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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
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
Interferon gamma and IL 2
Histamine; post capillary venules - vasodilation
...

2. What is the white pulp of the spleen?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Carbohydrate
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IgM and IgG

3. 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)
The igA found in breast milk
Barrel hoop basement membrane fenestrations
If there is class switching and plasma cell production (that is when memory cells are produced)

4. what secretes IL 4?
Activates cytotoxic CD 8 T cells as second signal
Basophils! THey want IG E class switch!
Glycoproteins; HLA
except hyperacute

5. What are the two signals required for B cell class switching? Which is the second signal?
delayed!
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Severe pyogenic infections early in life
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

6. Describe the complement independent Type II hypersenstivity reaction. Give an example.
IL 4 - 5 - 10 - 6
In the germinal center of secondary follicles (In the paler center)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Superficial inguinal

7. What is colostrum?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
C5a
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
The igA found in breast milk

8. Which antibody mediates immunity to worms? how?
T cell precursor
IgE; by activating eosinophils
Graves
Type IV

9. what ensure that a memory response is generated?
If there is class switching and plasma cell production (that is when memory cells are produced)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Activates Th1 helper cells; Macrophages

10. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
encapsulated
Tetanus - Botulinum - HBV - Rabies
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Antidesmoglein

11. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
IgM and IgD
Anti Jo -1
Type IV
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

12. Which disease is associated with DR3?
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
DM type I
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
By transcytosis

13. What are the symptoms of serum sickness?
Remove encapsulated bacateria
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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)
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

14. Give three examples of bacteria that use antigenic variation and how.
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Not thymus - BM
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

15. What is the main function of IL 8?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
A chemotactic factor for neutrophils
Antibody mediated cytotoxicity; either complement dependent or complement independent
MS - hay fever - SLE - goodpastures

16. What happens in a deficiency of C3?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
MHC I; from RER with help of the B2 microglobulin
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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)

17. What are the autoantibodies for polymyositis and dermatomyositis?
Lymphocytes
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
acute phase reactants
Anti Jo -1

18. What are the autoantibodies for myasthenia gravis?
Viral neutralization of igM and IgG!
Anti Ach receptor
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
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

19. What are the autoantibodies for autoimmune hepatitis?
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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
cannot cross placenta
Anti smooth muscle

20. What is the presentation of hyperIgM syndrome?
...
IgG
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Severe pyogenic infections early in life

21. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Histamine; post capillary venules - vasodilation
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

22. What are the autoantibodies for type I diabetes mellitus?
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
Anti glutamate carboxylase and anti insulin
Glycoproteins; HLA
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

23. hat is the presentation of Jobs syndrome or Hyper IgE?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
NK cells
IL 4 - 5 - 10 - 6

24. Which type of selection of thymic development provides central tolerance?
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
Negative selection
dimer

25. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Hereditary angioedema; PNH
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Hemochromatosis

26. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
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 :(
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

27. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Bind FcG for antibody dependent cellular cytotoxicity
...

28. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
MHC class molecules bind to KIRS or CD94 to prevent killing
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

29. What are the main cell surface proteins on B cells?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Internal iliac
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

30. What does granulysin do?
heavy chains
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

31. What is recomb beta interferon used for?
MS
Anemias (esp due to renal failure)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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

32. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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

33. Which disease is associated with DR7?
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
Cyclosporine - OKT3
Cytokine IL 10 secreted by Th2
Steroid responsive nephrotic syndrome

34. The ______ in the BM are DN - the DP are in the cortex of thymus
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
When you select for which MHC it will have; take out the lymphs that self react
T cell precursor
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

35. ________ regulate the cell mediated response.
S. aureus - E. Coli - aspergillus
DM type I
Immunosuppression after kidney transplantation
Humoral

36. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Celiac
Axillary
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Th cells fail to produce interferon gamma; a lot of IgE

37. What are the autoantibodies for graves?
Anti TSh receptor
Antidote for digoxin intoxication
Active; passive - fast but short half life (3 weeks!)
Its a serine protease that activates apoptosis; NK and CD8

38. which antibodies prevent antigens from binding mucosal surfaces?
IgA
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Bind FcG for antibody dependent cellular cytotoxicity
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

39. What lymph node drains the testes?
Complement activation (active in both)
...
Para aortic
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

40. What are the main symptoms of T cell immunodeficiencies?
carboxy terminal
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

41. What is three common causes of severe combined immunodef? What is the result of all three?
Bind FcG for antibody dependent cellular cytotoxicity
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
type four
Thrombocytopenia

42. In thymic development - What is the positive selection? negative selections?
DM type I
When you select for which MHC it will have; take out the lymphs that self react
MHC II - B7
Superficial inguinal

43. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Anti U1 RNP (ribonucleoprotein)
Activate macrophages
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
secondary

44. What cytokines to Th2 secrete?
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
False! B cell class switching requires a second signal
IL 4 - 5 - 10 - 6
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

45. What are the autoantibodies for Celiac disease?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Negative nitroblue tetrazolium reduction test

46. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
not Ab mediated
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

47. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Immunoflourescent staining of tissue biopsies
Anti U1 RNP (ribonucleoprotein)
neutrophilia!
Paracortex

48. describe the pathogenesis of delayed type IV hypersensitivity
By transcytosis
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
S. aureus - E. Coli - aspergillus
pentamer

49. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
encapsulated

50. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Tetanus - Botulinum - HBV - Rabies
IL 5
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

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USMLE Step 1 Immunology

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