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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 you test for type III hypersensitivity?
2 heavy chains and two light chains
Immunoflourescent staining of tissue biopsies
cannot cross placenta
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

2. To what portion of the Antibody do the complements bind?
Viral neutralization of igM and IgG!
Fc
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
Popliteal

3. How is the antigen loaded onto a MHC II?
A - B - C; all the D's
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
IgM
IgAs in mothers breast milk!

4. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
except hyperacute
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Th2; Th1
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

5. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Antimicrosomal and antithyroglobulin
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IL 1 and IL 6
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

6. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
T cell dysfunction
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

7. What does interferon gamma do? What two type of cells does it attack mostly?
S. aureus - E. Coli - aspergillus
dimer
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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

8. What are the autoantibodies for wegeners granulomatosis?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
TNF alpha and IL1
Rheumatic arthritis
Immunoflourescent staining of tissue biopsies

9. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
RNA segment reassortment
Bind FcG for antibody dependent cellular cytotoxicity
delayed!

10. What are the two signals required for B cell class switching? Which is the second signal?
Local infection/inflammation; infection of the ln itself; metastasis
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Graves
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

11. What is an example of a parasite showing antigenic variation?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
SP infections
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

12. what cell surface proteins are on all APCs?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Antidote for digoxin intoxication
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
MHC II - B7

13. is IgM an opsonizer?
Negative!
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
IL 3; supports growth and differentiation of bone marrow stem cells
B - T - and NK cells

14. Which antibodies can be multimeric?
IgG
IgM and IgA
IgG
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

15. How does the alternative pathway lead to MAC activation?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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
Humoral
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

16. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The igA found in breast milk
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Its main effect is a defect in Ab opsonization for killing
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

17. How is the thymus organized? what happens in each section?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
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
Cells that stil have weird parts of their membrane that macrophages usually bite off

18. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
Cells that stil have weird parts of their membrane that macrophages usually bite off
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Steroid responsive nephrotic syndrome

19. What are the symptoms of serum sickness?
Humoral
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

20. What are the autoantibodies for drug induced lupus?
Macrophages - Dendritic cells - B cells
Basophils! THey want IG E class switch!
Antihistone
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

21. How does igA cross the epithelium?
Inferior mesenteric
MHC class molecules bind to KIRS or CD94 to prevent killing
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

22. Which is the main antibody that provides passive immunity to infants?
IgE
Anti mitochondrial
Cells that stil have weird parts of their membrane that macrophages usually bite off
IgG

23. What are the PALS?
Macrophages - Dendritic cells - B cells
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
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Previous transfusion; pregnant woman whose fetus had paternal antigens

24. Give an example of someone who could get hyperacute transplant rejection.
Viral neutralization of igM and IgG!
Basophils! THey want IG E class switch!
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
Previous transfusion; pregnant woman whose fetus had paternal antigens

25. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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 :(
The igA found in breast milk
The patient could become cyanotic in the OR!

26. which cells have more complete tolerance - B or T cells?
T
Pernicious Anemia and Hashimotos
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
Its a serine protease that activates apoptosis; NK and CD8

27. Other than stimulating fever - what else does IL 6 do?
Yes
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Stimulate the liver to release acute phase reactants

28. What is three common causes of severe combined immunodef? What is the result of all three?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
Cytokine IL 10 secreted by Th2

29. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Stimulate the liver to release acute phase reactants
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

30. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Cross link
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Anti Ach receptor
All MHC 1/CD8

31. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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!
except hyperacute

32. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
NK cells
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

33. What is filgrastim and sargramostim? and What is it used for?
A - B - C; all the D's
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Edema and necrosis in that region
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

34. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
B - T - and NK cells
Superior mesenteric
...

35. Name the three opsonins
Sinusitis - otitis media - pneumonia
NK cells
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
CRP - C3b - IgM

36. What are the autoantibodies for graves?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Anti TSh receptor
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

37. How do you test for chronic granulomatous disease?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Immunoflourescent staining of tissue biopsies
Negative nitroblue tetrazolium reduction test
Antibody mediated cytotoxicity; either complement dependent or complement independent

38. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Yes
TGF beta and IL 10
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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

39. What is the most common selective Ig deficiency? What is the presentation?
Local infection/inflammation; infection of the ln itself; metastasis
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
DM type I
Internal iliac

40. __________ are a part of the innate system.
Antimicrosomal and antithyroglobulin
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
NK cells
not Ab mediated

41. what cell surface marker is used for NK cells as it is unique to them?
CD56
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
secondary
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

42. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
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
Glycoproteins; HLA
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

43. where are complements produced?
Anti Jo -1
Liver! (they are proteins circulating in the blood)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
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

44. What are the autoantibodies for sjorgens syndrome?
Bind FcG for antibody dependent cellular cytotoxicity
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Anti SS- A (anti RO) and Anti SS- B

45. How is i Th1 helper cell inhibited?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Antidesmoglein
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
Cytokine IL 10 secreted by Th2

46. which type of immunity is slow but long lasting? as opposed to...
Local infection/inflammation; infection of the ln itself; metastasis
Active; passive - fast but short half life (3 weeks!)
Anti SS- A (anti RO) and Anti SS- B
Anti smooth muscle

47. What are the two signals required for Th1 cells? what happens after then activated?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

48. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Bind FcG for antibody dependent cellular cytotoxicity
opsonizes
Antimicrosomal and antithyroglobulin
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

49. What is anergy? why does this occur?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

50. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Para aortic
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous 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
By transcytosis