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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 pathology of acute transplant rejection? is it reversible?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

2. What does Interferon alpha and beta do? how?
S. aureus - E. Coli - aspergillus
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Activates cytotoxic CD 8 T cells as second signal
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

3. what happens in a deficiency of C1 esterase inhibitor? DAF?
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Hereditary angioedema; PNH
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

4. What are the main symptoms of B cell immunodeficiencies?
SP infections
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Antibody mediated cytotoxicity; either complement dependent or complement independent
T

5. What lymph node drains the thigh?
Superficial inguinal
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

6. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Active; passive - fast but short half life (3 weeks!)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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
SP infections

7. what prevents NK cells from killing normal cells if their default is to kill?
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)
Interferon gamma; Th1
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
MHC class molecules bind to KIRS or CD94 to prevent killing

8. What is the pathogenesis of a candida skin test?
C5a
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Delayed type hypersensitivity

9. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
If there is class switching and plasma cell production (that is when memory cells are produced)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

10. What is the mechanism for sirolimus? what else it known as?
Popliteal
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

11. How is i Th1 helper cell inhibited?
Antimicrosomal and antithyroglobulin
Internal iliac
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Cytokine IL 10 secreted by Th2

12. What lymph node drains the sigmoid colon?
IL 15; IL 12 - interferon Beta and interferon alpha
Inferior mesenteric
MS
lowest concentration

13. What are the PALS?
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
All MHC 1/CD8
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

14. Which are the only two antiinflammatory cytokines?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
TGF beta and IL 10

15. What do multimeric antibodies require for assembly?
Viral neutralization of igM and IgG!
IgE; by activating eosinophils
A j chain
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

16. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Cross link
IgG
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)

17. For which toxins are preformed antibodies (passive) given?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Tetanus - Botulinum - HBV - Rabies

18. What is hereditary angioedema? What are the C3 levels?
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
Yes
IL 3; supports growth and differentiation of bone marrow stem cells
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

19. What are the two signals required for T cells? what happens after?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
T cell precursor
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

20. what secretes IL 4?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Basophils! THey want IG E class switch!

21. What is the general structure of an Ab?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
pathogenesis
2 heavy chains and two light chains

22. What are the autoantibodies for myasthenia gravis?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Antidote for digoxin intoxication
Anti Ach receptor

23. What are the autoantibodies for Celiac disease?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
IL 1 and IL 6
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Superior mesenteric

24. What is the clinical use for azathioprine?
MS - hay fever - SLE - goodpastures
...
Hereditary angioedema; PNH
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

25. What are the two signals required for B cell class switching? Which is the second signal?
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
T cell activation; no with CD 4 or CD 8
Para aortic
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

26. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Remove encapsulated bacateria
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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

27. So antibodies are the effectors for the humoral response. List some of their functions.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
T cell dysfunction

28. where do somatic hypermutation and class switching occur?
In the germinal center of secondary follicles (In the paler center)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

29. which cytokine inhibits TH2 cells? secreted by who?
2 heavy chains and two light chains
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
DM type I and RA
Interferon gamma; Th1

30. What is the pathology seen in chronic transplant rejection?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
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
IL 3; supports growth and differentiation of bone marrow stem cells
Antidesmoglein

31. what bacteria are a splenectomy patient most susceptible to? why?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
lowest concentration
Not thymus - BM

32. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Cells that stil have weird parts of their membrane that macrophages usually bite off
type four
IgM and IgD
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

33. What are the function of B cells?
CD56
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
IgG

34. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Antidesmoglein
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

35. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
False! B cell class switching requires a second signal
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
Glycoproteins; HLA
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

36. What are superantigens? give two examples.
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

37. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
T cell dysfunction
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
except hyperacute

38. What are the main Cell surface proteins on T cells?
lowest concentration
Anti TSh receptor
Rheumatic arthritis
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

39. What are some sinopulmonary infections?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
MS - hay fever - SLE - goodpastures
Sinusitis - otitis media - pneumonia

40. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Anemias (esp due to renal failure)
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

41. What are the autoantibodies for other vasculitides?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti TSh receptor
Th2; Th1
Local infection/inflammation; infection of the ln itself; metastasis

42. What is the defect in hyper IgM syndrome? What are the lab results?
Superficial inguinal
IgG
IL 15; IL 12 - interferon Beta and interferon alpha
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

43. What does IL 2 do?
False! B cell class switching requires a second signal
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Activates cytotoxic CD 8 T cells as second signal
T cell dysfunction

44. To what portion of the Antibody do the complements bind?
Fc
Axillary
Inferior mesenteric
Severe pyogenic infections early in life

45. IgM can fix complement but...
cannot cross placenta
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Superior mesenteric

46. A lymph node is a ________ lymphoid organ.
Edema and necrosis in that region
IgAs in mothers breast milk!
secondary
IgM and IgG

47. What lymph node drains the anal canal (below the pectinate line)?
Superficial inguinal
Activates Th1 helper cells; Macrophages
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

48. in which immunodef order do you see a lot of pus? no pus?
Interferon gamma and IL 2
Edema and necrosis in that region
When you select for which MHC it will have; take out the lymphs that self react
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

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

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50. other than eat and bite RBCs what else do Macrophages of spleen do>
cannot cross placenta
Remove encapsulated bacateria
pale central germinal centers
encapsulated