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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 autoantibodies for scleroderma (CREST)? scleroderma diffuse?
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
Antibody mediated cytotoxicity; either complement dependent or complement independent

2. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
IgAs in mothers breast milk!
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Fc

3. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
IgG
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

4. What is recomb gamma interferon used for?
Delayed type hypersensitivity
Chronic granulomatous disease
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Th2; Th1

5. The alternative pathway is the only constutively...
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
active complement pathway
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

6. What are the three types of lymphocytes?
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
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
B - T - and NK cells
Negative nitroblue tetrazolium reduction test

7. 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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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
A - B - C; all the D's

8. What type of fenestrations are found in the red pulp of the spleen?
Anti Ach receptor
Humoral
Barrel hoop basement membrane fenestrations
Paracortex

9. What lymph node drains the scrotum?
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
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
MS
Superficial inguinal

10. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
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
SP infections
encapsulated

11. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Superficial inguinal
A j chain
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

12. Describe the complement independent Type II hypersenstivity reaction. Give an example.
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
IL 15; IL 12 - interferon Beta and interferon alpha
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

13. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

14. What do mature naive B lymphocytes express?
All MHC 1/CD8
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
IgM and IgD
Activate macrophages

15. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
A - B - C; all the D's
Para aortic
Activate macrophages

16. What is filgrastim and sargramostim? and What is it used for?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
CRP - C3b - IgM
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

17. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Anti TSh receptor
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

18. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
T
T cell precursor

19. What are the major functions of Antibodies?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
neutrophilia!
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

20. where do somatic hypermutation and class switching occur?
Anti topoisomerase
except hyperacute
In the germinal center of secondary follicles (In the paler center)
Negative!

21. What are some sinopulmonary infections?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Fc
Sinusitis - otitis media - pneumonia
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

22. other than mediating shock - what else does TNF alpha do? who releases it mainly?
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)
Activates Th1 helper cells; Macrophages
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

23. Complements are...
IgM and IgG
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
DM type I and RA
acute phase reactants

24. which B and T cell disorder presents with specifically low IgM?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
2 heavy chains and two light chains
Wiskott Aldrich syndrome
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

25. What is the clinical use for azathioprine?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
...
MHC II - B7
Inferior mesenteric

26. What is the common variable immunodeficiency ? How is it different from Brutons?
No because no peptide fragment!
S. aureus - E. Coli - aspergillus
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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

27. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Paracortex
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

28. What are the autoantibodies for Mixed connective tissue disease?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Anti U1 RNP (ribonucleoprotein)
DM type I and RA
The igA found in breast milk

29. 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)?
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
T cell dysfunction
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

30. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Lymphocytes
IL 3; supports growth and differentiation of bone marrow stem cells
Its main effect is a defect in Ab opsonization for killing
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)

31. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Th2; Th1
Lymphocytes

32. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
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
Alternative splicing of mRNA
...
Activate macrophages

33. are Th cells involved in trapping of antigens of endotoxin/LPS?
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
neutrophilia!
No because no peptide fragment!
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

34. What is the pathology seen in chronic transplant rejection?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
opsonizes
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

35. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Influenza; antigenic shift; antigenic drift
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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

36. So antibodies are the effectors for the humoral response. List some of their functions.
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Anti glutamate carboxylase and anti insulin
B - T - and NK cells

37. What is the pathogenesis of acute transplant rejection? When does it occur?
IL 15; IL 12 - interferon Beta and interferon alpha
NK 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
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

38. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton
Paracortex; viral infection
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

39. What happens in a secondary follicle?
Rheumatic arthritis
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Tetanus - Botulinum - HBV - Rabies
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

40. What does granulysin do?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
...
Lymphocytes
Antidote for digoxin intoxication

41. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
heavy chains
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

42. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Kill them because they have CD16 on them that recognize the FcG portion
Anti viral and anti tumor
Chronic granulomatous disease
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

43. The MALT/GALT are not...
Histamine; post capillary venules - vasodilation
Paracortex
encapsulated
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

44. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Paracortex; viral infection
Cross link
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

45. Other than stimulating fever - what else does IL 6 do?
C5a
Stimulate the liver to release acute phase reactants
Receiving preformed Antibodies
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

46. Which diseases are associated with DR2?
Negative selection
RNA segment reassortment
Cross link
MS - hay fever - SLE - goodpastures

47. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Acts as second signal on B cells to induce class switching to IgE and IgG
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

48. What are the symptoms of serum sickness?
SP infections
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
T cell activation; no with CD 4 or CD 8
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

49. How fast does it occur?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Its a serine protease that activates apoptosis; NK and CD8
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
The patient could become cyanotic in the OR!

50. What is anergy? why does this occur?
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
A chemotactic factor for neutrophils
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)