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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. To what portion of the Antibody do the complements bind?
Fc
Para aortic
Popliteal
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

2. What is the common variable immunodeficiency ? How is it different from Brutons?
By transcytosis
isotype
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
encapsulated

3. What is the general structure of an Ab?
2 heavy chains and two light chains
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Anemias (esp due to renal failure)
carboxy terminal

4. What are the symptoms of serum sickness?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Its main effect is a defect in Ab opsonization for killing
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

5. What does IL 10 do? who is secreted by?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

6. What are four results of a splenectomy?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
IgM and IgA
Fc
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

7. What is colostrum?
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
delayed!
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
The igA found in breast milk

8. when can graft versus host disease? What is the result?
A recomb cytokine of IL 2; RCC and metastatic melanoma
MHC I - CD16 - CD56
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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

9. What are the autoantibodies for pemphigus bulgaris?
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Antidesmoglein

10. What is muromonab - CD3 (OKT3)
pathogenesis
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

11. What are the autoantibodies for pernicious anemia?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti IF
Anti alpha subunit 3 of collagen on type IV bm

12. 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?
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Axillary
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

13. other than C3a - what other complement acts as an anaphyloxin?
Cyclosporine - OKT3
Edema and necrosis in that region
C5a
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

14. Give an example of someone who could get hyperacute transplant rejection.
Previous transfusion; pregnant woman whose fetus had paternal antigens
Sinusitis - otitis media - pneumonia
Humoral
IgE

15. What lymph node drains the rectum (above the pectinate line)?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Type IV
Internal iliac

16. What is the most common example of passive immunity?
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
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
IgAs in mothers breast milk!
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

17. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
except hyperacute
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

18. which of the hypersensitivity reactions is not Ab mediated?
Pernicious Anemia and Hashimotos
DM type I and RA
DM type I
Type IV

19. can igG cross the placenta?
Anti Jo -1
Yes
By transcytosis
Kill them because they have CD16 on them that recognize the FcG portion

20. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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
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
cannot cross placenta

21. Which disease is associated with DR7?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Steroid responsive nephrotic syndrome
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
SP infections

22. How do you test for chronic granulomatous disease?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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
Negative nitroblue tetrazolium reduction test
CD21 on B cells (although there is T cell lymphocytosis in EBV)

23. How is i Th1 helper cell inhibited?
Para aortic
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Cytokine IL 10 secreted by Th2
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

24. Leukocyte adhesion defect presents with...
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
neutrophilia!
When you select for which MHC it will have; take out the lymphs that self react
Activates Th1 helper cells; Macrophages

25. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Anti SS- A (anti RO) and Anti SS- B
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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)
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

26. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
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
Influenza; antigenic shift; antigenic drift
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
T cell precursor

27. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
IgM and IgA
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

28. What are the autoantibodies for primary biliary cirrhosis?
IgE
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Anti mitochondrial

29. What type of side chains are found on Fc region of an antibody?
Carbohydrate
Active; passive - fast but short half life (3 weeks!)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Antimicrosomal and antithyroglobulin

30. which of the transplant rejections is antibody mediated? why does it occur?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
IL 5
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

31. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
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
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Activate macrophages

32. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
opsonizes
DM type I and RA
Paracortex; viral infection
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

33. What does interferon gamma do to be antiviral?
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
Celiac
Increases expression of MHC I and MHC II and also activates NK cells
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

34. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Internal iliac
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
Tetanus - Botulinum - HBV - Rabies

35. What is digoxin immune Fab used for?
Interferon gamma; Th1
Antidote for digoxin intoxication
IgG
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

36. What is the pathogenesis of a hypersensitivity reaction?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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

37. What are howell jolly bodies?
Graves
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
...
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

38. What is the pathogenesis of acute transplant rejection? When does it occur?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

39. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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
Glycoproteins; HLA
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

40. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Antimicrosomal and antithyroglobulin
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

41. What are the autoantibodies for goodpastures syndrome?
Active; passive - fast but short half life (3 weeks!)
Anti alpha subunit 3 of collagen on type IV bm
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
Superficial inguinal

42. Which are the only two antiinflammatory cytokines?
Secretory component
Anemias (esp due to renal failure)
mesenchymal
TGF beta and IL 10

43. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Liver! (they are proteins circulating in the blood)
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
Its main effect is a defect in Ab opsonization for killing
Chronic granulomatous disease

44. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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
DM type I and RA

45. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
pathogenesis
Its main effect is a defect in Ab opsonization for killing
Anti viral and anti tumor
Negative nitroblue tetrazolium reduction test

46. The idiotype; the Fc portion determines the...
Interferon gamma; Th1
Daclizumab; prevent ACUTE rejection of renal transplant
isotype
IL 5

47. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
mesenchymal
IL 4 - 5 - 10 - 6
IgE; by activating eosinophils
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

48. Which is the main antibody that provides passive immunity to infants?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
SP infections
Negative nitroblue tetrazolium reduction test
IgG

49. what cell surface proteins are on all APCs?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
not Ab mediated
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
MHC II - B7

50. What are the two signals required for Th1 cells? what happens after then activated?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
MHC II - B7
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

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USMLE Step 1 Immunology

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