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Test your basic knowledge |
USMLE Step 1 Immunology
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Study First
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 are the cell surface proteins on NK cells?
mesenchymal
MHC I - CD16 - CD56
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
2. What links the adaptive and innate immunity?
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
IL 3; supports growth and differentiation of bone marrow stem cells
Complement activation (active in both)
Type IV
3. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
IgE
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
4. ________ regulate the cell mediated response.
except hyperacute
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!
Humoral
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
5. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
CD56
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Yes
6. What are the autoantibodies for pernicious anemia?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Anemias (esp due to renal failure)
Anti IF
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
7. what cell surface proteins are on all APCs?
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
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
active complement pathway
MHC II - B7
8. can igG cross the placenta?
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)
Yes
Th2; Th1
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
9. Which HLA's are included in MHC I? MHC II?
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10. What is the clinical use of Muromonab?
MS
IL 5
Immunosuppression after kidney transplantation
Previous transfusion; pregnant woman whose fetus had paternal antigens
11. What are the autoantibodies for graves?
IgG
Anti TSh receptor
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
12. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Steroid responsive nephrotic syndrome
Anti topoisomerase
Bind FcG for antibody dependent cellular cytotoxicity
Influenza; antigenic shift; antigenic drift
13. What lymph node drains the breast?
Anti viral and anti tumor
Axillary
Macrophages - Dendritic cells - B cells
Antimicrosomal and antithyroglobulin
14. What are the autoantibodies for autoimmune hepatitis?
Popliteal
lowest concentration
Anti smooth muscle
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
15. What are the autoantibodies for systemic sclerosis?
Anti topoisomerase
Rheumatic arthritis
Complement activation (active in both)
Remove encapsulated bacateria
16. In general What are T cells good for?
acute phase reactants
Anti viral and anti tumor
DM type I and RA
Immunoflourescent staining of tissue biopsies
17. What is the most common selective Ig deficiency? What is the presentation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
18. What is a type I hypersensitivity reaction? What is atopic?
By transcytosis
C5a
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
When you select for which MHC it will have; take out the lymphs that self react
19. What is the main function of interferons?
Yes
Secretory component
Axillary
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
20. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Celiac
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
21. What does interferon gamma do? What two type of cells does it attack mostly?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Superficial inguinal
22. What is muromonab - CD3 (OKT3)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Kill them because they have CD16 on them that recognize the FcG portion
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
NK cells
23. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
neutrophilia!
Antimicrosomal and antithyroglobulin
Edema and necrosis in that region
24. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Activates cytotoxic CD 8 T cells as second signal
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Basophils! THey want IG E class switch!
25. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Remove encapsulated bacateria
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
26. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Cross link
IgG
27. The Fc region is found on the...
All MHC 1/CD8
Anemias (esp due to renal failure)
carboxy terminal
secondary
28. Which disease is associated with B8?
Graves
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
29. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
IgM and IgG
A chemotactic factor for neutrophils
MS
30. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
IgG
pathogenesis
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
31. what ensure that a memory response is generated?
If there is class switching and plasma cell production (that is when memory cells are produced)
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
Anti TSh receptor
T cell activation; no with CD 4 or CD 8
32. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
33. How does igA cross the epithelium?
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
By transcytosis
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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!
34. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
T cell activation; no with CD 4 or CD 8
Paracortex; viral infection
If there is class switching and plasma cell production (that is when memory cells are produced)
2 heavy chains and two light chains
35. 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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Delayed type hypersensitivity
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
36. What cytokines to Th2 secrete?
Activate macrophages
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 4 - 5 - 10 - 6
type four
37. What does interferon gamma do to be antiviral?
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
Increases expression of MHC I and MHC II and also activates NK cells
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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
38. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Rheumatic arthritis
except hyperacute
Chronic granulomatous disease
Antidesmoglein
39. What is passive immunity?
Receiving preformed Antibodies
S. aureus - E. Coli - aspergillus
delayed!
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
40. What is recomb gamma interferon used for?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Humoral
Chronic granulomatous disease
41. Which disease is associated with HLA A3?
Liver! (they are proteins circulating in the blood)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Hemochromatosis
Activates cytotoxic CD 8 T cells as second signal
42. What lymph node drains the duodenum - jejunum?
Anti Ach receptor
encapsulated
Superior mesenteric
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
43. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Immunoflourescent staining of tissue biopsies
Superficial inguinal
44. are Th cells involved in trapping of antigens of endotoxin/LPS?
A j chain
IgE
No because no peptide fragment!
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
45. give an example of how influenza does a major antigenic shift.
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
RNA segment reassortment
Not thymus - BM
Th cells fail to produce interferon gamma; a lot of IgE
46. What are the function of B cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
except hyperacute
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
opsonizes
47. IgE has the ___________ in the serum
lowest concentration
MHC class molecules bind to KIRS or CD94 to prevent killing
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
S. aureus - E. Coli - aspergillus
48. What is serum sickness? give an example.
opsonizes
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
The patient could become cyanotic in the OR!
49. What are the T cell functions?
Secretory component
T cell activation; no with CD 4 or CD 8
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
2 heavy chains and two light chains
50. T/F B cells do not require a second signal
Not thymus - BM
mesenchymal
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
False! B cell class switching requires a second signal