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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.
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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 happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
No because no peptide fragment!
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
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

2. What is the presentation of scid? treatment?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

3. What does IL 2 do?
Activates cytotoxic CD 8 T cells as second signal
CRP - C3b - IgM
Th cells fail to produce interferon gamma; a lot of IgE
Secretory component

4. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Its a serine protease that activates apoptosis; NK and CD8
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Paracortex; viral infection
When you select for which MHC it will have; take out the lymphs that self react

5. What is the treatment of acute transplant rejection?
opsonizes
Cyclosporine - OKT3
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
Kill them because they have CD16 on them that recognize the FcG portion

6. Other than stimulating fever - what else does IL 6 do?
Not thymus - BM
SP infections
Stimulate the liver to release acute phase reactants
Thrombocytopenia

7. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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
Complement activation (active in both)
IL 5

8. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
B - T - and NK cells
Popliteal
dimer
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

9. which interleukin receptor is required for NK development? activation?
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
Antihistone
IL 15; IL 12 - interferon Beta and interferon alpha

10. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Anti Ach receptor
IL 5
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)

11. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
IL 4 - 5 - 10 - 6
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
MHC I; from RER with help of the B2 microglobulin

12. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Histamine; post capillary venules - vasodilation
dimer
Antidesmoglein
Secretory component

13. Which MHC presents intracellular peptides? how so?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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
MHC I; from RER with help of the B2 microglobulin
B - T - and NK cells

14. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Anti viral and anti tumor
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Th cells fail to produce interferon gamma; a lot of IgE

15. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
A chemotactic factor for neutrophils
MHC I - CD16 - CD56

16. 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?
Anti mitochondrial
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Lymphocytes

17. What are C1 - C2 - C3 - C4 important for?
Superficial inguinal
Viral neutralization of igM and IgG!
Anti SS- A (anti RO) and Anti SS- B
cannot cross placenta

18. To what portion of the Antibody do the complements bind?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Fc
In the germinal center of secondary follicles (In the paler center)
TNF alpha and IL1

19. Only the _______ contribute to the Fc region
No because no peptide fragment!
mesenchymal
Celiac
heavy chains

20. How do you test for chronic granulomatous disease?
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
Activates Th1 helper cells; Macrophages
IL 1 and IL 6
Negative nitroblue tetrazolium reduction test

21. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
pathogenesis
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Complement activation (active in both)
isotype

22. What is the most common example of passive immunity?
IgAs in mothers breast milk!
Stimulate the liver to release acute phase reactants
...
TLR ad nuclear receptors

23. What are the autoantibodies for drug induced lupus?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Antihistone

24. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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
Acts as second signal on B cells to induce class switching to IgE and IgG

25. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Fab portion
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

26. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Negative nitroblue tetrazolium reduction test
Humoral
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
B - T - and NK cells

27. What is the presentation of hyperIgM syndrome?
dimer
Paracortex; viral infection
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Severe pyogenic infections early in life

28. What lymph node drains the lateral side of the dorsum of the foot?
mesenchymal
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Popliteal
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

29. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Activate macrophages
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

30. What is the main function of IL 12? other than macrophages who else can release IL 12?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
cannot cross placenta
Antimicrosomal and antithyroglobulin

31. What are the function of B cells?
Antibody mediated cytotoxicity; either complement dependent or complement independent
A chemotactic factor for neutrophils
Graves
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

32. What are the autoantibodies for wegeners granulomatosis?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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
Viral neutralization of igM and IgG!
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

33. What are the two signals to kill for NK cells?
Basophils! THey want IG E class switch!
Anti Jo -1
Increases expression of MHC I and MHC II and also activates NK cells
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

34. What is the pathogenesis of acute transplant rejection? When does it occur?
Daclizumab; prevent ACUTE rejection of renal transplant
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

35. What are the PALS?
Complement activation (active in both)
T cell precursor
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

36. The secondary follicles have __________; primary follicles are dense
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
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
pale central germinal centers
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

37. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
A chemotactic factor for neutrophils

38. Which helper T cells' development is induced by IL 4? IL 12?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Th2; Th1
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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

39. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Active; passive - fast but short half life (3 weeks!)
Th cells fail to produce interferon gamma; a lot of IgE
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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

40. What lymph node drains the rectum (above the pectinate line)?
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
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Internal iliac

41. what happens in a deficiency of C1 esterase inhibitor? DAF?
Thrombocytopenia
In the germinal center of secondary follicles (In the paler center)
Hereditary angioedema; PNH
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

42. 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)?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IgE; by activating eosinophils
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
MS

43. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
No because no peptide fragment!
Anti glutamate carboxylase and anti insulin
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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

44. What is thrombopoietin used for?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Anti IF
Thrombocytopenia

45. What are the two signals required for B cell class switching? Which is the second signal?
S. aureus - E. Coli - aspergillus
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Tetanus - Botulinum - HBV - Rabies

46. What is an example of a parasite showing antigenic variation?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Internal iliac
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Chronic granulomatous disease

47. What cytokines to Th2 secrete?
False! B cell class switching requires a second signal
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
IL 4 - 5 - 10 - 6
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

48. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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
Popliteal

49. What is the pathogenesis of a hypersensitivity reaction?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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
Anti SS- A (anti RO) and Anti SS- B
Liver! (they are proteins circulating in the blood)

50. The MALT/GALT are not...
Antidote for digoxin intoxication
C5a
encapsulated
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