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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. What is oprelevkin? and What is it used for?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Recom IL 11; thrombocytopenia

2. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Viral neutralization of igM and IgG!

3. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
Not thymus - BM
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
Cyclosporine - OKT3

4. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Antidesmoglein
False! B cell class switching requires a second signal
Glycoproteins; HLA
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

5. What is chronic mucocutaneous candidiasis d/t?
In the germinal center of secondary follicles (In the paler center)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
IgM and IgA
T cell dysfunction

6. What are the cell surface proteins for Macrophages? which two are for opsonins?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Liver! (they are proteins circulating in the blood)
Activate macrophages
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

7. Type Iv hypersensitivity is...
B - T - and NK cells
delayed!
Type IV
T cell precursor

8. What are C1 - C2 - C3 - C4 important for?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
secondary
Active; passive - fast but short half life (3 weeks!)
Viral neutralization of igM and IgG!

9. other than C3a - what other complement acts as an anaphyloxin?
Wiskott Aldrich syndrome
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)
C5a
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

10. What does IL 4 do?
Acts as second signal on B cells to induce class switching to IgE and IgG
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Activate macrophages
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

11. Which diseases are associated with DR4?
TNF alpha and IL1
carboxy terminal
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
DM type I and RA

12. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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

13. 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
Graves
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
IgM and IgD

14. What are the autoantibodies for graves?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Anti TSh receptor
opsonizes

15. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Delayed type hypersensitivity
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Th2; Th1
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

16. which antibodies prevent antigens from binding mucosal surfaces?
Paracortex
IgA
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
except hyperacute

17. What is colostrum?
The igA found in breast milk
TNF alpha and IL1
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
IL 15; IL 12 - interferon Beta and interferon alpha

18. What is the most common example of passive immunity?
secondary
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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
IgAs in mothers breast milk!

19. IgE has the ___________ in the serum
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
The patient could become cyanotic in the OR!
IL 15; IL 12 - interferon Beta and interferon alpha
lowest concentration

20. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Superficial inguinal
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

21. What is a type I hypersensitivity reaction? What is atopic?
Anti IF
Th2; Th1
A j chain
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

22. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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 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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Local infection/inflammation; infection of the ln itself; metastasis

23. Describe the capsular structure of a lymph node; What are the functions of the LN?
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
IL 15; IL 12 - interferon Beta and interferon alpha
MHC I - CD16 - CD56
Recom IL 11; thrombocytopenia

24. Which disease is associated with B8?
Graves
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
C5a
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

25. What is the main function of TNF alpha? How does it do this?
type four
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Stimulate the liver to release acute phase reactants
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

26. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
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
Macrophages - Dendritic cells - B cells
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

27. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
...
TNF alpha and IL1
Receiving preformed Antibodies
Daclizumab; prevent ACUTE rejection of renal transplant

28. What is the toxicity of azathioprine?
Immunoflourescent staining of tissue biopsies
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
...
Antidesmoglein

29. What is the pathology in hyperacute transplant rejection?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
2 heavy chains and two light chains
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

30. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
CD56
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Alternative splicing of mRNA
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

31. what cell surface proteins are on all APCs?
cannot cross placenta
Hemochromatosis
Activate macrophages
MHC II - B7

32. Which antibodies can be multimeric?
IgM and IgA
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
Chronic granulomatous disease

33. What is the pathology seen in chronic transplant rejection?
Antihistone
Activates cytotoxic CD 8 T cells as second signal
active complement pathway
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

34. What links the adaptive and innate immunity?
Complement activation (active in both)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

35. What are the main cell surface proteins on B cells?
Pernicious Anemia and Hashimotos
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

36. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
IgA
Humoral
Hemochromatosis

37. Which is the most abundant antibody in blood?
TNF alpha and IL1
Anti Jo -1
Kill them because they have CD16 on them that recognize the FcG portion
IgG

38. IgM can fix complement but...
Axillary
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
cannot cross placenta
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

39. What is the presentation of Brutons agammaglobulinemia?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
IL 3; supports growth and differentiation of bone marrow stem cells
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

40. IgM can exist as a _______ also
Negative selection
not Ab mediated
pentamer
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

41. what happens in a deficiency of C1 esterase inhibitor? DAF?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Hereditary angioedema; PNH
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Activates Th1 helper cells; Macrophages

42. what bacteria are a splenectomy patient most susceptible to? why?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Anti SS- A (anti RO) and Anti SS- B
Previous transfusion; pregnant woman whose fetus had paternal antigens
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

43. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
All MHC 1/CD8
IL 1 and IL 6
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Graves

44. The alternative pathway is the only constutively...
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)
active complement pathway
Carbohydrate
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

45. Type IV hypersensitivity is i...
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IgG
not Ab mediated

46. The lymphocytes are ________ origin
Popliteal
mesenchymal
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

47. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Th cells fail to produce interferon gamma; a lot of IgE
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
delayed!
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

48. Describe complement dependent Type II hypersensitivity. Give an example.
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
If there is class switching and plasma cell production (that is when memory cells are produced)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

49. What are the three types of APCs?
Increases expression of MHC I and MHC II and also activates NK cells
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Glycoproteins; HLA
Macrophages - Dendritic cells - B cells

50. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Cytokine IL 10 secreted by Th2
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
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