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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.
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 ensure that a memory response is generated?
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
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
If there is class switching and plasma cell production (that is when memory cells are produced)

2. What is the defect in hyper IgM syndrome? What are the lab results?
Anti viral and anti tumor
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
T cell activation; no with CD 4 or CD 8
No because no peptide fragment!

3. IgM can fix complement but...
Rheumatic arthritis
CD56
Barrel hoop basement membrane fenestrations
cannot cross placenta

4. What does it mean if there are igM in the serum at birth?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Receiving preformed Antibodies
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Humoral

5. which of the hypersensitivity reactions is not Ab mediated?
...
Type IV
When you select for which MHC it will have; take out the lymphs that self react
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

6. What is thrombopoietin used for?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
IgA
Thrombocytopenia

7. For which toxins are preformed antibodies (passive) given?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
Tetanus - Botulinum - HBV - Rabies
IgG

8. What lymph node drains the testes?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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
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
Para aortic

9. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
Previous transfusion; pregnant woman whose fetus had paternal antigens
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

10. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

11. What is the pathology seen in chronic transplant rejection?
Popliteal
By transcytosis
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

12. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
In the germinal center of secondary follicles (In the paler center)
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Cytokine IL 10 secreted by Th2

13. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Basophils! THey want IG E class switch!
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
IgAs in mothers breast milk!
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

14. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
When you select for which MHC it will have; take out the lymphs that self react

15. How does complement link innate and adaptive?
IgM and IgG
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Chronic granulomatous disease
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

16. What are the autoantibodies for graves?
Anti TSh receptor
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Histamine; post capillary venules - vasodilation
IgM and IgD

17. What is the pathogenesis of acute transplant rejection? When does it occur?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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
Popliteal
T

18. What are the autoantibodies for primary biliary cirrhosis?
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
MHC class molecules bind to KIRS or CD94 to prevent killing
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
Anti mitochondrial

19. which B and T cell disorder presents with specifically low IgM?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Wiskott Aldrich syndrome
A chemotactic factor for neutrophils
pale central germinal centers

20. What are MHC's necessary for? By themselves?
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
Anti Ach receptor
...
T cell activation; no with CD 4 or CD 8

21. which of the transplant rejections is antibody mediated? why does it occur?
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
A - B - C; all the D's
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

22. 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
MHC II - B7
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Secretory component

23. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
MHC class molecules bind to KIRS or CD94 to prevent killing
Anti Jo -1
Not thymus - BM
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

24. What is the autoantibody for SLE that is nonspecific? Specific?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
secondary
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

25. The Fc region is found on the...
carboxy terminal
Hereditary angioedema; PNH
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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

26. What are some catalase positive organisms?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Interferon gamma and IL 2
S. aureus - E. Coli - aspergillus

27. The alternative pathway is the only constutively...
Pernicious Anemia and Hashimotos
Thrombocytopenia
active complement pathway
Superior mesenteric

28. which antibody is involved in the primary response or immediate response to an antigen?
Receiving preformed Antibodies
IgM
IgG
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

29. What is the general structure of an Ab?
Local infection/inflammation; infection of the ln itself; metastasis
Anemias (esp due to renal failure)
2 heavy chains and two light chains
T cell precursor

30. What lymph node drains the rectum (above the pectinate line)?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Internal iliac
DM type I
Superficial inguinal

31. The pathogenesis of contact dermatitis is ________ hypersensitivity
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
type four
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

32. ________ regulate the cell mediated response.
Paracortex; viral infection
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
Sinusitis - otitis media - pneumonia
Humoral

33. What is three common causes of severe combined immunodef? What is the result of all three?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Negative nitroblue tetrazolium reduction test
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

34. What are the autoantibodies for pernicious anemia?
Anti IF
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Daclizumab; prevent ACUTE rejection of renal transplant

35. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Antimicrosomal and antithyroglobulin
Activate macrophages
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Its a serine protease that activates apoptosis; NK and CD8

36. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Negative selection
Anti viral and anti tumor
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

37. What is the presentation of hyperIgM syndrome?
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
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
IL 15; IL 12 - interferon Beta and interferon alpha
Severe pyogenic infections early in life

38. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Superior mesenteric
IL 15; IL 12 - interferon Beta and interferon alpha
Activate macrophages
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

39. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
T cell precursor
IL 15; IL 12 - interferon Beta and interferon alpha

40. What is digoxin immune Fab used for?
IL 5
T cell precursor
Antidote for digoxin intoxication
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. what happens in a deficiency of C1 esterase inhibitor? DAF?
The igA found in breast milk
Hereditary angioedema; PNH
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

42. where are complements produced?
Receiving preformed Antibodies
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
Liver! (they are proteins circulating in the blood)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

43. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Lymphocytes

44. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
TLR ad nuclear receptors
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
When you select for which MHC it will have; take out the lymphs that self react

45. What is a type I hypersensitivity reaction? What is atopic?
Its a serine protease that activates apoptosis; NK and CD8
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

46. What are the autoantibodies for drug induced lupus?
Antihistone
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
dimer

47. IgE has the ___________ in the serum
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti alpha subunit 3 of collagen on type IV bm
lowest concentration
Anti Jo -1

48. __________ are a part of the innate system.
C5a
Barrel hoop basement membrane fenestrations
NK cells
Rheumatic arthritis

49. which type of immunity is slow but long lasting? as opposed to...
IgAs in mothers breast milk!
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Active; passive - fast but short half life (3 weeks!)
IgA

50. What can cause a lymph node enlargement?
Secretory component
IgM and IgG
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Local infection/inflammation; infection of the ln itself; metastasis