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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 T cell functions?
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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
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

2. Other than stimulating fever - what else does IL 6 do?
C5a
TLR ad nuclear receptors
DM type I
Stimulate the liver to release acute phase reactants

3. What lymph node drains the rectum (above the pectinate line)?
MHC I - CD16 - CD56
Internal iliac
Anti TSh receptor
Humoral

4. what cell surface proteins are on all APCs?
MHC II - B7
heavy chains
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

5. What is the defect in hyper IgM syndrome? What are the lab results?
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
IL 15; IL 12 - interferon Beta and interferon alpha
IgG
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

6. What does granzyme do? who secretes it?
Tetanus - Botulinum - HBV - Rabies
Its a serine protease that activates apoptosis; NK and CD8
MHC I; from RER with help of the B2 microglobulin
Active; passive - fast but short half life (3 weeks!)

7. What bugs can actually infect the lymph node itself?
Alternative splicing of mRNA
opsonizes
heavy chains
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

8. What is chronic mucocutaneous candidiasis d/t?
Increases expression of MHC I and MHC II and also activates NK cells
T cell dysfunction
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

9. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
Its a serine protease that activates apoptosis; NK and CD8
TNF alpha and IL1
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

10. What lymph node drains the testes?
Para aortic
B - T - and NK 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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

11. which of the transplant rejections is antibody mediated? why does it occur?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Chronic granulomatous disease

12. What type of side chains are found on Fc region of an antibody?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Carbohydrate
Para aortic

13. describe the classic complement pathway.
Kill them because they have CD16 on them that recognize the FcG portion
Anti U1 RNP (ribonucleoprotein)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Anti IF

14. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
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
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
cannot cross placenta
TNF alpha and IL1

15. What is the pathology of acute transplant rejection? is it reversible?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
IL 3; supports growth and differentiation of bone marrow stem cells
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

16. Which disease is associated with HLA A3?
Hemochromatosis
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

17. What happens in a secondary follicle?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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 :(
Rheumatic arthritis

18. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Lymphocytes
Antihistone

19. The two heavy chains of an antibody contribute to the...
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Antidote for digoxin intoxication
Fab portion

20. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Histamine; post capillary venules - vasodilation
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
By transcytosis

21. What kinds of receptors activate innate immunity?
Local infection/inflammation; infection of the ln itself; metastasis
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Immunoflourescent staining of tissue biopsies
TLR ad nuclear receptors

22. other than eat and bite RBCs what else do Macrophages of spleen do>
The patient could become cyanotic in the OR!
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
C5a
Remove encapsulated bacateria

23. Complements are...
acute phase reactants
Steroid responsive nephrotic syndrome
Pernicious Anemia and Hashimotos
MHC I - CD16 - CD56

24. What does IL 2 do?
Fab portion
Type IV
Activates cytotoxic CD 8 T cells as second signal
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

25. How is the thymus organized? what happens in each section?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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
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
IgA

26. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Celiac
Recom IL 11; thrombocytopenia

27. How does the alternative pathway lead to MAC activation?
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
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
IgM and IgG

28. where do somatic hypermutation and class switching occur?
IL 1 and IL 6
Activate macrophages
In the germinal center of secondary follicles (In the paler center)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

29. For which toxins are preformed antibodies (passive) given?
IL 1 and IL 6
Yes
Tetanus - Botulinum - HBV - Rabies
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 :(

30. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Macrophages - Dendritic cells - B cells
TGF beta and IL 10
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

31. What are the autoantibodies for other vasculitides?
Rheumatic arthritis
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Influenza; antigenic shift; antigenic drift

32. What type of fenestrations are found in the red pulp of the spleen?
Barrel hoop basement membrane fenestrations
Popliteal
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

33. what ensure that a memory response is generated?
RNA segment reassortment
If there is class switching and plasma cell production (that is when memory cells are produced)
IgA
CRP - C3b - IgM

34. What are the mediators that mast cells release?
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!
carboxy terminal
Activates Th1 helper cells; Macrophages
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

35. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
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
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
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Cross link

36. 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?
IgG
Chronic granulomatous disease
Activate macrophages
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

37. 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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
...
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

38. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Negative selection
Cyclosporine - OKT3

39. which of the hypersensitivity reactions is not Ab mediated?
Type IV
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 :(
Carbohydrate
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

40. What is recomb gamma interferon used for?
Chronic granulomatous disease
Anti viral and anti tumor
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
C5a

41. The ______ in the BM are DN - the DP are in the cortex of thymus
Th cells fail to produce interferon gamma; a lot of IgE
T cell precursor
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

42. when can graft versus host disease? What is the result?
delayed!
Fab portion
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
Antidote for digoxin intoxication

43. which antibodies can bind complement?
CD56
IgM and IgG
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Humoral

44. 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)?
lowest concentration
Superior mesenteric
carboxy terminal
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

45. which B and T cell disorder presents with specifically low IgM?
DM type I and RA
pentamer
Wiskott Aldrich syndrome
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

46. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
IgG
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
Steroid responsive nephrotic syndrome
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

47. What does granulysin do?
Bind FcG for antibody dependent cellular cytotoxicity
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
dimer
T

48. What are MHC's necessary for? By themselves?
Acts as second signal on B cells to induce class switching to IgE and IgG
Para aortic
MS - hay fever - SLE - goodpastures
T cell activation; no with CD 4 or CD 8

49. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
Anti Jo -1
Anti Ach receptor
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

50. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
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
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