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72 Cards in this Set

  • Front
  • Back
IL-1
made by mac's
cause acute inflam
cause chemokine production to recruit leukocytes
endothelium to express adhesion molecules
endogenous pyrogen
IL-2
Secreted by Th cells
growth of helper and cytotoxic T cells
IL-3
secreted by activated T cells
growth and differentiation of bone marrow stem cells, similar function to GM-CSF
IL-4
Secreted by Th2 cells
Promotes growth of B cells
class switching to IgE and IgG
IL-5
Secreted by Th2 cells
promotes differentiation of B cells
enhances class switching to IgA
production and activiation of eosinophils
IL-6
Secreted by Th cells and mac's
Stimulates production of acute-phase reactants and immunoglobulins
IL-8
secreted by mac's
major chemotactic factor for neutrophils
IL-10
secreted by regulatory T cells
inhibits actions of activated T cells
IL-12
Secreted by B cells and mac's
activated by NK and Th1 cells
IFN-gamma
secreted by Th1
stimulates mac's
TNF
from macrophages. mediates septic shock. causes leukocyte recrutiment, vascular leak.
Helper T cells
Surface proteins
CD4, TCR, CD3, CD28, CD40L
Cytotoxic T cells

Surface proteins
CD8, TCR, CD3
B cells
IgM, B7, CD19, CD20, CD21, CD40, MHC II
Macrophages

Surface proteins
MHC II, B7, CD40, CD14
Receptors for Fc and C3b
NK cells

Surface proteins
Receptors for MHC I, CD16, CD56
All cells except mature red cells
MHC I
Type I Hypersensitivity
Anaphylactic and atopic.

free Ag cross-links IgE on presensitized mast cells and basophils, that release vasoactive amines like histamine.

Rxn develops rapidly after Ag exposure to preformed antibody.
Type II Hypersensitivity
Antibody mediated.

IgM, IgG bind to fixed Ag on enemy cell, leading to lysis, by complement or phagocytosis

Cy-2-toxic - Membrane Attack Complex
Type III Hypersensitivity
Immune Complex - Ag-Ab complexes activate complement, attracting neutrophils that release lysomal enzymes

Serum Sickness - Ab to foreign proteins are produced, and immune complexes form and deposited in tissues.

Arthus rx - local subacute type III rxn. Intradermal injection of Ab induces antibodies which form Ag-Ab complexes in skin. edema, necrosis, complement activation.
Serum Sickness
Type of type III hypersensitivity, where Ag-Ab complexes are deposited into tissues where they fix complement and make damage.

Now mostly caused by drugs.

Fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days after Ag exposure
Type IV Hypersensitivity
Delayed T cell mediated type.

sensitived T cells encounter antigen the release lymphokines, leading to mac activation.

not antibody mediated.
T lymphocytes, Transplant rejection, TB skin test, Touching (contact dermatitis)
Diseases assoc w/ Type I hypersensitivity
anaphylaxis
Allergic rhinitis
Diseases assoc w/ Type II hypersensitivity
Hemolytic anemia
ITP
Erythroblastosis fetalis
Rheumatic fever
Goodpasture's syndrome
Bullous pemphigoid
Graves' disease
Myasthenia gravis
Diseases assoc w/ Type III hypersensitivity
SLE
Rheumatoid arthritis
Polyarteritis nodusm
Poststreptococcal glomerulonephritis
Serum Sickness
Arthrus rxn
Hypersensitivity pneumonitis
Diseases assoc w/ Type IV hypersensitivity
Type 1 diabetes mellitus
Multiple sclerosis
Guillain-Barre's syndrome
Hashimoto thyroiditis
GvHD
PPD
Contact Dermatitis
Bruton's agammaglobulinemia
X-linked recessive defect in tyr kinase gene assoc w/ low levels of all classes of Ig's, decreased B cells.

recurrent Bacterial infxns after age 6 (when maternal IgG decline) in boys
Thymic aplasia
DiGeorge syndrome
Thymus and parathyroids fail to develop from 3rd and 4th pharyngeal pouches.

Present w/ tetany due to T cell deficiency.

Congenital defects of heart and great vessels. 22q11 deletion
SCID
defect in early stem cell differentiation.

recurrent viral, bacterial, fungal and protozoal infexctions.

many causes = failure to make MHCII antigens, defective IL-2, adenosine deaminase deficiency
IL-12 receptor deficiency
Decreased activation of T cells

present w/ disseminated mycobacterial infxns due to decreased Th1 response
hyper-IgM syndrome
Decreased activation of B cells.

defect in CD40L on CD4 T helper cells, leads to inability to class switch. High levels of IgM, very low levels of IgG, IgA and IgE

Presents early in life w/ severe pyogenic infxns
Wiskott-Aldrich syndrome
Decreased activation of B cells

X-linked defect in ability to mount IgM response to capsular polysaccharides of bacteria. Assoc w/ elevated IgA (A for Aldrich), normal IgE, low IgM.

Sx - Triad. recurrent pyogenic infxns, thrombocytopenic purpura, Eczema
Job's Syndrome
Decreased activation of Neutrophils.

Failure of IFNg production by T helper cells. Neutrophils fail to respond to chemotactic stimuli.

Sx - coarse Facies, cold (noninflamed) staphylococcal Abscesses, retained primary Teeth, elevated IgE, Dermatologic problems like Eczema (FATED)
Leukocyte adhesion deficiency syndrome - type 1
defect in LFA-1 integrin proteins on phagocytes. presents early w/ recurrent bacterial infxns, absent pus formation, delayed separation of umbilicus
Chediak-Higashi Disease
Autosomal recessive. Defect in microtubular function and lysosomal emptying of phagocytic cells.

Presents w/ recurrent pyogenic infxns by staph, strep, partial albinism and peripheral neuropathy
Chronic granulomatous disease
defect in phagocytosis of neutrophils b/c lack of NADPH oxidase or similar enzymes.

marked susceptibility to opportunistic infxns w/ bacteria, esp S. aureus, E.coli, and Aspergillus. Confirmed w/ negative nitroblue tetrazolium dye reduction
Chronic mucocutaneous candidiasis
T cell dysfunction specifically against Candida albicans. presents with skin and mucous membrane Candida infxns
Selective immunoglobulin deficiency
Deficiency in specific class of Ig's, maybe b/c defect in isotype switching.

Selective IgA deficiency is most common selective Ig deficiency. present w/ sinus and lung infxns, milk allergies and diarrhea common.
Ataxia-telangiectasia
defect in DNA repair enzymes w/ assoc IgA deficiency. presents w/ cerebelar problems (ataxia) and spider angiomas (telangiectasias)
Common variable immunodeficiency
Normal number of circulating B cells, but decreased plasma cells from a defect in maturation. decreased Ig, cna be acquired in 20s - 30s.
Cyclosporine
binds cyclophilins, complex blocks differentiation and activation of T cells by inhibiting calcineurin, preventing production of IL-2 and its receptor.

used after transplant and w/ selected autoimmune disorders.

Predisposes patients to viral infections and lymphoma; nephrotoxic (need mannitol diuresis)
Tacrolimus FK506
similar to cyclosporine, binds to FK-binding protein, inhibiting secretion of IL-2 and other cytokines.

immunosuppressives used in organ transplants.

Toxicities: nephrotoxicity, peripheral neuropathy, hypertension, pleural effusion, hyperglycemia
Azathioprine
antimetabolite precursor of 6-mercaptopurine that interferes with metabolism and synthesis of nucleic acids. toxic to proliferating lymphocytes.

Kidney transplantation, autoimmune disorders (glomerulonephritis, hemolytic anemia)

Tox - bone marrow suppression, metabolite mercaptopurine is metabolized by xanthine oxidase; toxic effects may be increased by allopurionol
Muromonab - CD3
Monoclonal antibody that binds to CD3 epsilon chain on surface of T cells. Blocks cellular interaction w/ CD3 protein responsible for T cell signal transduction.

immunosuppression after kidney transplant.

cytokine release syndrome, hypersensitivity rxn
Sirolimus (rapamycin)
binds to mTOR. inhibits T cell proliferation in response to IL-2.

immunosuppression after kidney transplant w/ cyclosporine and corticosteroids.

tox - hyperlipidemia, thrombocytopenia, leukopenia
Mycophenolate mofetil
inhibits de novo guanine synthesis and blocks lymphocyte production.
Daclizumab
monoclonal antibody with high affinity for IL-2 receptor on activated T cells
Hyperacute rejection
antibody mediated due to preformed antidonor antibodies in the transplant recipient. occurs within minutes after transplantation
Acute rejection
cell mediated due to cytotoxic T lymphocytes reacting against foreign MHCs. occurs weeks after transplantation. Reversible with immunosuppressants such as cyclosporine and OKT3
Chronic rejection
antibody-mediated vascular damage (fibrinoid necrosis); occurs months to years after transplant. irreversible
Graft versus Host disease
grafted immunocompetent T cells proliferate in the irradiated immunocompromised host and reject cells with foreign proteins, resulting in severe organ dysfunction.

Sx - maculopapular rash, jaundice, hepatosplenomegaly, diarrhea
Anti-nuclear antibodies
SLE
Ant-dsDNA, anti-Smith (snRNP)
Specific for SLE
Antihistone
Drug-induced lupus
Anti-IgG
Rheumatoid Factor!

Rhuematoid arthritis
Anticentromere
Scleroderma CREST
Anti-Scl70
Scleroderma diffuse
Antimitochondrial
Primary biliary cirrhosis
Antigliadin
Celiac disease
Anti-basment membrane
Goodpasture's disease
Anti-epithelial cell
Pemphigus vulgaris
Antimicrosomal
Antithyroglobulin
Hashimoto's thyroiditis
Anti--Jo-1
Polymyositis, dermatomyositis
Anti-SSA (Ro)
Anti-SSB (La)
Sjogren's syndrome
Anti-U1 RNP
(ribonucleoprotein)
Mixed connective tissue
Anti-smooth muscle
Autoimmune hepatitis
Anti-glutamate decarboxylase
Type 1 diabetes mellitus
c-ANCA
Wegener's granulomatosis
p-ANCA
Other vasculitides
HLA- B8

Disease association
Grave's disease
Celiac sprue
HLA-DR2
Multiple sclerosis
Hay fever
SLE
Goodpastures
HLA-DR5 associated w/
Pernicious anemia
Hashimoto's thyroiditis