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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. Which cytokines do Th2 release and For what?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Local infection/inflammation; infection of the ln itself; metastasis

2. describe the classic complement pathway.
Glycoproteins; HLA
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
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

3. What are the autoantibodies for graves?
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
Anti TSh receptor
IL 4 - 5 - 10 - 6
Cytokine IL 10 secreted by Th2

4. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
secondary
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
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

5. What does IL 5 do?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
except hyperacute
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

6. What is hereditary angioedema? What are the C3 levels?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

7. What is the presentation of common variable immunodef? and What are the labs?
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
Activate macrophages
Wiskott Aldrich syndrome
CRP - C3b - IgM

8. What are the labs in brutons agammaglobulinemia?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

9. Type Iv hypersensitivity is...
delayed!
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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)
Rheumatic arthritis

10. which cytokine inhibits TH2 cells? secreted by who?
Glycoproteins; HLA
Fab portion
TLR ad nuclear receptors
Interferon gamma; Th1

11. What does CD16 on NK cells do?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Antibody mediated cytotoxicity; either complement dependent or complement independent
Bind FcG for antibody dependent cellular cytotoxicity
DM type I and RA

12. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
lowest concentration
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

13. The idiotype; the Fc portion determines the...
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
isotype
Humoral
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

14. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
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
IgG
Anti topoisomerase
Its main effect is a defect in Ab opsonization for killing

15. in which immunodef order do you see a lot of pus? no pus?
Glycoproteins; HLA
except hyperacute
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
S. aureus - E. Coli - aspergillus

16. What is the mechanism for sirolimus? what else it known as?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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

17. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
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
Superior mesenteric
RNA segment reassortment
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

18. What are the main cell surface proteins on B cells?
In the germinal center of secondary follicles (In the paler center)
...
Cyclosporine - OKT3
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

19. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
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
Bind FcG for antibody dependent cellular cytotoxicity
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

20. What is Aldesleukin? What is it used for
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)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
A recomb cytokine of IL 2; RCC and metastatic melanoma
Histamine; post capillary venules - vasodilation

21. What does granulysin do?
Liver! (they are proteins circulating in the blood)
Remove encapsulated bacateria
Anti SS- A (anti RO) and Anti SS- B
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

22. What are the autoantibodies for Mixed connective tissue disease?
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 U1 RNP (ribonucleoprotein)
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
Local infection/inflammation; infection of the ln itself; metastasis

23. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Type IV
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
Pernicious Anemia and Hashimotos

24. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
CRP - C3b - IgM
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

25. Which type of selection of thymic development provides central tolerance?
Negative selection
Anti viral and anti tumor
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
Its a serine protease that activates apoptosis; NK and CD8

26. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Hemochromatosis
Th cells fail to produce interferon gamma; a lot of IgE
Inferior mesenteric
Rheumatic arthritis

27. What cytokines are released by Th1 cells?
Type IV
Interferon gamma and IL 2
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

28. which antibody is involved in the primary response or immediate response to an antigen?
IgM
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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 :(
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

29. What are some catalase positive organisms?
SP infections
Negative selection
S. aureus - E. Coli - aspergillus
Paracortex

30. which of the transplant rejections is antibody mediated? why does it occur?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
MHC class molecules bind to KIRS or CD94 to prevent killing
Sinusitis - otitis media - pneumonia

31. What is immune complex disease? give an example.
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Cross link

32. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
MHC I; from RER with help of the B2 microglobulin
Receiving preformed Antibodies
Previous transfusion; pregnant woman whose fetus had paternal antigens
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

33. What are the T cell functions?
Graves
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
IL 1 and IL 6

34. Which is the most abundant antibody in blood?
isotype
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
CRP - C3b - IgM
IgG

35. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
lowest concentration
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

36. What lymph node drains the stomach?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Celiac
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

37. What is the main function of IL 8?
A chemotactic factor for neutrophils
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
By transcytosis
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

38. What is the main function of interferons?
Superficial inguinal
Immunosuppression after kidney transplantation
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

39. T/F B cells do not require a second signal
Negative nitroblue tetrazolium reduction test
False! B cell class switching requires a second signal
Anti smooth muscle
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

40. other than C3a - what other complement acts as an anaphyloxin?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Antidote for digoxin intoxication
C5a
Sinusitis - otitis media - pneumonia

41. What lymph node drains the lateral side of the dorsum of the foot?
SP infections
Antimicrosomal and antithyroglobulin
secondary
Popliteal

42. What happens in a secondary follicle?
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

43. How is sirolimus different from tacrolimus?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

44. What are the autoantibodies for myasthenia gravis?
Superficial inguinal
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Anti Ach receptor
IL 1 and IL 6

45. From where do cytokines come from?
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Lymphocytes
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

46. What is passive immunity?
Antimicrosomal and antithyroglobulin
pathogenesis
Receiving preformed Antibodies
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

47. What is the most common selective Ig deficiency? What is the presentation?
B - T - and NK cells
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Liver! (they are proteins circulating in the blood)

48. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Interferon gamma and IL 2
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 :(
Anti smooth muscle
delayed!

49. are Th cells involved in trapping of antigens of endotoxin/LPS?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Severe pyogenic infections early in life
No because no peptide fragment!
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

50. What do mature naive B lymphocytes express?
IL 5
IgM and IgD
Anemias (esp due to renal failure)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)