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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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1. What is the clinical use for sirolimus? what should you combine it with?
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

2. describe the pathogenesis of delayed type IV hypersensitivity
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

3. is IgM an opsonizer?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Negative!
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

4. 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
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
secondary
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

5. Other than stimulating fever - what else does IL 6 do?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Stimulate the liver to release acute phase reactants
Increases expression of MHC I and MHC II and also activates NK cells

6. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
IgG
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
...
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

7. What is colostrum?
TLR ad nuclear receptors
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
The igA found in breast milk
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

8. A lymph node is a ________ lymphoid organ.
secondary
Receiving preformed Antibodies
Antibody mediated cytotoxicity; either complement dependent or complement independent
Type IV

9. 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?
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Superficial inguinal
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

10. Which HLA's are included in MHC I? MHC II?

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11. Describe the Mannose Lectin pathway
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
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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

12. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
False! B cell class switching requires a second signal
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

13. What is Aldesleukin? What is it used for
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
A recomb cytokine of IL 2; RCC and metastatic melanoma
DM type I and RA
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

14. What is the pathology of acute transplant rejection? is it reversible?
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
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

15. How is the thymus organized? what happens in each section?
IgG
Cyclosporine - OKT3
Acts as second signal on B cells to induce class switching to IgE and IgG
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

16. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
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
IgAs in mothers breast milk!
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

17. What lymph node drains the duodenum - jejunum?
Superior mesenteric
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

18. Only the _______ contribute to the Fc region
Complement activation (active in both)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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
heavy chains

19. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
A - B - C; all the D's
Thrombocytopenia
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
Negative!

20. Complements are...
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
acute phase reactants

21. What is serum sickness? give an example.
Yes
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
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
TLR ad nuclear receptors

22. The pathogenesis of contact dermatitis is ________ hypersensitivity
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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)
Chronic granulomatous disease
type four

23. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
MS
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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
Anti IF

24. 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?
Paracortex; viral infection
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
Acts as second signal on B cells to induce class switching to IgE and IgG
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

25. What type of fenestrations are found in the red pulp of the spleen?
Barrel hoop basement membrane fenestrations
A recomb cytokine of IL 2; RCC and metastatic melanoma
Rheumatic arthritis
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

26. what ensure that a memory response is generated?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
If there is class switching and plasma cell production (that is when memory cells are produced)
IL 4 - 5 - 10 - 6

27. What are some catalase positive organisms?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
CD56
S. aureus - E. Coli - aspergillus
Popliteal

28. What is the receptor for EBV? On what cells is that located?
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
A j chain
IL 1 and IL 6
CD21 on B cells (although there is T cell lymphocytosis in EBV)

29. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
opsonizes
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
except hyperacute
Anti IF

30. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
CRP - C3b - IgM
T cell dysfunction
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

31. which antibodies can bind complement?
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
IgM and IgG
Alternative splicing of mRNA
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

32. can igG cross the placenta?
Sinusitis - otitis media - pneumonia
IL 4 - 5 - 10 - 6
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Yes

33. ________ regulate the cell mediated response.
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Humoral
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

34. What are the cell surface proteins for Macrophages? which two are for opsonins?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Interferon gamma and IL 2

35. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
IL 4
Chronic granulomatous disease
not Ab mediated

36. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

37. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
dimer
Glycoproteins; HLA
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

38. What cytokines to Th2 secrete?
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
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
Activate macrophages
IL 4 - 5 - 10 - 6

39. For which toxins are preformed antibodies (passive) given?
mesenchymal
Tetanus - Botulinum - HBV - Rabies
Antidote for digoxin intoxication
secondary

40. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

41. other than C3a - what other complement acts as an anaphyloxin?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
C5a
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

42. What does IgA pick up from epithelial cells before being secreted?
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
Secretory component
Yes
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

43. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Anti smooth muscle

44. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
...
Influenza; antigenic shift; antigenic drift
Sinusitis - otitis media - pneumonia

45. Which are the only two antiinflammatory cytokines?
IL 4 - 5 - 10 - 6
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
TGF beta and IL 10
not Ab mediated

46. What does interferon gamma do to be antiviral?
Anti Jo -1
Celiac
Increases expression of MHC I and MHC II and also activates NK cells
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

47. hat is the presentation of Jobs syndrome or Hyper IgE?
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Anti IF
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

48. in which immunodef order do you see a lot of pus? no pus?
mesenchymal
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
T cell precursor

49. What is an example of a parasite showing antigenic variation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

50. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
DM type I and RA
By transcytosis