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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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1. Which is the main antibody in the delayed or secondary response to an antigen?
IgG
Alternative splicing of mRNA
Anti SS- A (anti RO) and Anti SS- B
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

2. where do NK cells develop?
isotype
Not thymus - BM
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

3. what happens in a deficiency of C1 esterase inhibitor? DAF?
TGF beta and IL 10
Hereditary angioedema; PNH
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Rheumatic arthritis

4. What is the receptor for EBV? On what cells is that located?
Anti Ach receptor
By transcytosis
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

5. What are four results of a splenectomy?
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
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

6. What do multimeric antibodies require for assembly?
IgAs in mothers breast milk!
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
A j chain

7. Which HLA's are included in MHC I? MHC II?

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8. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Edema and necrosis in that region
Superficial inguinal
T cell precursor

9. What are the autoantibodies for polymyositis and dermatomyositis?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Wiskott Aldrich syndrome
Anti Jo -1

10. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Interferon gamma; Th1
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
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

11. Describe complement dependent Type II hypersensitivity. Give an example.
TNF alpha and IL1
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
Liver! (they are proteins circulating in the blood)
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

12. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
CD56
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
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
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

13. describe the classic complement pathway.
Receiving preformed Antibodies
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

14. Leukocyte adhesion defect presents with...
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
acute phase reactants
In the germinal center of secondary follicles (In the paler center)
neutrophilia!

15. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Bind FcG for antibody dependent cellular cytotoxicity
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

16. which interleukin receptor is required for NK development? activation?
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Anti Ach receptor
IL 15; IL 12 - interferon Beta and interferon alpha

17. What are the main cell surface proteins on B cells?
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
Fc
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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

18. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
Axillary
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
IgA
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

19. What is oprelevkin? and What is it used for?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Lymphocytes
Recom IL 11; thrombocytopenia

20. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
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
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
Remove encapsulated bacateria

21. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
IL 1 and IL 6
Rheumatic arthritis

22. describe the pathogenesis of delayed type IV hypersensitivity
When you select for which MHC it will have; take out the lymphs that self react
IgM
Anti Jo -1
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

23. What is the pathogenesis of HyperIgE syndrome? What are the labs?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Th cells fail to produce interferon gamma; a lot of IgE

24. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
Stimulate the liver to release acute phase reactants
carboxy terminal
Cyclosporine - OKT3

25. what mediates the type II hypersensitivity? What are the two different methods?
Anti glutamate carboxylase and anti insulin
Antibody mediated cytotoxicity; either complement dependent or complement independent
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
IgM and IgD

26. 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
opsonizes
Chronic granulomatous disease
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

27. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Wiskott Aldrich syndrome
No because no peptide fragment!
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

28. So antibodies are the effectors for the humoral response. List some of their functions.
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
TGF beta and IL 10
IgM and IgD
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

29. The secondary follicles have __________; primary follicles are dense
IL 3; supports growth and differentiation of bone marrow stem cells
Antidesmoglein
pale central germinal centers
T

30. What lymph node drains the upper limb?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Axillary
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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

31. What does it mean if there are igM in the serum at birth?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

32. What are the autoantibodies for pemphigus bulgaris?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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
Stimulate the liver to release acute phase reactants
Antidesmoglein

33. What is an example of a parasite showing antigenic variation?
mesenchymal
Liver! (they are proteins circulating in the blood)
A chemotactic factor for neutrophils
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

34. What are the main symptoms of B cell immunodeficiencies?
2 heavy chains and two light chains
SP infections
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
T cell activation; no with CD 4 or CD 8

35. 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)?
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
Anti viral and anti tumor
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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

36. What lymph node drains the sigmoid colon?
T
Inferior mesenteric
Liver! (they are proteins circulating in the blood)
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

37. What is muromonab - CD3 (OKT3)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Th cells fail to produce interferon gamma; a lot of IgE
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

38. What are target cells?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Cells that stil have weird parts of their membrane that macrophages usually bite off
Local infection/inflammation; infection of the ln itself; metastasis
TNF alpha and IL1

39. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
secondary
RNA segment reassortment
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

40. What is the toxicity of muromonab?
The igA found in breast milk
Celiac
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

41. How is i Th1 helper cell inhibited?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Basophils! THey want IG E class switch!
Cytokine IL 10 secreted by Th2
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

42. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Anti topoisomerase
Wiskott Aldrich syndrome
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!
IL 1 and IL 6

43. What is the defect in hyper IgM syndrome? What are the lab results?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
except hyperacute
Its a serine protease that activates apoptosis; NK and CD8

44. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Stimulate the liver to release acute phase reactants
Yes
except hyperacute
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

45. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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

46. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Lymphocytes
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

47. What lymph node drains the lateral side of the dorsum of the foot?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
Popliteal

48. What is the main cytokine that activates eosinophils?
A j chain
IL 5
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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

49. What are superantigens? give two examples.
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Interferon gamma; Th1
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

50. What is the general structure of an Ab?
Celiac
...
2 heavy chains and two light chains
Superficial inguinal

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USMLE Step 1 Immunology

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