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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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1. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Rheumatic arthritis
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
MHC I - CD16 - CD56

2. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
IgAs in mothers breast milk!
Previous transfusion; pregnant woman whose fetus had paternal antigens
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

3. What is epo used for?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Anemias (esp due to renal failure)
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

4. What lymph node drains the thigh?
Axillary
Negative nitroblue tetrazolium reduction test
Superficial inguinal
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

5. What is the presentation of common variable immunodef? and What are the labs?
Anti smooth muscle
CRP - C3b - IgM
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

6. In general What are T cells good for?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Anti viral and anti tumor
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
The igA found in breast milk

7. What are the autoantibodies for wegeners granulomatosis?
B - T - and NK cells
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Antibody mediated cytotoxicity; either complement dependent or complement independent
Rheumatic arthritis

8. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
Antidesmoglein
Macrophages - Dendritic cells - B cells
Popliteal

9. is IgM an opsonizer?
Negative!
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
Anti IF
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

10. What does interferon gamma do? What two type of cells does it attack mostly?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
active complement pathway
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

11. What is recomb alpha interferon used for?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Para aortic

12. IgE has the ___________ in the serum
lowest concentration
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
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

13. Type IV hypersensitivity is i...
Chronic granulomatous disease
not Ab mediated
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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

14. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Histamine; post capillary venules - vasodilation
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
mesenchymal

15. What happens in a secondary follicle?
IgM and IgA
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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

16. What is the pathogenesis of a hypersensitivity reaction?
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
Th2; Th1
The patient could become cyanotic in the OR!
Daclizumab; prevent ACUTE rejection of renal transplant

17. 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)?
Complement activation (active in both)
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 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

18. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
A recomb cytokine of IL 2; RCC and metastatic melanoma
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Hemochromatosis

19. hat is the presentation of Jobs syndrome or Hyper IgE?
B - T - and NK cells
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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 :(

20. What is an example of a parasite showing antigenic variation?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Anti glutamate carboxylase and anti insulin
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

21. The ______ in the BM are DN - the DP are in the cortex of thymus
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Glycoproteins; HLA
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
T cell precursor

22. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Th2; Th1
MHC II - B7
Paracortex
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

23. What lymph node drains the stomach?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
isotype
Celiac
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

24. What is a type I hypersensitivity reaction? What is atopic?
A chemotactic factor for neutrophils
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

25. other than mediating shock - what else does TNF alpha do? who releases it mainly?
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
IgG
Activates Th1 helper cells; Macrophages
B - T - and NK cells

26. Which is the main antibody in the delayed or secondary response to an antigen?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IgG
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 :(
Anti TSh receptor

27. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
delayed!
dimer
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

28. What are the PALS?
IgE
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
active complement pathway
Interferon gamma and IL 2

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

30. what bacteria are a splenectomy patient most susceptible to? why?
Superficial inguinal
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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

31. What lymph node drains the lateral side of the dorsum of the foot?
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
Hereditary angioedema; PNH
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Popliteal

32. What is immune complex disease? give an example.
Anti mitochondrial
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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

33. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Anti Jo -1
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)
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
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

34. what secretes IL 4?
Basophils! THey want IG E class switch!
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Complement activation (active in both)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

35. 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?
IL 5
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
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

36. What are some sinopulmonary infections?
...
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
IgM
Sinusitis - otitis media - pneumonia

37. which antibody activate mast cells - basophils - and eosinophils?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IgE
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Anti glutamate carboxylase and anti insulin

38. How does igA cross the epithelium?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Type IV
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
By transcytosis

39. where are complements produced?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
pale central germinal centers
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Liver! (they are proteins circulating in the blood)

40. What are the autoantibodies for other vasculitides?
Humoral
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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

41. What is the clinical use for sirolimus? what should you combine it with?
IgM
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)

42. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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

43. Which is the most abundant antibody in blood?
IgG
T
MHC class molecules bind to KIRS or CD94 to prevent killing
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

44. which antibody is involved in the primary response or immediate response to an antigen?
Anti smooth muscle
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
IgM

45. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

46. What are the autoantibodies for Celiac disease?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
...
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)

47. What are target cells?
Anti IF
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Cells that stil have weird parts of their membrane that macrophages usually bite off
Its main effect is a defect in Ab opsonization for killing

48. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Cross link
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
cannot cross placenta
Daclizumab; prevent ACUTE rejection of renal transplant

49. What does interferon gamma do to be antiviral?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Barrel hoop basement membrane fenestrations
IL 4
Increases expression of MHC I and MHC II and also activates NK cells

50. What is the pathogenesis of acute transplant rejection? When does it occur?
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
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
DM type I
S. aureus - E. Coli - aspergillus