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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. The secondary follicles have __________; primary follicles are dense
T cell activation; no with CD 4 or CD 8
...
pale central germinal centers
IgM and IgG

2. What lymph node drains the scrotum?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
MHC class molecules bind to KIRS or CD94 to prevent killing
Superficial inguinal
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

3. What are the three types of APCs?
Macrophages - Dendritic cells - B cells
A j chain
Negative selection
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

4. What lymph node drains the lateral side of the dorsum of the foot?
Activate macrophages
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Popliteal
TLR ad nuclear receptors

5. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
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
Glycoproteins; HLA
TGF beta and IL 10
Increases expression of MHC I and MHC II and also activates NK cells

6. What are the autoantibodies for Celiac disease?
IL 15; IL 12 - interferon Beta and interferon alpha
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
B - T - and NK cells

7. What are the autoantibodies for hashimotos?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Antimicrosomal and antithyroglobulin
By transcytosis
acute phase reactants

8. other than eat and bite RBCs what else do Macrophages of spleen do>
not Ab mediated
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Remove encapsulated bacateria
carboxy terminal

9. which antibodies can bind complement?
Antidote for digoxin intoxication
Anti glutamate carboxylase and anti insulin
T cell precursor
IgM and IgG

10. What are C1 - C2 - C3 - C4 important for?
A j chain
Yes
Cytokine IL 10 secreted by Th2
Viral neutralization of igM and IgG!

11. which of the hypersensitivity reactions is not Ab mediated?
Type IV
IgE
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

12. In thymic development - What is the positive selection? negative selections?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
T cell activation; no with CD 4 or CD 8
IgA
When you select for which MHC it will have; take out the lymphs that self react

13. 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
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
opsonizes
MHC II - B7

14. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Cytokine IL 10 secreted by Th2
Thrombocytopenia
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

15. What is the clinical use of Muromonab?
Immunosuppression after kidney transplantation
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
except hyperacute
Paracortex; viral infection

16. What does IL 4 do?
IL 5
Bind FcG for antibody dependent cellular cytotoxicity
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Acts as second signal on B cells to induce class switching to IgE and IgG

17. What is the toxicity of azathioprine?
MHC I; from RER with help of the B2 microglobulin
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)
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
...

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

19. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
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
Bind FcG for antibody dependent cellular cytotoxicity
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

20. can igG cross the placenta?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Yes
Cytokine IL 10 secreted by Th2
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

21. The Fc region is found on the...
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
carboxy terminal
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
In the germinal center of secondary follicles (In the paler center)

22. What does granulysin do?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Anti U1 RNP (ribonucleoprotein)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

23. To what portion of the Antibody do the complements bind?
Fc
T cell activation; no with CD 4 or CD 8
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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

24. What are the main cell surface proteins on B cells?
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

25. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Activate macrophages
Activates Th1 helper cells; Macrophages
Cytokine IL 10 secreted by Th2
Alternative splicing of mRNA

26. A lymph node is a ________ lymphoid organ.
secondary
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
isotype
Its main effect is a defect in Ab opsonization for killing

27. What are howell jolly bodies?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IgG
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

28. What type of side chains are found on Fc region of an antibody?
Tetanus - Botulinum - HBV - Rabies
Carbohydrate
Th2; Th1
Anti mitochondrial

29. What is a factor that is a predictor for a bad transplantation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
S. aureus - E. Coli - aspergillus
When you select for which MHC it will have; take out the lymphs that self react

30. Which cytokines do Th2 release and For what?
Its a serine protease that activates apoptosis; NK and CD8
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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

31. IgE has the ___________ in the serum
lowest concentration
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Rheumatic arthritis

32. What are the three types of lymphocytes?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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
B - T - and NK cells

33. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Anti SS- A (anti RO) and Anti SS- B
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

34. What is serum sickness? give an example.
active complement pathway
T cell dysfunction
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
Anti mitochondrial

35. How does igA cross the epithelium?
Interferon gamma and IL 2
Superficial inguinal
By transcytosis
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

36. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
secondary
All MHC 1/CD8
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

37. What are the labs in brutons agammaglobulinemia?
Immunoflourescent staining of tissue biopsies
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

38. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
Histamine; post capillary venules - vasodilation
Anti SS- A (anti RO) and Anti SS- B
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

39. What are the autoantibodies for myasthenia gravis?
TGF beta and IL 10
Anti Ach receptor
If there is class switching and plasma cell production (that is when memory cells are produced)
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

40. What does IL 2 do?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Activates cytotoxic CD 8 T cells as second signal
Anti U1 RNP (ribonucleoprotein)
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

41. Give three examples of bacteria that use antigenic variation and how.
Basophils! THey want IG E class switch!
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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
Wiskott Aldrich syndrome

42. which cells have more complete tolerance - B or T cells?
dimer
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
The igA found in breast milk
T

43. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
IgG
Carbohydrate
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

44. What are the autoantibodies for drug induced lupus?
Influenza; antigenic shift; antigenic drift
Antihistone
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Antibody mediated cytotoxicity; either complement dependent or complement independent

45. What bugs can actually infect the lymph node itself?
Anti TSh receptor
type four
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
carboxy terminal

46. What is passive immunity?
Receiving preformed Antibodies
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
Immunosuppression after kidney transplantation

47. where are complements produced?
Liver! (they are proteins circulating in the blood)
Paracortex
Negative selection
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

48. What are the autoantibodies for polymyositis and dermatomyositis?
IL 5
neutrophilia!
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Anti Jo -1

49. How does complement link innate and adaptive?
Para aortic
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

50. Name the three opsonins
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 1 and IL 6
CRP - C3b - IgM
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction