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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. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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
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
IgM and IgA

2. Leukocyte adhesion defect presents with...
Delayed type hypersensitivity
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
IgG
neutrophilia!

3. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
IgAs in mothers breast milk!
except hyperacute
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
...

4. hat is the presentation of Jobs syndrome or Hyper IgE?
MHC II - B7
CD56
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
NK cells

5. What is the presentation of hyperIgM syndrome?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Inferior mesenteric
MHC I - CD16 - CD56
Severe pyogenic infections early in life

6. What are the major functions of Antibodies?
All MHC 1/CD8
Cross link
Type IV
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

7. what bacteria are a splenectomy patient most susceptible to? why?
2 heavy chains and two light chains
A j chain
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
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

8. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Anemias (esp due to renal failure)
MHC I - CD16 - CD56
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Interferon gamma; Th1

9. which of the hypersensitivity reactions is not Ab mediated?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Type IV
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
type four

10. which cytokine inhibits TH2 cells? secreted by who?
pentamer
Interferon gamma; Th1
Liver! (they are proteins circulating in the blood)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

11. Which type of selection of thymic development provides central tolerance?
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
Negative selection
dimer
pentamer

12. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Anti TSh receptor
Hemochromatosis
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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

13. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
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
2 heavy chains and two light chains
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

14. What cytokines to Th2 secrete?
When you select for which MHC it will have; take out the lymphs that self react
Bind FcG for antibody dependent cellular cytotoxicity
IL 4 - 5 - 10 - 6
Anti IF

15. How does the alternative pathway lead to MAC activation?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Negative nitroblue tetrazolium reduction test
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

16. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Cells that stil have weird parts of their membrane that macrophages usually bite off
IgM
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
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

17. How is i Th1 helper cell inhibited?
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep
Cytokine IL 10 secreted by Th2
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Macrophages - Dendritic cells - B cells

18. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
neutrophilia!
Superior mesenteric
Histamine; post capillary venules - vasodilation
The igA found in breast milk

19. What is the main cytokine released by T cells? What does it do
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
IL 3; supports growth and differentiation of bone marrow stem cells
Daclizumab; prevent ACUTE rejection of renal transplant
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

20. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Anti IF
A recomb cytokine of IL 2; RCC and metastatic melanoma
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

21. Which disease is associated with B8?
Graves
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
Anti Jo -1
Carbohydrate

22. What is epo used for?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Axillary
Anemias (esp due to renal failure)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

23. what secretes IL 4?
IL 4
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Basophils! THey want IG E class switch!
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

24. 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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
dimer

25. What do multimeric antibodies require for assembly?
MHC I; from RER with help of the B2 microglobulin
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Negative!
A j chain

26. when can graft versus host disease? What is the result?
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Hereditary angioedema; PNH

27. Describe complement dependent Type II hypersensitivity. Give an example.
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
type four
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

28. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Celiac
Influenza; antigenic shift; antigenic drift
In the germinal center of secondary follicles (In the paler center)

29. The MALT/GALT are not...
IgG
encapsulated
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Thrombocytopenia

30. What is recomb beta interferon used for?
IL 15; IL 12 - interferon Beta and interferon alpha
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
MS
Stimulate the liver to release acute phase reactants

31. 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
Anti TSh receptor
opsonizes
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

32. How does complement link innate and adaptive?
Anti viral and anti tumor
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

33. Which cytokines do Th2 release and For what?
Anti viral and anti tumor
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Its a serine protease that activates apoptosis; NK and CD8
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

34. The lymphocytes are ________ origin
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
mesenchymal
TGF beta and IL 10
acute phase reactants

35. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Pernicious Anemia and Hashimotos
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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
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

36. Which antibody mediates immunity to worms? how?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IgE; by activating eosinophils
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

37. describe the pathogenesis of delayed type IV hypersensitivity
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

38. What is an example of a parasite showing antigenic variation?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Th2; Th1

39. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
If there is class switching and plasma cell production (that is when memory cells are produced)
Its main effect is a defect in Ab opsonization for killing
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 :(
Negative selection

40. IgE has the ___________ in the serum
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
lowest concentration
A j chain
T

41. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Hereditary angioedema; PNH
Kill them because they have CD16 on them that recognize the FcG portion
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

42. What are the mediators that mast cells release?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
IgAs in mothers breast milk!

43. What are the autoantibodies for pemphigus bulgaris?
Antidesmoglein
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
B - T - and NK cells
MHC I - CD16 - CD56

44. What are the autoantibodies for pernicious anemia?
Superficial inguinal
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Anti IF

45. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
IgG
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

46. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
cannot cross placenta
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

47. What are the main cell surface proteins on B cells?
MHC I; from RER with help of the B2 microglobulin
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

48. what will NK cells do to cells covered in IgG Ab? why?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Kill them because they have CD16 on them that recognize the FcG portion
Immunoflourescent staining of tissue biopsies
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

49. What are the T cell functions?
Anemias (esp due to renal failure)
IgM
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Its a serine protease that activates apoptosis; NK and CD8

50. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Th cells fail to produce interferon gamma; a lot of IgE
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
IgA