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 does interferon gamma do? What two type of cells does it attack mostly?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Interferon gamma and IL 2
IgAs in mothers breast milk!

2. What lymph node drains the upper limb?
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
Axillary
Pernicious Anemia and Hashimotos
Celiac

3. Which are the only two antiinflammatory cytokines?
IgM and IgA
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
TGF beta and IL 10
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

4. Describe the Mannose Lectin pathway
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 :(
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
Interferon gamma and IL 2
Cells that stil have weird parts of their membrane that macrophages usually bite off

5. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
delayed!
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

6. What are the three types of APCs?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Paracortex
T
Macrophages - Dendritic cells - B cells

7. What type of fenestrations are found in the red pulp of the spleen?
isotype
Its a serine protease that activates apoptosis; NK and CD8
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Barrel hoop basement membrane fenestrations

8. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
T cell activation; no with CD 4 or CD 8
RNA segment reassortment
Acts as second signal on B cells to induce class switching to IgE and IgG
Paracortex; viral infection

9. what cytokine does basophils secrete?
IL 4
MHC class molecules bind to KIRS or CD94 to prevent killing
acute phase reactants
Barrel hoop basement membrane fenestrations

10. What does IL 2 do?
not Ab mediated
Activates cytotoxic CD 8 T cells as second signal
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
Negative!

11. which of the transplant rejections is antibody mediated? why does it occur?
Graves
IL 1 and IL 6
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
T cell dysfunction

12. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Anti Ach receptor

13. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Popliteal
heavy chains
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
Glycoproteins; HLA

14. Which MHC presents intracellular peptides? how so?
Not thymus - BM
Negative!
MHC I; from RER with help of the B2 microglobulin
S. aureus - E. Coli - aspergillus

15. What are the autoantibodies for sjorgens syndrome?
Negative nitroblue tetrazolium reduction test
Anti SS- A (anti RO) and Anti SS- B
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

16. other than eat and bite RBCs what else do Macrophages of spleen do>
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Antidote for digoxin intoxication
Remove encapsulated bacateria
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

17. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Edema and necrosis in that region
Rheumatic arthritis
Internal iliac
Interferon gamma and IL 2

18. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Superior mesenteric
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Anti Jo -1

19. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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
NK cells
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 :(

20. what cell surface proteins are on all APCs?
MHC II - B7
Thrombocytopenia
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

21. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
TNF alpha and IL1

22. Other than stimulating fever - what else does IL 6 do?
heavy chains
When you select for which MHC it will have; take out the lymphs that self react
Anti IF
Stimulate the liver to release acute phase reactants

23. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Superficial inguinal
Cytokine IL 10 secreted by Th2
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
Anti glutamate carboxylase and anti insulin

24. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Cyclosporine - OKT3
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!
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

25. What is the main function of IL 8?
Histamine; post capillary venules - vasodilation
Anti smooth muscle
encapsulated
A chemotactic factor for neutrophils

26. What are the two signals required for B cell class switching? Which is the second signal?
IgM
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Its a serine protease that activates apoptosis; NK and CD8

27. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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
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

28. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Celiac
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
...
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)

29. What is an example of a parasite showing antigenic variation?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Kill them because they have CD16 on them that recognize the FcG portion
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
active complement pathway

30. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
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
In the germinal center of secondary follicles (In the paler center)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IL 5

31. Give three examples of bacteria that use antigenic variation and how.
Paracortex
Th cells fail to produce interferon gamma; a lot of IgE
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

32. What are the autoantibodies for drug induced lupus?
Antihistone
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Cytokine IL 10 secreted by Th2

33. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Interferon gamma; Th1
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Daclizumab; prevent ACUTE rejection of renal transplant

34. What lymph node drains the breast?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Popliteal
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Axillary

35. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
IgE; by activating eosinophils

36. what happens in a deficiency of C1 esterase inhibitor? DAF?
A chemotactic factor for neutrophils
carboxy terminal
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Hereditary angioedema; PNH

37. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Barrel hoop basement membrane fenestrations

38. Type IV hypersensitivity is i...
Sinusitis - otitis media - pneumonia
not Ab mediated
IL 4 - 5 - 10 - 6
In the germinal center of secondary follicles (In the paler center)

39. T/F B cells do not require a second signal
False! B cell class switching requires a second signal
Internal iliac
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
No because no peptide fragment!

40. What is the autoantibody for SLE that is nonspecific? Specific?
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 nuclear Antibodies (ANA); Anti dsDNA - anti Smith
MS - hay fever - SLE - goodpastures
encapsulated

41. What are four results of a splenectomy?
Superior mesenteric
C5a
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Paracortex; viral infection

42. What is the clinical use for sirolimus? what should you combine it with?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

43. What are the PALS?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
A recomb cytokine of IL 2; RCC and metastatic melanoma

44. What are the autoantibodies for pernicious anemia?
Its a serine protease that activates apoptosis; NK and CD8
Anti IF
T cell dysfunction
except hyperacute

45. Which antibodies can be multimeric?
IgM and IgA
Active; passive - fast but short half life (3 weeks!)
IL 1 and IL 6
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)

46. What is immune complex disease? give an example.
IgAs in mothers breast milk!
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

47. What is the pathogenesis of HyperIgE syndrome? What are the labs?
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
IL 5
Th cells fail to produce interferon gamma; a lot of IgE
IgAs in mothers breast milk!

48. What is three common causes of severe combined immunodef? What is the result of all three?
Superficial inguinal
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Humoral
Complement activation (active in both)

49. From where do cytokines come from?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Lymphocytes

50. What lymph node drains the duodenum - jejunum?
Superior mesenteric
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
A recomb cytokine of IL 2; RCC and metastatic melanoma
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)