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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 happens in a deficiency of C3?
Interferon gamma; Th1
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Viral neutralization of igM and IgG!
T cell precursor

2. To what disease do the autoantibodies to IgG (rheumatoid factor)?
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
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Rheumatic arthritis

3. What is anergy? why does this occur?
A chemotactic factor for neutrophils
secondary
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
IgE; by activating eosinophils

4. The two heavy chains of an antibody contribute to the...
Fab portion
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
acute phase reactants
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

5. What lymph node drains the breast?
MHC I - CD16 - CD56
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Axillary

6. How is the thymus organized? what happens in each section?
pentamer
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

7. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Cyclosporine - OKT3
Paracortex; viral infection
Stimulate the liver to release acute phase reactants
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

8. How does the alternative pathway lead to MAC activation?
B - T - and NK cells
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
Daclizumab; prevent ACUTE rejection of renal transplant
IgM and IgD

9. Which are the only two antiinflammatory cytokines?
Cytokine IL 10 secreted by Th2
TGF beta and IL 10
Negative!
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

10. What is recomb beta interferon used for?
MS
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IgG
Remove encapsulated bacateria

11. What is the main function of IL 8?
Th2; Th1
T cell dysfunction
A chemotactic factor for neutrophils
Previous transfusion; pregnant woman whose fetus had paternal antigens

12. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
In the germinal center of secondary follicles (In the paler center)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
...

13. which antibodies prevent antigens from binding mucosal surfaces?
IgA
The igA found in breast milk
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

14. describe the classic complement pathway.
T cell activation; no with CD 4 or CD 8
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
DM type I and RA
Para aortic

15. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Negative selection
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Activates Th1 helper cells; Macrophages

16. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Tetanus - Botulinum - HBV - Rabies
Influenza; antigenic shift; antigenic drift
S. aureus - E. Coli - aspergillus

17. Which is the most abundant antibody in blood?
T cell dysfunction
Interferon gamma; Th1
IgG
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

18. other than mediating shock - what else does TNF alpha do? who releases it mainly?
heavy chains
Activates Th1 helper cells; Macrophages
pentamer
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

19. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
mesenchymal
Superficial inguinal

20. which of the hypersensitivity reactions is not Ab mediated?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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
Type IV
Anti mitochondrial

21. How is the antigen loaded onto a MHC II?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
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
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
IgA

22. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
TLR ad nuclear receptors

23. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Internal iliac
Graves
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 :(

24. Complements are...
Immunoflourescent staining of tissue biopsies
Tetanus - Botulinum - HBV - Rabies
MHC I; from RER with help of the B2 microglobulin
acute phase reactants

25. What are the autoantibodies for sjorgens syndrome?
Delayed type hypersensitivity
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anti SS- A (anti RO) and Anti SS- B
pale central germinal centers

26. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
...
Anti alpha subunit 3 of collagen on type IV bm
MS

27. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Histamine; post capillary venules - vasodilation
encapsulated
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

28. 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
Influenza; antigenic shift; antigenic drift
Severe pyogenic infections early in life
Immunoflourescent staining of tissue biopsies

29. 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
IL 4
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
MHC I; from RER with help of the B2 microglobulin

30. What are the autoantibodies for other vasculitides?
pathogenesis
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Superficial inguinal
Hereditary angioedema; PNH

31. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
TGF beta and IL 10
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
A j chain
A - B - C; all the D's

32. IgE has the ___________ in the serum
IL 15; IL 12 - interferon Beta and interferon alpha
lowest concentration
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

33. describe the pathogenesis of delayed type IV hypersensitivity
Delayed type hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Anti U1 RNP (ribonucleoprotein)
Macrophages - Dendritic cells - B cells

34. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Cyclosporine - OKT3
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

35. what mediates the type II hypersensitivity? What are the two different methods?
The igA found in breast milk
Celiac
Interferon gamma; Th1
Antibody mediated cytotoxicity; either complement dependent or complement independent

36. what will NK cells do to cells covered in IgG Ab? why?
Kill them because they have CD16 on them that recognize the FcG portion
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Axillary

37. What are the autoantibodies for graves?
IgG
MHC I - CD16 - CD56
Anti TSh receptor
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

38. which antibodies can bind complement?
IgM and IgG
Anti topoisomerase
Its main effect is a defect in Ab opsonization for killing
C5a

39. What can cause a lymph node enlargement?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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
Local infection/inflammation; infection of the ln itself; metastasis
active complement pathway

40. What is a factor that is a predictor for a bad transplantation?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

41. 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
Kill them because they have CD16 on them that recognize the FcG portion
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
CD21 on B cells (although there is T cell lymphocytosis in EBV)

42. What is the treatment of acute transplant rejection?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Cyclosporine - OKT3
Immunosuppression after kidney transplantation

43. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
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
lowest concentration
Glycoproteins; HLA
Paracortex; viral infection

44. which B and T cell disorder presents with specifically low IgM?
Antimicrosomal and antithyroglobulin
Wiskott Aldrich syndrome
Anti viral and anti tumor
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

45. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
A recomb cytokine of IL 2; RCC and metastatic melanoma
cannot cross placenta
All MHC 1/CD8

46. other than C3a - what other complement acts as an anaphyloxin?
C5a
Antimicrosomal and antithyroglobulin
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
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

47. __________ are a part of the innate system.
Wiskott Aldrich syndrome
Activate macrophages
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
NK cells

48. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Th cells fail to produce interferon gamma; a lot of IgE
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
If there is class switching and plasma cell production (that is when memory cells are produced)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

49. which antibody is involved in the primary response or immediate response to an antigen?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IL 3; supports growth and differentiation of bone marrow stem cells
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IgM

50. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
IL 15; IL 12 - interferon Beta and interferon alpha
MHC II - B7
Anti glutamate carboxylase and anti insulin