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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 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?
Anti IF
Anti Jo -1
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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

2. which B and T cell disorder presents with specifically low IgM?
Activates cytotoxic CD 8 T cells as second signal
lowest concentration
Wiskott Aldrich syndrome
Popliteal

3. What are the autoantibodies for wegeners granulomatosis?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Anti topoisomerase
pathogenesis
A j chain

4. What is the clinical use for sirolimus? what should you combine it with?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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
opsonizes

5. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Acts as second signal on B cells to induce class switching to IgE and IgG
IL 4 - 5 - 10 - 6
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
TLR ad nuclear receptors

6. What is chronic mucocutaneous candidiasis d/t?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Immunoflourescent staining of tissue biopsies
T cell dysfunction
Axillary

7. What is the treatment of acute transplant rejection?
IgE; by activating eosinophils
Cyclosporine - OKT3
Celiac
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

8. In thymic development - What is the positive selection? negative selections?
Increases expression of MHC I and MHC II and also activates NK cells
Cells that stil have weird parts of their membrane that macrophages usually bite off
When you select for which MHC it will have; take out the lymphs that self react
Negative!

9. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
IgG
active complement pathway
TLR ad nuclear receptors

10. Which helper T cells' development is induced by IL 4? IL 12?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Th2; Th1
If there is class switching and plasma cell production (that is when memory cells are produced)
No because no peptide fragment!

11. What are the two signals required for T cells? what happens after?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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

12. What are the autoantibodies for sjorgens syndrome?
Steroid responsive nephrotic syndrome
isotype
Anti SS- A (anti RO) and Anti SS- B
Cells that stil have weird parts of their membrane that macrophages usually bite off

13. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

14. What do mature naive B lymphocytes express?
IgM and IgD
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Negative nitroblue tetrazolium reduction test
Kill them because they have CD16 on them that recognize the FcG portion

15. which of the transplant rejections is antibody mediated? why does it occur?
Barrel hoop basement membrane fenestrations
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or 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
The patient could become cyanotic in the OR!

16. How fast does it occur?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
carboxy terminal
The patient could become cyanotic in the OR!
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

17. Only the _______ contribute to the Fc region
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
heavy chains
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
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

18. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Axillary
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
Graves
Influenza; antigenic shift; antigenic drift

19. Which disease is associated with DR3?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Wiskott Aldrich syndrome
DM type I

20. are Th cells involved in trapping of antigens of endotoxin/LPS?
No because no peptide fragment!
opsonizes
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Anti IF

21. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Liver! (they are proteins circulating in the blood)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

22. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Antimicrosomal and antithyroglobulin
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Hemochromatosis

23. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
TGF beta and IL 10
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

24. The alternative pathway is the only constutively...
active complement pathway
pentamer
...
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

25. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
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
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

26. Which diseases are associated with DR5?
A j chain
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
No because no peptide fragment!
Pernicious Anemia and Hashimotos

27. what cell surface proteins are on all APCs?
MHC II - B7
IgE
Internal iliac
Fc

28. What is the receptor for EBV? On what cells is that located?
cannot cross placenta
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Anti IF

29. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
T cell precursor
IgM and IgG
Chronic granulomatous disease
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

30. What are C1 - C2 - C3 - C4 important for?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Viral neutralization of igM and IgG!
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
Steroid responsive nephrotic syndrome

31. what ensure that a memory response is generated?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
If there is class switching and plasma cell production (that is when memory cells are produced)
B - T - and NK cells
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

32. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Increases expression of MHC I and MHC II and also activates NK cells
Activates Th1 helper cells; Macrophages
MHC I - CD16 - CD56
Glycoproteins; HLA

33. what secretes IL 4?
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
Basophils! THey want IG E class switch!
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
pentamer

34. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
T
Chronic granulomatous disease
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

35. What is the pathology seen in chronic transplant rejection?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Anti Ach receptor

36. How does complement link innate and adaptive?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
IgM and IgA
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

37. 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?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

38. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
Basophils! THey want IG E class switch!

39. What are the mediators that mast cells release?
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Bind FcG for antibody dependent cellular cytotoxicity

40. What is the most common selective Ig deficiency? What is the presentation?
Antihistone
Glycoproteins; HLA
Cyclosporine - OKT3
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

41. IgM can exist as a _______ also
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
By transcytosis
acute phase reactants
pentamer

42. How does igA cross the epithelium?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
By transcytosis
DM type I

43. From where do cytokines come from?
Lymphocytes
Hereditary angioedema; PNH
acute phase reactants
IgG

44. The lymphocytes are ________ origin
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
mesenchymal
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

45. what mediates the type II hypersensitivity? What are the two different methods?
MS - hay fever - SLE - goodpastures
Antibody mediated cytotoxicity; either complement dependent or complement independent
Interferon gamma and IL 2
IgA

46. The two heavy chains of an antibody contribute to the...
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Fab portion
Hereditary angioedema; PNH
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

47. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
IgM and IgD
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
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
TGF beta and IL 10

48. What are the autoantibodies for pemphigus bulgaris?
Axillary
cannot cross placenta
Antidesmoglein
active complement pathway

49. What lymph node drains the anal canal (below the pectinate line)?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IgG
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
Superficial inguinal

50. What are howell jolly bodies?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Severe pyogenic infections early in life
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