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. What is chronic mucocutaneous candidiasis d/t?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
T cell dysfunction
...
Anti Jo -1

2. What does CD16 on NK cells do?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
Bind FcG for antibody dependent cellular cytotoxicity

3. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Kill them because they have CD16 on them that recognize the FcG portion
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Immunoflourescent staining of tissue biopsies

4. what cell surface marker is used for NK cells as it is unique to them?
Recom IL 11; thrombocytopenia
CRP - C3b - IgM
CD56
...

5. What is the pathogenesis of acute transplant rejection? When does it occur?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

6. What is a factor that is a predictor for a bad transplantation?
NK cells
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
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

7. IgG...
IgE; by activating eosinophils
opsonizes
Tetanus - Botulinum - HBV - Rabies
False! B cell class switching requires a second signal

8. What are the mediators that mast cells release?
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!
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

9. What is passive immunity?
Fab portion
Active; passive - fast but short half life (3 weeks!)
Receiving preformed Antibodies
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

10. Which disease is associated withB B27?
pathogenesis
TGF beta and IL 10
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Anti smooth muscle

11. What are the cell surface proteins on NK cells?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
IgA
MHC I - CD16 - CD56

12. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
Steroid responsive nephrotic syndrome
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

13. What is hereditary angioedema? What are the C3 levels?
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
Tetanus - Botulinum - HBV - Rabies
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)
pentamer

14. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
T cell dysfunction
Anti SS- A (anti RO) and Anti SS- B
Anti IF

15. What are the autoantibodies for polymyositis and dermatomyositis?
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
DM type I
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Anti Jo -1

16. What is the main function of interferons?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
TLR ad nuclear receptors

17. 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)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
Carbohydrate

18. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
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 :(
Anti IF
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

19. what will NK cells do to cells covered in IgG Ab? why?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Stimulate the liver to release acute phase reactants
Kill them because they have CD16 on them that recognize the FcG portion
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

20. Which helper T cells' development is induced by IL 4? IL 12?
Celiac
pale central germinal centers
Th2; Th1
Para aortic

21. What is the clinical use for azathioprine?
...
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Anti Ach receptor
Chronic granulomatous disease

22. What lymph node drains the lateral side of the dorsum of the foot?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Popliteal
Increases expression of MHC I and MHC II and also activates NK cells

23. What lymph node drains the rectum (above the pectinate line)?
T
Pernicious Anemia and Hashimotos
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
Internal iliac

24. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
IgE; by activating eosinophils
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

25. Which is the most abundant antibody in blood?
IgM and IgD
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Antihistone
IgG

26. How is i Th1 helper cell inhibited?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Cytokine IL 10 secreted by Th2
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Tetanus - Botulinum - HBV - Rabies

27. What is the toxicity of muromonab?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

28. What is the most common selective Ig deficiency? What is the presentation?
RNA segment reassortment
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
Delayed type hypersensitivity
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

29. What is the general structure of an Ab?
2 heavy chains and two light chains
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Recom IL 11; thrombocytopenia
Delayed type hypersensitivity

30. What are target cells?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
MHC II - B7
Cells that stil have weird parts of their membrane that macrophages usually bite off

31. What are superantigens? give two examples.
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
Activates cytotoxic CD 8 T cells as second signal
IgA
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

32. What are the autoantibodies for graves?
Its main effect is a defect in Ab opsonization for killing
Interferon gamma and IL 2
Anti TSh receptor
Secretory component

33. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Anti viral and anti tumor
except hyperacute
When you select for which MHC it will have; take out the lymphs that self react
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

34. The lymphocytes are ________ origin
MHC II - B7
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
mesenchymal

35. which antibodies can bind complement?
No because no peptide fragment!
Paracortex
Activates Th1 helper cells; Macrophages
IgM and IgG

36. What happens in a deficiency of C3?
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
Anti topoisomerase
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

37. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
encapsulated
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Negative nitroblue tetrazolium reduction test

38. which antibodies prevent antigens from binding mucosal surfaces?
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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
T cell activation; no with CD 4 or CD 8
IgA

39. What is the common variable immunodeficiency ? How is it different from Brutons?
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
T
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

40. Complements are...
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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
acute phase reactants

41. What is the late phase reaction of anaphylaxis allergy? what mediates it?
TNF alpha and IL1
pentamer
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)
carboxy terminal

42. what mediates the type II hypersensitivity? What are the two different methods?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Fc
Popliteal
Humoral

43. What does IL 2 do?
Activates cytotoxic CD 8 T cells as second signal
A j chain
Sinusitis - otitis media - pneumonia
No because no peptide fragment!

44. What is filgrastim and sargramostim? and What is it used for?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Activate macrophages
Sinusitis - otitis media - pneumonia
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

45. What is colostrum?
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
Complement activation (active in both)
Acts as second signal on B cells to induce class switching to IgE and IgG
The igA found in breast milk

46. What is the marginal zone of the spleen? what happens there?
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
Lymphocytes
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
...

47. To what portion of the Antibody do the complements bind?
not Ab mediated
Fc
Cytokine IL 10 secreted by Th2
cannot cross placenta

48. IgM can exist as a _______ also
Interferon gamma and IL 2
Immunoflourescent staining of tissue biopsies
Th cells fail to produce interferon gamma; a lot of IgE
pentamer

49. What lymph node drains the duodenum - jejunum?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Anti TSh receptor
Anti smooth muscle
Superior mesenteric

50. What are the main cell surface proteins on B cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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)
Recom IL 11; thrombocytopenia
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP