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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. What lymph node drains the sigmoid colon?
neutrophilia!
Inferior mesenteric
Recom IL 11; thrombocytopenia
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

2. 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)
IgG
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

3. What is serum sickness? give an example.
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
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
active complement pathway
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

4. What lymph node drains the upper limb?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Axillary
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
T cell precursor

5. what will NK cells do to cells covered in IgG Ab? why?
Interferon gamma; Th1
Macrophages - Dendritic cells - B cells
Kill them because they have CD16 on them that recognize the FcG portion
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 :(

6. Describe the capsular structure of a lymph node; What are the functions of the LN?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
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

7. What is muromonab - CD3 (OKT3)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
...

8. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
pentamer
Humoral

9. describe the classic complement pathway.
Lymphocytes
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
In the germinal center of secondary follicles (In the paler center)
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

10. What does IL 4 do?
Activates cytotoxic CD 8 T cells as second signal
Its a serine protease that activates apoptosis; NK and CD8
Cytokine IL 10 secreted by Th2
Acts as second signal on B cells to induce class switching to IgE and IgG

11. Give three examples of bacteria that use antigenic variation and how.
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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

12. What is the pathology seen in chronic transplant rejection?
T
Tetanus - Botulinum - HBV - Rabies
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Glycoproteins; HLA

13. What are the autoantibodies for graves?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anti TSh receptor
A chemotactic factor for neutrophils
Anti viral and anti tumor

14. What is the main cytokine that activates eosinophils?
Rheumatic arthritis
IL 5
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Humoral

15. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
Anti topoisomerase
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

16. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Superficial inguinal
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Superficial inguinal
Internal iliac

17. What is the pathology in hyperacute transplant rejection?
IL 4
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
C5a
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

18. in which immunodef order do you see a lot of pus? no pus?
Immunoflourescent staining of tissue biopsies
Superficial inguinal
T cell activation; no with CD 4 or CD 8
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

19. What lymph node drains the thigh?
Superficial inguinal
MHC class molecules bind to KIRS or CD94 to prevent killing
Remove encapsulated bacateria
Activates cytotoxic CD 8 T cells as second signal

20. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
IgE; by activating eosinophils
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Hereditary angioedema; PNH

21. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
Anti Jo -1
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
Type IV

22. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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
Edema and necrosis in that region

23. What is chronic mucocutaneous candidiasis d/t?
IgE
Antidesmoglein
Activates Th1 helper cells; Macrophages
T cell dysfunction

24. Which cytokines do Th2 release and For what?
MHC class molecules bind to KIRS or CD94 to prevent killing
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

25. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
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
Viral neutralization of igM and IgG!
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
IgA

26. What is recomb beta interferon used for?
DM type I and RA
acute phase reactants
MS
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

27. How is i Th1 helper cell inhibited?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Cytokine IL 10 secreted by Th2
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

28. What are the autoantibodies for myasthenia gravis?
Influenza; antigenic shift; antigenic drift
Anti Ach receptor
IL 5
Negative nitroblue tetrazolium reduction test

29. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Cross link
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

30. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

31. What is hereditary angioedema? What are the C3 levels?
A chemotactic factor for neutrophils
Activate macrophages
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
All MHC 1/CD8

32. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IgG
The patient could become cyanotic in the OR!

33. What are the three types of lymphocytes?
Complement activation (active in both)
B - T - and NK cells
Anti smooth muscle
Macrophages - Dendritic cells - B cells

34. What do mature naive B lymphocytes express?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
IgM and IgD
CRP - C3b - IgM
Cells that stil have weird parts of their membrane that macrophages usually bite off

35. What lymph node drains the anal canal (below the pectinate line)?
Anti mitochondrial
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
Th2; Th1
Superficial inguinal

36. IgM can exist as a _______ also
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Lymphocytes
pentamer
IgM

37. What is the toxicity of muromonab?
CD56
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
MHC I - CD16 - CD56
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

38. What are the autoantibodies for systemic sclerosis?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Anti topoisomerase
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
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

39. What does Interferon alpha and beta do? how?
Humoral
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

40. What is a type I hypersensitivity reaction? What is atopic?
Interferon gamma; Th1
Anti alpha subunit 3 of collagen on type IV bm
If there is class switching and plasma cell production (that is when memory cells are produced)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

41. The idiotype; the Fc portion determines the...
isotype
Anti viral and anti tumor
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

42. what prevents NK cells from killing normal cells if their default is to kill?
Activates cytotoxic CD 8 T cells as second signal
Receiving preformed Antibodies
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
MHC class molecules bind to KIRS or CD94 to prevent killing

43. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
NK cells
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

44. which antibodies can bind complement?
Inferior mesenteric
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
IgM and IgG
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

45. How does the alternative pathway lead to MAC activation?
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
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

46. What is filgrastim and sargramostim? and What is it used for?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Alternative splicing of mRNA
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

47. What is the main cytokine released by T cells? What does it do
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
IL 3; supports growth and differentiation of bone marrow stem cells
RNA segment reassortment
DM type I and RA

48. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
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
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
IgE; by activating eosinophils

49. Give an example of someone who could get hyperacute transplant rejection.
Previous transfusion; pregnant woman whose fetus had paternal antigens
Anti Ach receptor
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

50. What does CD16 on NK cells do?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
IgE; by activating eosinophils
Bind FcG for antibody dependent cellular cytotoxicity
dimer

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USMLE Step 1 Immunology

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