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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 is the pathogenesis of HyperIgE syndrome? What are the labs?
DM type I
IgG
Daclizumab; prevent ACUTE rejection of renal transplant
Th cells fail to produce interferon gamma; a lot of IgE

2. What lymph node drains the lateral side of the dorsum of the foot?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Lymphocytes
Para aortic
Popliteal

3. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
...
TNF alpha and IL1
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anti U1 RNP (ribonucleoprotein)

4. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Edema and necrosis in that region
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

5. What cytokines to Th2 secrete?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Receiving preformed Antibodies
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
IL 4 - 5 - 10 - 6

6. To what portion of the Antibody do the complements bind?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Fc
Anti Jo -1
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

7. What are the two signals required for T cells? what happens after?
Wiskott Aldrich syndrome
Paracortex
active complement pathway
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

8. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
T
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
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
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

9. What are MHC's necessary for? By themselves?
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
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
T cell activation; no with CD 4 or CD 8
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

10. which interleukin receptor is required for NK development? activation?
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 15; IL 12 - interferon Beta and interferon alpha
IL 5
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

11. What is serum sickness? give an example.
MHC class molecules bind to KIRS or CD94 to prevent killing
DM type I and RA
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

12. What is the toxicity of muromonab?
Anti IF
Antihistone
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

13. What lymph node drains the rectum (above the pectinate line)?
IgM and IgD
Internal iliac
All MHC 1/CD8
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

14. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
A chemotactic factor for neutrophils
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

15. 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
Complement activation (active in both)
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
Daclizumab; prevent ACUTE rejection of renal transplant

16. What links the adaptive and innate immunity?
The patient could become cyanotic in the OR!
heavy chains
Complement activation (active in both)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

17. What is muromonab - CD3 (OKT3)
pale central germinal centers
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Popliteal
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

18. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
MHC II - B7
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

19. ________ regulate the cell mediated response.
Humoral
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
IgM
lowest concentration

20. what will NK cells do to cells covered in IgG Ab? why?
The igA found in breast milk
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Kill them because they have CD16 on them that recognize the FcG portion
Negative!

21. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Hemochromatosis
Negative!

22. Which antibody mediates immunity to worms? how?
Graves
IgE; by activating eosinophils
IL 4 - 5 - 10 - 6
Antimicrosomal and antithyroglobulin

23. describe the classic complement pathway.
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
TNF alpha and IL1
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
MS

24. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Paracortex; viral infection
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Macrophages - Dendritic cells - B cells

25. What are the autoantibodies for hashimotos?
Its a serine protease that activates apoptosis; NK and CD8
Antimicrosomal and antithyroglobulin
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

26. 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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Cross link
pentamer

27. what bacteria are a splenectomy patient most susceptible to? why?
2 heavy chains and two light chains
IgG
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
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

28. Only the _______ contribute to the Fc region
heavy chains
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IL 4
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

29. What is the most common example of passive immunity?
C5a
Activates Th1 helper cells; Macrophages
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IgAs in mothers breast milk!

30. Leukocyte adhesion defect presents with...
IgM and IgA
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
Anti TSh receptor
neutrophilia!

31. Which MHC presents intracellular peptides? how so?
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
A j chain
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
MHC I; from RER with help of the B2 microglobulin

32. What does IL 2 do?
Activates cytotoxic CD 8 T cells as second signal
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Active; passive - fast but short half life (3 weeks!)
Celiac

33. where are complements produced?
Anti U1 RNP (ribonucleoprotein)
T
Liver! (they are proteins circulating in the blood)
T cell precursor

34. Type IV hypersensitivity is i...
Internal iliac
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
not Ab mediated
S. aureus - E. Coli - aspergillus

35. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Paracortex
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Basophils! THey want IG E class switch!

36. Which is the main antibody in the delayed or secondary response to an antigen?
IgG
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Carbohydrate

37. which of the transplant rejections is antibody mediated? why does it occur?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Barrel hoop basement membrane fenestrations

38. What is the main function of interferons?
RNA segment reassortment
Wiskott Aldrich syndrome
Barrel hoop basement membrane fenestrations
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

39. What are superantigens? give two examples.
Basophils! THey want IG E class switch!
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
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

40. what cell surface proteins are on all APCs?
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
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
Activate macrophages
MHC II - B7

41. What is the toxicity of azathioprine?
...
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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

42. What does granulysin do?
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
Anti glutamate carboxylase and anti insulin
Type IV
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

43. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
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
acute phase reactants
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
type four

44. Which disease is associated with DR3?
DM type I
Sinusitis - otitis media - pneumonia
Antimicrosomal and antithyroglobulin
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

45. Which is the most abundant antibody in blood?
IgG
Activates Th1 helper cells; Macrophages
Immunoflourescent staining of tissue biopsies
Yes

46. The Fc region is found on the...
carboxy terminal
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

47. which B and T cell disorder presents with specifically low IgM?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Wiskott Aldrich syndrome
active complement pathway

48. where do somatic hypermutation and class switching occur?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Local infection/inflammation; infection of the ln itself; metastasis
In the germinal center of secondary follicles (In the paler center)
The igA found in breast milk

49. are Th cells involved in trapping of antigens of endotoxin/LPS?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Antihistone
No because no peptide fragment!

50. 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
Chronic granulomatous disease
Cytokine IL 10 secreted by Th2
Interferon gamma and IL 2