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81 Cards in this Set

  • Front
  • Back
Origin of the thymus
3rd branchial pouch
CD8 cells bind to MHC class:
I (8 x 1 = 4 x 2)
CD4 cells bind to MHC class:
II (8 x 1 = 4 x 2)
CD4 cells become Th2 cells in the presence of:
CD4 cells become Th1 cells in the presence of:
Th1 cells make the following cytokines:
IL-2 and INF-gamma to activate mphage and CD8 cells
Th2 cells make the following cytokines:
IL-2, IL-4 and IL-5 and help B cells make antibodies
MHC-I and MHC-II molecules are expressed on these cells:

What genes are they encoded on?
MHC - 1 = almost all nucleated cells
MHC - II = APCs only

Encoded on the HLA genes of chromo 6
What is the TCR complex composed of and what cells is it on?
CD-3 --> for cell signaling
delta chain

It is on CD4 and CD8 cells
For CD4 cells, what are the molecules on the APC that bind to what molecules on the T cell?
MHC II on APC - TCR on T cell (signal 1)
B7 - CD 28 (signal 2, costimulation)
CD 40 - CD 40L (which tells APC to make more B7)
For CD8 cells, what are the 2 signals needed for activation?
signal 1: MHC-I bound to TCR
signal 2: IL-2 from the CD4 cells
What are the characteristics of the Fab fragment of an antibody?
amino terminal

contains the hypervariable regions on the light and heavy chains

responsible for antigen recognition
What are the characteristics of the Fc fragment of an antibody?
Constant (no variability, all heavy chains)

Carboxy terminal

Complement binding (to IgM and IgG)

Has carbohydrate side chains
The mature B lymphocytes first express these types of Ig's (before isotype switching)
IgM and IgD
secondary response.
Most abundant
Fixes complement
the only one that crosses the placenta
opsonizes bacteria, toxins, viruses
Prevents attachment to mucous membranes
Does not fix complement
Monomer or dimer
Picks up secretory component from endothelial cells
Primary antigen response
Fixes complement
Monomer or pentamer
unknown fxn
Mediates type I hypersensitivity reaction
--> release of mediators from mast cells and basophils
Mediates immunity to worms
Lowest concentration in serum
Made by: mphages
Stimulates: T cells, B cells, mphage, epithelial cells
Causes: fever
Made by: Th1 and Th2 cells
Stimulates: CD4 and CD8 cells
Causes: growth
Made by: activated T cells
Stimulates: Bone marrow stem cells
Causes: growth and differentiation (like GM-CSF)
Made by: Th2 cells
Stimulates: B cells, T cells
Causes: Growth, enchances class switching to IgE. Increases differentiation to Th2 cells
Made by: Th2 cells
Stimulates: B cells, eosinophils
Causes: class switching to IgA. Increase in eosinophils
Made by: Th1 and Th2 cells and mphages
Causes: production of acute phase reactants and Ig
Causes: neutrophil chemotaxis
Made by: Th2 cells
Stimulates: Th2 and Th1 cells
Causes: stimulates Th2 cells, inhibits Th1 cells
Made by: B cells, mphages
Stimulates: NK and Th1
Causes: activation, increase in Th1 differentiation
Made by: Th1 cells
Stimulates: Macrophages
Causes: increase in MHC I and II expression and antigen presentation
Made by: mphages
Stimulates: Th1 and Th2 and B cells, neutrophils
Causes: Increase in IL-2 production, increase in B cell proliferation, neutrophil activation, dendritic cell migration to lymph nodes
Made by: CD4 and others
Causes: inhibition of T cell activation
Complement defends against this type of bacteria:
gram negative
The classic pathway is activated by:
IgG or IgM
The lectin and alternative pathways are activated by:
microbial surface proteins
The classic and alternative pathways converge at this complement component:
C3 in each --> C5 --> C5b, 6, 7 --> membrane attack complex (C5b, 6, 7, 8, 9) --> lysis
Interferons work by:
inducing the cellular production of proteins that inhibit viral protein synthesis by degrading viral mRNA
Deficiency in C1 esterase inhibitor causes:
hereditary angioedema from overactive complement (classic pathway)
Deficiency of C3 causes:
severe recurrent pyogenic sinus and respiratory infections
Deficiency of C6-C8 causes:
Neisseria bacteremia
Deficiency of decay-accelerating factor (DAF) causes:
paroxysmal nocturnal hemoglobinuria (PNH)
Type I hypersensitivity
IgE on presensitized mast cells and basophils --> vasoactive amine release
Due to preformed antibody
mediators: Th2, mast, IgE, eosinophils

examples: Allergic rhinitis, bronchil asthma, anaphylaxis
Type II hypersensitivity
Antibody mediated - IgM and IgG attacks cell --> complement lysis or phagocytosis.

Examples: Graves, Hashimotos, Pernicious anemia, pemphigus, transfusion rxns, rheumatic fever, farmers lung
Type III hypersensitivity
Immune complex mediated - IgG and IgM
Complement is activated (classic), neutrophils are activated.
Complexes deposited in skin, kidney, joints
Causes local vasculitis

Examples: serum sickness, rheumatoid arthritis, glomerulonephritis, sxs of malaria and SLE
Type IV hypersensitivity
Delayed, T cell mediated
Takes 2-3 days to occur
Lymphocytes activate mphage --> giant cells

Examples: Contact dermatitis (poison ivy), temporal arteritis, transplant rejection, celiac disease, sxs of leprosy and TB (PPD)
Type V hypersensitivity
Like type II but in Britain where the Abs bind to specific cell receptors

Ex/ Myasthenia gravis and graves disease
Name that hypersensitivity reaction:
1. Guillain-barre
2. ITP
3. Bullous pemphigoid
4. Lupus
5. Post-strep glomerulonephritis
6. Arthus reaction
7. Hypersensitivity pneumonitis
1. Type IV
2. Type II
3. Type II
4. Type III
5. Type III
6. Type III
7. Type III
Bruton's agammaglobulinemia
X linked recessive
defect in tyrosine kinase gene
Pre-B cells can't mature
Low levels of all immunoglobulins

Sxs: bacterial infections after 6 mo

Path: no tonsils, apparently nl thymus
DiGeorge syndrome
22q11 deletion
Thymic aplasia due to failed development of the 3rd and 4th branchial pouches

Sxs: hypocalcemia, tetany, T cell absence, recurrent viral and fungal infections

Path: heart defects, great vessel defects
Caused by: mutant IL-2 receptor, adenosine deaminase deficiency, failure to synthesize MHC-II proteins.

Sxs: failure to thrive, opportunistic infections
IL-12 receptor deficiency
Presents with disseminated mycobacterial infections

(it is supposed to stimulate Th1 differentiation and NK cells)
hyper-IgM syndrome
Defect in CD40 ligand on CD4 cells
Inability to class switch

Sxs: elevated IgM, very low everything else, severe pyogenic infections
Wiskott-Aldrich syndrome
X linked
No IgM response to bacterial capsules
Primary defect unknown

Sxs: elevated IgA, low IgM, nl IgE. Recurrent pyogenic infections, thrombocytopenic purpura, eczema, increase in malignancy and lymphoma
Job's syndrome
Failure of gamma-interferon production by helper T cells
No neutrophil chemotaxis

Sxs: noninflamed staphylococcal abscesses, eczema, coarse facies, retained primary teeth, high levels of IgE
Leukocyte adhesion deficiency syndrome
Defect in LFA-1 adhesion proteins on phagocytes

Sxs: severe pyogenic and fungal infections, delayed umbilical separation
Chediak-Higashi disease
Autosomal recessive
Defect in MT fxn and lysosomal emptying of phagocytic cells (lysosomes and phagosomes can't fuse)

Sxs: recurrent staph and strep infections, partial albinism, peripheral neuropathy
Chronic granulomatous disease
Lack of NADPH oxidase activity
Decrease in neutrophil fxn

Sxs: opporutinistic infections (S. aureus, E. coli, Apergillus)

Dx: negative nitroblue tetrazolium dye reduction test
Chronic mucocutaneous candidiasis
T cell dysfxn against Candida
Selective immunoglobulin deficiency
Most commonly an IgA deficiency

Sxs: chronic sinus and lung infections, milk allergies, diarrhea
Defect in DNA repair enzymes
IgA deficiency

Sxs: cerebellar problems, spider angiomas
Common variable immunodeficiency
Normal levels of B cells but decrease in plasma cells and Ig

Can be acquired in 20-30s
Antinuclear antibodies
SLE, nonspecific
SLE, specific
SLE, specific
Drug-induced lupus
= rheumatoid factor
= p-ANCA, c-ANCA
scleroderma (CREST)
anti-Scl 70
scleroderma (diffuse)
primary biliary cirrhosis
celiac disease
anti-basement membrade
anti-epithelial cell
pemphigus vulgaris
hashimoto's thyroiditis
polymyositis, dermatomyositis
ankylosing spondylitis
inflammatory bowel disease
reiter's syndrome
celiac sprue
hay fever
DM type I
DM type I
pernicious anemia
steroid-responsive nephrotic syndrome