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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 are the two signals required for B cell class switching? Which is the second signal?
A - B - C; all the D's
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Carbohydrate
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

2. what mediates the type II hypersensitivity? What are the two different methods?
Humoral
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
Cyclosporine - OKT3
Antibody mediated cytotoxicity; either complement dependent or complement independent

3. Which cytokines do Th2 release and For what?
Delayed type hypersensitivity
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

4. What do mature naive B lymphocytes express?
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
Influenza; antigenic shift; antigenic drift
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
IgM and IgD

5. For which toxins are preformed antibodies (passive) given?
Receiving preformed Antibodies
Tetanus - Botulinum - HBV - Rabies
...
Active; passive - fast but short half life (3 weeks!)

6. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
carboxy terminal
Anti SS- A (anti RO) and Anti SS- B
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
IgM

7. What is recomb alpha interferon used for?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
encapsulated
Anti TSh receptor
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

8. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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 LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
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
IgM and IgG

9. What are the autoantibodies for pernicious anemia?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Anti IF
Superficial inguinal

10. What cytokines are released by Th1 cells?
Interferon gamma and IL 2
not Ab mediated
Steroid responsive nephrotic syndrome
Complement activation (active in both)

11. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Cytokine IL 10 secreted by Th2
Receiving preformed Antibodies
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

12. Which type of selection of thymic development provides central tolerance?
MHC I - CD16 - CD56
MS - hay fever - SLE - goodpastures
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Negative selection

13. What can cause a lymph node enlargement?
Activate macrophages
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Local infection/inflammation; infection of the ln itself; metastasis

14. What is an example of a parasite showing antigenic variation?
Anti viral and anti tumor
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
RNA segment reassortment

15. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Yes
Activate macrophages

16. What are the mediators that mast cells release?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Lymphocytes
In the germinal center of secondary follicles (In the paler center)

17. What is the clinical use of Muromonab?
...
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Immunosuppression after kidney transplantation
Severe pyogenic infections early in life

18. What are the autoantibodies for goodpastures syndrome?
...
Anti alpha subunit 3 of collagen on type IV bm
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
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 :(

19. What is the most common example of passive immunity?
Active; passive - fast but short half life (3 weeks!)
IgAs in mothers breast milk!
IgG
active complement pathway

20. How do you test for type III hypersensitivity?
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
MHC I; from RER with help of the B2 microglobulin
Not thymus - BM
Immunoflourescent staining of tissue biopsies

21. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
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
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
Delayed type hypersensitivity

22. What are the main Cell surface proteins on T cells?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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
Superficial inguinal
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

23. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
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
Cytokine IL 10 secreted by Th2
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
C5a

24. What is anergy? why does this occur?
Edema and necrosis in that region
IgM and IgG
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

25. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Daclizumab; prevent ACUTE rejection of renal transplant
All MHC 1/CD8
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
When you select for which MHC it will have; take out the lymphs that self react

26. What is the white pulp of the spleen?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

27. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
Fc
Anti Jo -1
Tetanus - Botulinum - HBV - Rabies

28. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
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!
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
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

29. Name 5 ways Antibody diversity is generated?
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
Hemochromatosis
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
Sinusitis - otitis media - pneumonia

30. What is recomb gamma interferon used for?
Chronic granulomatous disease
If there is class switching and plasma cell production (that is when memory cells are produced)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Anti IF

31. What is the main cytokine that activates eosinophils?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IL 5
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
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

32. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Negative nitroblue tetrazolium reduction test
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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
acute phase reactants

33. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

34. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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

35. What does granulysin do?
Cytokine IL 10 secreted by Th2
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Anti smooth muscle
Complement activation (active in both)

36. What are superantigens? give two examples.
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

37. What lymph node drains the rectum (above the pectinate line)?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Internal iliac
MS - hay fever - SLE - goodpastures
Viral neutralization of igM and IgG!

38. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
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
TLR ad nuclear receptors
CD56

39. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Antidote for digoxin intoxication
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

40. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

41. Describe the Mannose Lectin pathway
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
S. aureus - E. Coli - aspergillus
dimer
Anti Ach receptor

42. Which disease is associated with HLA A3?
Anti U1 RNP (ribonucleoprotein)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Hemochromatosis
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

43. which type of immunity is slow but long lasting? as opposed to...
Active; passive - fast but short half life (3 weeks!)
DM type I
False! B cell class switching requires a second signal
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

44. What are the autoantibodies for wegeners granulomatosis?
Fc
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Celiac

45. which of the hypersensitivity reactions is not Ab mediated?
Type IV
Basophils! THey want IG E class switch!
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
DM type I and RA

46. How does igA cross the epithelium?
IL 3; supports growth and differentiation of bone marrow stem cells
Daclizumab; prevent ACUTE rejection of renal transplant
MHC I - CD16 - CD56
By transcytosis

47. can igG cross the placenta?
IgG
Yes
MS - hay fever - SLE - goodpastures
Macrophages - Dendritic cells - B cells

48. Name the three opsonins
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
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

49. which of the transplant rejections is antibody mediated? why does it occur?
Immunoflourescent staining of tissue biopsies
Receiving preformed Antibodies
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
By transcytosis

50. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Cross link
Complement activation (active in both)
Activates Th1 helper cells; Macrophages