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Test your basic knowledge |
USMLE Step 1 Immunology
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Study First
Subjects
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health-sciences
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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. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Antidesmoglein
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
2. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
NK 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
SP infections
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
3. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Receiving preformed Antibodies
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
...
4. 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
When you select for which MHC it will have; take out the lymphs that self react
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Anti Ach receptor
5. What is filgrastim and sargramostim? and What is it used for?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
encapsulated
Superficial inguinal
6. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Anemias (esp due to renal failure)
IgM and IgD
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
7. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Th2; Th1
Anti glutamate carboxylase and anti insulin
8. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
Negative selection
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
9. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
lowest concentration
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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
10. How fast does it occur?
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)
Local infection/inflammation; infection of the ln itself; metastasis
Anti TSh receptor
The patient could become cyanotic in the OR!
11. what prevents NK cells from killing normal cells if their default is to kill?
MHC class molecules bind to KIRS or CD94 to prevent killing
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Increases expression of MHC I and MHC II and also activates NK cells
False! B cell class switching requires a second signal
12. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
13. are Th cells involved in trapping of antigens of endotoxin/LPS?
pathogenesis
Humoral
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
No because no peptide fragment!
14. What are the T cell functions?
Superficial inguinal
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Interferon gamma; Th1
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
15. What bugs can actually infect the lymph node itself?
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
dimer
Steroid responsive nephrotic syndrome
16. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Liver! (they are proteins circulating in the blood)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
17. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
S. aureus - E. Coli - aspergillus
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
18. What lymph node drains the lateral side of the dorsum of the foot?
TGF beta and IL 10
False! B cell class switching requires a second signal
Popliteal
MHC class molecules bind to KIRS or CD94 to prevent killing
19. What are the labs in brutons agammaglobulinemia?
In the germinal center of secondary follicles (In the paler center)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
type four
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
20. What lymph node drains the breast?
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!
When you select for which MHC it will have; take out the lymphs that self react
Axillary
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
21. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Celiac
Histamine; post capillary venules - vasodilation
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
22. What is recomb alpha interferon used for?
A recomb cytokine of IL 2; RCC and metastatic melanoma
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Negative selection
Paracortex
23. What is the clinical use for sirolimus? what should you combine it with?
Th cells fail to produce interferon gamma; a lot of IgE
Thrombocytopenia
CD56
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
24. What are the autoantibodies for sjorgens syndrome?
delayed!
pathogenesis
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Anti SS- A (anti RO) and Anti SS- B
25. What are the function of B cells?
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Acts as second signal on B cells to induce class switching to IgE and IgG
The igA found in breast milk
26. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
C5a
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
27. Which is the main antibody in the delayed or secondary response to an antigen?
Anti mitochondrial
Not thymus - BM
IgG
Anti glutamate carboxylase and anti insulin
28. What are the cell surface proteins on NK cells?
Antidesmoglein
MHC I - CD16 - CD56
Para aortic
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!
29. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Steroid responsive nephrotic syndrome
30. IgE has the ___________ in the serum
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
lowest concentration
31. What lymph node drains the thigh?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Superficial inguinal
Th cells fail to produce interferon gamma; a lot of IgE
When you select for which MHC it will have; take out the lymphs that self react
32. What is serum sickness? give an example.
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
DM type I
T cell activation; no with CD 4 or CD 8
Antihistone
33. which antibody activate mast cells - basophils - and eosinophils?
A j chain
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Kill them because they have CD16 on them that recognize the FcG portion
IgE
34. what cell surface proteins are on all APCs?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Local infection/inflammation; infection of the ln itself; metastasis
MHC II - B7
Immunoflourescent staining of tissue biopsies
35. What is the clinical use for azathioprine?
By transcytosis
Inferior mesenteric
...
Delayed type hypersensitivity
36. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
Pernicious Anemia and Hashimotos
The patient could become cyanotic in the OR!
Fc
37. What are MHC's necessary for? By themselves?
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
Inferior mesenteric
T cell activation; no with CD 4 or CD 8
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
38. What lymph node drains the stomach?
Influenza; antigenic shift; antigenic drift
Anemias (esp due to renal failure)
Celiac
Bind FcG for antibody dependent cellular cytotoxicity
39. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Its a serine protease that activates apoptosis; NK and CD8
MHC II - B7
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
40. Give three examples of bacteria that use antigenic variation and how.
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Anti glutamate carboxylase and anti insulin
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
41. What does granzyme do? who secretes it?
MHC class molecules bind to KIRS or CD94 to prevent killing
Complement activation (active in both)
IgM and IgG
Its a serine protease that activates apoptosis; NK and CD8
42. Which is the main antibody that provides passive immunity to infants?
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
IgG
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
43. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
Histamine; post capillary venules - vasodilation
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
44. What are the autoantibodies for autoimmune hepatitis?
pathogenesis
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Anti smooth muscle
45. Describe complement dependent Type II hypersensitivity. Give an example.
carboxy terminal
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
IgM and IgD
46. What is the common variable immunodeficiency ? How is it different from Brutons?
Stimulate the liver to release acute phase reactants
Anti Ach receptor
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
...
47. What are the cell surface proteins for Macrophages? which two are for opsonins?
Hereditary angioedema; PNH
isotype
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
48. which antibodies prevent antigens from binding mucosal surfaces?
IL 1 and IL 6
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
IgA
Th2; Th1
49. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Previous transfusion; pregnant woman whose fetus had paternal antigens
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
50. What is colostrum?
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
TLR ad nuclear receptors
The igA found in breast milk