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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. So antibodies are the effectors for the humoral response. List some of their functions.
IL 1 and IL 6
Interferon gamma; Th1
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

2. What are the cell surface proteins on NK cells?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
MHC I - CD16 - CD56
Negative!

3. What is the defect in hyper IgM syndrome? What are the lab results?
No because no peptide fragment!
MHC class molecules bind to KIRS or CD94 to prevent killing
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
MHC II - B7

4. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
IgAs in mothers breast milk!
Antibody mediated cytotoxicity; either complement dependent or complement independent

5. what mediates the type II hypersensitivity? What are the two different methods?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Anti IF
pentamer
Anemias (esp due to renal failure)

6. IgM can exist as a _______ also
pentamer
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

7. What are the two signals to kill for NK cells?
Severe pyogenic infections early in life
IgM
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

8. From where do cytokines come from?
Lymphocytes
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Humoral

9. What does interferon gamma do to be antiviral?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Antidesmoglein
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
Increases expression of MHC I and MHC II and also activates NK cells

10. Which disease is associated withB B27?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Anti glutamate carboxylase and anti insulin
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

11. What are MHC's necessary for? By themselves?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
T cell activation; no with CD 4 or CD 8
pentamer

12. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
T
Humoral
TGF beta and IL 10

13. What is muromonab - CD3 (OKT3)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IgE
Pernicious Anemia and Hashimotos
Interferon gamma and IL 2

14. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Superficial inguinal
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
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

15. which B and T cell disorder presents with specifically low IgM?
Antihistone
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
Interferon gamma and IL 2
Wiskott Aldrich syndrome

16. Give an example of someone who could get hyperacute transplant rejection.
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
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
Antidote for digoxin intoxication

17. What are the main cell surface proteins on B cells?
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

18. What are the autoantibodies for polymyositis and dermatomyositis?
Paracortex; viral infection
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Anti Jo -1
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

19. Name 5 ways Antibody diversity is generated?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
Anti TSh receptor
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

20. What does Interferon alpha and beta do? how?
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
All MHC 1/CD8
cannot cross placenta
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

21. What is the late phase reaction of anaphylaxis allergy? what mediates it?
RNA segment reassortment
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)
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

22. which antibodies can bind complement?
IgA
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
IgM and IgG
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

23. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Paracortex; viral infection
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
active complement pathway

24. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Increases expression of MHC I and MHC II and also activates NK cells

25. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Steroid responsive nephrotic syndrome
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Its a serine protease that activates apoptosis; NK and CD8
Histamine; post capillary venules - vasodilation

26. where do NK cells develop?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Not thymus - BM
2 heavy chains and two light chains
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

27. What kinds of receptors activate innate immunity?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
TLR ad nuclear receptors
Anti IF

28. What does IL 10 do? who is secreted by?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Superficial inguinal
T cell precursor

29. The ______ in the BM are DN - the DP are in the cortex of thymus
pathogenesis
T cell precursor
IgM and IgA
Viral neutralization of igM and IgG!

30. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
By transcytosis
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IgM and IgD

31. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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

32. Type IV hypersensitivity is i...
not Ab mediated
Cells that stil have weird parts of their membrane that macrophages usually bite off
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
secondary

33. what characterizes an arthus reaction?
Edema and necrosis in that region
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

34. What are the mediators that mast cells release?
Anti IF
Para aortic
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

35. Which helper T cells' development is induced by IL 4? IL 12?
Th2; Th1
Anti TSh receptor
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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

36. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
All MHC 1/CD8
Lymphocytes
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

37. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
IgM
Negative selection
heavy chains
...

38. What is the main function of IL 12? other than macrophages who else can release IL 12?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Activates cytotoxic CD 8 T cells as second signal
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

39. What is the toxicity of muromonab?
IgG
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
NK cells
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

40. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
Paracortex; viral infection
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
active complement pathway

41. which type of immunity is slow but long lasting? as opposed to...
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
A chemotactic factor for neutrophils
Active; passive - fast but short half life (3 weeks!)
carboxy terminal

42. Which disease is associated with HLA A3?
Hemochromatosis
Th2; Th1
In the germinal center of secondary follicles (In the paler center)
Its a serine protease that activates apoptosis; NK and CD8

43. What are the PALS?
Increases expression of MHC I and MHC II and also activates NK cells
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Daclizumab; prevent ACUTE rejection of renal transplant

44. What happens in a secondary follicle?
Hereditary angioedema; PNH
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
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

45. Which disease is associated with DR7?
Recom IL 11; thrombocytopenia
Steroid responsive nephrotic syndrome
...
MS

46. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Influenza; antigenic shift; antigenic drift

47. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
IgE
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

48. which antibody is involved in the primary response or immediate response to an antigen?
IgM
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
Antihistone
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

49. What are the two signals required for Th1 cells? what happens after then activated?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
A - B - C; all the D's
Antihistone

50. What are the major functions of Antibodies?
Anti alpha subunit 3 of collagen on type IV bm
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Basophils! THey want IG E class switch!
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)