 11; thrombocytopenia
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
IL 1 and IL 6
Delayed type hypersensitivity

10. What are the autoantibodies for Mixed connective tissue disease?
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
Anti U1 RNP (ribonucleoprotein)
T cell activation; no with CD 4 or CD 8
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

11. IgM can exist as a _______ also
pentamer
Carbohydrate
delayed!
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

12. What is anergy? why does this occur?
Anti viral and anti tumor
Th cells fail to produce interferon gamma; a lot of IgE
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

13. What is epo used for?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anemias (esp due to renal failure)
Anti SS- A (anti RO) and Anti SS- B
T cell precursor

14. What is the main cytokine that activates eosinophils?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
CD56
IL 5
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

15. What are target cells?
active complement pathway
Cells that stil have weird parts of their membrane that macrophages usually bite off
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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

16. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Alternative splicing of mRNA
Type IV
T

17. which of the hypersensitivity reactions is not Ab mediated?
TNF alpha and IL1
Type IV
False! B cell class switching requires a second signal
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

18. Which diseases are associated with DR5?
Pernicious Anemia and Hashimotos
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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

19. What are the autoantibodies for primary biliary cirrhosis?
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
RNA segment reassortment
Anti mitochondrial

20. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
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
Glycoproteins; HLA

21. What is thrombopoietin used for?
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
Thrombocytopenia
MS - hay fever - SLE - goodpastures
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

22. What is the autoantibody for SLE that is nonspecific? Specific?
Type IV
Remove encapsulated bacateria
Liver! (they are proteins circulating in the blood)
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

23. What lymph node drains the scrotum?
Superficial inguinal
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Sinusitis - otitis media - pneumonia
MHC I; from RER with help of the B2 microglobulin

24. Which disease is associated withB B27?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Not thymus - BM
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

25. what ensure that a memory response is generated?
If there is class switching and plasma cell production (that is when memory cells are produced)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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

26. What do multimeric antibodies require for assembly?
When you select for which MHC it will have; take out the lymphs that self react
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
A j chain
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

27. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Antidesmoglein
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Superior mesenteric

28. Complements are...
acute phase reactants
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Negative!
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

29. Which disease is associated with B8?
except hyperacute
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Graves
Negative selection

30. 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?
RNA segment reassortment
Activate macrophages
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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

31. What are the cell surface proteins for Macrophages? which two are for opsonins?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Recom IL 11; thrombocytopenia
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

32. other than C3a - what other complement acts as an anaphyloxin?
C5a
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Activates cytotoxic CD 8 T cells as second signal
RNA segment reassortment

33. Give three examples of bacteria that use antigenic variation and how.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
except hyperacute
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
IL 5

34. which antibodies can bind complement?
IgM and IgG
Activate macrophages
MHC I; from RER with help of the B2 microglobulin
SP infections

35. what secretes IL 4?
Activate macrophages
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
Not thymus - BM
Basophils! THey want IG E class switch!

36. What lymph node drains the duodenum - jejunum?
Superior mesenteric
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
All MHC 1/CD8
Interferon gamma; Th1

37. How does the alternative pathway lead to MAC activation?
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
Anti Ach receptor
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Anti SS- A (anti RO) and Anti SS- B

38. What are the autoantibodies for sjorgens syndrome?
Cytokine IL 10 secreted by Th2
isotype
Anti SS- A (anti RO) and Anti SS- B
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

39. What does interferon gamma do? What two type of cells does it attack mostly?
Superficial inguinal
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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

40. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
DM type I
By transcytosis

41. What is a factor that is a predictor for a bad transplantation?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
type four
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

42. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Type IV
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Complement activation (active in both)
Anti U1 RNP (ribonucleoprotein)

43. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Activates cytotoxic CD 8 T cells as second signal
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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

44. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Anti Ach receptor
Influenza; antigenic shift; antigenic drift
The igA found in breast milk
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

45. hat is the presentation of Jobs syndrome or Hyper IgE?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Th cells fail to produce interferon gamma; a lot of IgE
Cytokine IL 10 secreted by Th2
Axillary

46. What lymph node drains the upper limb?
Axillary
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
Barrel hoop basement membrane fenestrations
Anti Jo -1

47. What is the toxicity of muromonab?
Daclizumab; prevent ACUTE rejection of renal transplant
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Acts as second signal on B cells to induce class switching to IgE and IgG

48. What are some sinopulmonary infections?
DM type I and RA
2 heavy chains and two light chains
Sinusitis - otitis media - pneumonia
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

49. What is the common variable immunodeficiency ? How is it different from Brutons?
Antimicrosomal and antithyroglobulin
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
Its main effect is a defect in Ab opsonization for killing
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!

50. can igG cross the placenta?
Carbohydrate
Yes
Type IV
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!