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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. How does the alternative pathway lead to MAC activation?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
IgG
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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

2. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Antihistone
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
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

3. What does Interferon alpha and beta do? how?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Basophils! THey want IG E class switch!
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

4. What is the toxicity of muromonab?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Activate macrophages
Basophils! THey want IG E class switch!
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

5. Which is the main antibody in the delayed or secondary response to an antigen?
IgG
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Not thymus - BM

6. The two heavy chains of an antibody contribute to the...
Fab portion
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Edema and necrosis in that region
Anti topoisomerase

7. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
False! B cell class switching requires a second signal
Tetanus - Botulinum - HBV - Rabies
DM type I

8. T/F B cells do not require a second signal
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Antimicrosomal and antithyroglobulin
False! B cell class switching requires a second signal
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

9. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
T cell precursor
All MHC 1/CD8
Complement activation (active in both)

10. What are the main symptoms of T cell immunodeficiencies?
Activates cytotoxic CD 8 T cells as second signal
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
Cells that stil have weird parts of their membrane that macrophages usually bite off

11. What are the autoantibodies for Mixed connective tissue disease?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Antidote for digoxin intoxication
Anti U1 RNP (ribonucleoprotein)
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

12. Which antibodies can be multimeric?
IgM and IgA
Axillary
Secretory component
C5a

13. How is i Th1 helper cell inhibited?
Cross link
Cytokine IL 10 secreted by Th2
Bind FcG for antibody dependent cellular cytotoxicity
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

14. what happens in a deficiency of C1 esterase inhibitor? DAF?
secondary
A - B - C; all the D's
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
Hereditary angioedema; PNH

15. What is the mechanism for sirolimus? what else it known as?
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
IgE
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
Cross link

16. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Histamine; post capillary venules - vasodilation
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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

17. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Acts as second signal on B cells to induce class switching to IgE and IgG
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

18. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
except hyperacute
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
NK cells

19. which of the hypersensitivity reactions is not Ab mediated?
IgAs in mothers breast milk!
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Type IV

20. What are the two signals to kill for NK cells?
Fc
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anti TSh receptor

21. What does IL 10 do? who is secreted by?
IgM and IgA
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
If there is class switching and plasma cell production (that is when memory cells are produced)

22. What lymph node drains the breast?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Severe pyogenic infections early in life
Axillary
Popliteal

23. What does IgA pick up from epithelial cells before being secreted?
Superficial inguinal
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Secretory component
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

24. What is recomb gamma interferon used for?
T cell activation; no with CD 4 or CD 8
Negative!
Chronic granulomatous disease
Macrophages - Dendritic cells - B cells

25. where are complements produced?
delayed!
RNA segment reassortment
Liver! (they are proteins circulating in the blood)
Activates Th1 helper cells; Macrophages

26. In general What are T cells good for?
Anti viral and anti tumor
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

27. What are the main symptoms of B cell immunodeficiencies?
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
Its a serine protease that activates apoptosis; NK and CD8
SP infections
neutrophilia!

28. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
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
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Influenza; antigenic shift; antigenic drift

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?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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
RNA segment reassortment
Severe pyogenic infections early in life

30. 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).
Antimicrosomal and antithyroglobulin
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!
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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

31. which cells have more complete tolerance - B or T cells?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Edema and necrosis in that region
T
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

32. What are the cell surface proteins for Macrophages? which two are for opsonins?
Recom IL 11; thrombocytopenia
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

33. What is oprelevkin? and What is it used for?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Stimulate the liver to release acute phase reactants
Recom IL 11; thrombocytopenia
IL 3; supports growth and differentiation of bone marrow stem cells

34. What is colostrum?
The igA found in breast milk
Negative nitroblue tetrazolium reduction test
Negative selection
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

35. Name 5 ways Antibody diversity is generated?
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Acts as second signal on B cells to induce class switching to IgE and IgG

36. 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?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
C5a
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Anemias (esp due to renal failure)

37. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Secretory component
Recom IL 11; thrombocytopenia
MS - hay fever - SLE - goodpastures
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

38. What is the marginal zone of the spleen? what happens there?
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
IgG
IgA
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

39. What is filgrastim and sargramostim? and What is it used for?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

40. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Histamine; post capillary venules - vasodilation
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

41. What lymph node drains the upper limb?
Chronic granulomatous disease
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Axillary
Acts as second signal on B cells to induce class switching to IgE and IgG

42. What does IL 5 do?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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
Severe pyogenic infections early in life
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

43. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

44. How is the thymus organized? what happens in each section?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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
Th cells fail to produce interferon gamma; a lot of IgE

45. Monomer in circulation - ___ when secreted
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
...
dimer
Its main effect is a defect in Ab opsonization for killing

46. 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
MHC I; from RER with help of the B2 microglobulin
Anti viral and anti tumor
neutrophilia!

47. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Superficial inguinal

48. What are the three types of lymphocytes?
TLR ad nuclear receptors
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
B - T - and NK cells

49. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Immunoflourescent staining of tissue biopsies
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!
Th2; Th1
All MHC 1/CD8

50. What are the autoantibodies for pemphigus bulgaris?
NK cells
Local infection/inflammation; infection of the ln itself; metastasis
Antidesmoglein
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)