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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 presentation of scid? treatment?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
...
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Fc

2. What links the adaptive and innate immunity?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
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
Complement activation (active in both)

3. What are C1 - C2 - C3 - C4 important for?
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
Viral neutralization of igM and IgG!
Anti glutamate carboxylase and anti insulin
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

4. What cytokines to Th2 secrete?
Internal iliac
pale central germinal centers
Para aortic
IL 4 - 5 - 10 - 6

5. What are the autoantibodies for autoimmune hepatitis?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Anti smooth muscle
Antihistone
MS

6. How is i Th1 helper cell inhibited?
A recomb cytokine of IL 2; RCC and metastatic melanoma
IL 5
Cytokine IL 10 secreted by Th2
Anti glutamate carboxylase and anti insulin

7. What is thrombopoietin used for?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Cytokine IL 10 secreted by Th2
Thrombocytopenia
Internal iliac

8. What does IL 2 do?
Activates cytotoxic CD 8 T cells as second signal
IgE; by activating eosinophils
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
Thrombocytopenia

9. Which antibody mediates immunity to worms? how?
...
Anti Ach receptor
IgE; by activating eosinophils
Anti topoisomerase

10. How is the antigen loaded onto a MHC II?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
All MHC 1/CD8
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

11. What is passive immunity?
Receiving preformed Antibodies
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
All MHC 1/CD8
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

12. What is the mechanism for sirolimus? what else it known as?
TGF beta and IL 10
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Wiskott Aldrich syndrome
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

13. What is filgrastim and sargramostim? and What is it used for?
Axillary
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
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Tetanus - Botulinum - HBV - Rabies

14. A lymph node is a ________ lymphoid organ.
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
secondary

15. What is the pathology of acute transplant rejection? is it reversible?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Antidesmoglein
RNA segment reassortment
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

16. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
IL 1 and IL 6
Antihistone
Paracortex; viral infection

17. What is oprelevkin? and What is it used for?
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
Recom IL 11; thrombocytopenia
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
Previous transfusion; pregnant woman whose fetus had paternal antigens

18. How do you test for chronic granulomatous disease?
Negative nitroblue tetrazolium reduction test
IL 3; supports growth and differentiation of bone marrow stem cells
Paracortex; viral infection
Anti topoisomerase

19. Which is the most abundant antibody in blood?
IgG
IL 5
Th cells fail to produce interferon gamma; a lot of IgE
lowest concentration

20. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Superficial inguinal
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

21. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
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
Chronic granulomatous disease
Histamine; post capillary venules - vasodilation
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

22. what prevents NK cells from killing normal cells if their default is to kill?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
MHC class molecules bind to KIRS or CD94 to prevent killing
IgM and IgG
Antidote for digoxin intoxication

23. What are MHC's necessary for? By themselves?
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
IgAs in mothers breast milk!
T cell activation; no with CD 4 or CD 8
Anti SS- A (anti RO) and Anti SS- B

24. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
RNA segment reassortment
except hyperacute
Axillary
Its main effect is a defect in Ab opsonization for killing

25. What is the main function of interferons?
Edema and necrosis in that region
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Histamine; post capillary venules - vasodilation

26. What is recomb beta interferon used for?
MS
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

27. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Cytokine IL 10 secreted by Th2
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Severe pyogenic infections early in life

28. What are the T cell functions?
IgE; by activating eosinophils
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

29. What is the white pulp of the spleen?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
mesenchymal
Acts as second signal on B cells to induce class switching to IgE and IgG

30. What is recomb gamma interferon used for?
Chronic granulomatous disease
Bind FcG for antibody dependent cellular cytotoxicity
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Complement activation (active in both)

31. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Anemias (esp due to renal failure)
Paracortex
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
Stimulate the liver to release acute phase reactants

32. What is Aldesleukin? What is it used for
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
A recomb cytokine of IL 2; RCC and metastatic melanoma
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

33. What are the autoantibodies for type I diabetes mellitus?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Paracortex
Anti glutamate carboxylase and anti insulin
Macrophages - Dendritic cells - B cells

34. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Anti mitochondrial
Pernicious Anemia and Hashimotos

35. What is the treatment of acute transplant rejection?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
IgE; by activating eosinophils
Cyclosporine - OKT3
Negative nitroblue tetrazolium reduction test

36. which antibodies can bind complement?
IgM and IgG
Fab portion
DM type I and RA
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

37. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Liver! (they are proteins circulating in the blood)

38. What is a type I hypersensitivity reaction? What is atopic?
Superficial inguinal
Graves
IL 5
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

39. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti alpha subunit 3 of collagen on type IV bm

40. What is chronic mucocutaneous candidiasis d/t?
Hemochromatosis
T cell dysfunction
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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

41. The Fc region is found on the...
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
carboxy terminal
NK cells
Viral neutralization of igM and IgG!

42. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
IgG

43. What lymph node drains the testes?
TNF alpha and IL1
Para aortic
Thrombocytopenia
DM type I and RA

44. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
carboxy terminal
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
C5a

45. Which type of selection of thymic development provides central tolerance?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Negative selection
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
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

46. What are some sinopulmonary infections?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Sinusitis - otitis media - pneumonia
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
Graves

47. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
T
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
Anti alpha subunit 3 of collagen on type IV bm
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

48. where do somatic hypermutation and class switching occur?
In the germinal center of secondary follicles (In the paler center)
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!
Celiac
Humoral

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

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50. What are the mediators that mast cells release?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Yes