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140 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Paracortex
|
hosues T cells, contains high endothelial venule, through which T and B cells enter from blood
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Lymph drainage of anal canal above pectinate line
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Internal iliac
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Lymph drainage of bladder
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external iliac (for superior portion), and internal iliac (for posterior portion)
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Lymph drainage of prostate
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internal iliac
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Red pulp of spleen
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contains splenic sinusoids and cords of billroth. The cords consist of reticular cells, RBCs, and macrophages that extend their processes through the discontinuous sinusoids to sample blood
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Splenic dysfunction
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decreased IgM leads to decreased complement activation, which leads to decreased C3b opsonization and susceptibility to encapsulated organisms
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Differentiation of Th2 cells
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constitutive IL-4 secretion
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Differentiation of Th1 cells
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IL-12 by macrophages and IFN-gamma by NK cells
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B2-microglobulin
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pairs w/ alpha chain of MHC I and aids in transport to the cell surface
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not expressed on RBCs
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MHC III
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encodes for complement, TNF
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HLA B8
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Graves' disease
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HLA DR2
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MS, hay fever, SLE, Goodpasture's
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HLA DR5
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Hashimoto's thyroiditis, Pernicious anemia
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HLA DR7
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steroid-responsive nephrotic syndrome
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T-cells kill...
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tumor cells, virus-infected cells, donor graft cells
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Natural killer cell enzymes
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perforin and granzymes. induce apoptosis of virally infected cells or tumor cells
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Cytokines that enhance NK cells
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IL-12, IFN-beta, IFN-alpha
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SUperantigens
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cross-link beta-region of TCR to MHC class II, resulting in uncoordinated release of IFN-gamma from Th1 cells and IL-1, IL-6, and TNF-alpha from macrophages
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Endotoxins/LPS
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directly stimulate macrophages by binding to endotoxin receptor CD14
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2 step activation of Th cells by APC
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Signal 1: MHC II and TCR interaction
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Signal 2: B7 on APC and CD28 on T-cell
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2 step activation of Tc cell by virus infected cell
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Signal 1: MHC I and TCR interaction
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Signal 2: IL-2 release from a Th cells activates Tc cell to kill virus-infected cell
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B and T cell coactivation
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CD28 on T-cell binds B7 on B-cell, leading to activation of T-helper cell
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CD40 on B-cell binds CD40L on T-cell, leading to activation of B-cell
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T-cell independent activation of B-cells
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Non-protein antigens and Mitogens
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Papain
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proteolytic enzyme used in experiments that cleaves antibodies at the hinge region, resulting in 2 identical Fab fragments and 1 Fc fragment
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Where are carbohydrate side chains located on an antibody
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On the Fc region
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Terminal deoxynucleotidyl transferase
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addition of nucleotides to DNA during recombination. Active only during B-cell heavy chain recombination and all of T-cell rearrangement
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IL-1
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secreted by macrophages. Causes acute inflammation, chemokine production, recruitment of leukocytes, expression of adhesion molecules, fever
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IL-2
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secreted by Th1 cells. Stimulates growth of helper and cytotoxic T-cells
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IL-3
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Secreted by activated T cells. Supports growth and differentiation of bone marrow cells (similar to GM-CSF)
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IL-4
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Secreted by Th2 cells. Promotes growth of B cells and enhances class switching to IgE and IgG
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IL-5
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Secreted by Th2 cells. Promotes differentiation of B-cells, enhances class switch to IgA, stimulates eosinophils
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IL-6
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Secreted by Th cells and macrophages. Stimulates production of acute-phase reactants from the liver and immunoglobulins from plasma cells
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IL-8
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Secreted by macrophages. Chemotactic factor for neutrophils
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IL-10
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secreted by Th2 cells. Activates Th2, inhibits Th1, inhibits IFN-gamma
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IL-12
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Secreted by B-cells and macrophages. Activates NK and Th1 cells
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IFN-gamma
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secreted by Th1 cells. Stimulates macrophages. Activates Th1, inhibits Th2
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TNF
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Secreted by macrophages. Mediates septic shock, causes leukocyte recruitment, vascular leak, cachexia
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IL-12 deficiency
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means that Th1 cells can't be made, which means that there will be an IFN-gamma deficiency
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Helper T-cell markers
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CD4, TCR, CD3, CD28, CD40L
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Cytotoxic T-cell markers
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CD8, TCR, CD3
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NK cell markers
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receptors for MHC 1, CD16, CD56
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Alternate pathway
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activated by microbial surfaces and cell surface components such as LPS or teichoic acid
|
initiates early, innate response that doesn't require antibody for activation
|
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Lectin pathway
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interacts w/ mannose on bacterial, viral, and fungal surfaces
|
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Classical pathway
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activated by antigen-antibody complexes (IgG, IgM)
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Major effector mechanism of humoral immunity
|
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Passive immunity given after infection with...
|
tetanus, botulinum, rabies, HBV
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Organisms w/ antigen variation
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salmonella (2 flagellar variants), Borrelia, Neisseria, Influenza, trypanosomes
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Mark of B-cell anergy
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decreased surface IgM
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Serum sickness
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caused by drugs, fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days after antigen exposure
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Scleroderma (diffuse) autoantibodies
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Anti-RNA polymerase III, anti-SCL-70 (topoisomerase I)
|
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CVID defect
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B-cell maturation, many causes
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CVID clinical and labs
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Clinical: usually seen in 20s and 30s, increased risk of autoimmune disease, lymphoma, sinopulmonary infections
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Labs: normal number of B-cells, decreased plasma cells, decreased immunoglobulins
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|
|
Hyper-IgE syndrome (Job's)
|
cells can't produce IFN-gamma
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FATED: course Facies, cold (noninflamed) staph Abscesses, retained primary Teeth, increased IgE, Dermatologic problems (eczema)
|
|
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IL-12 receptor deficiency
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decreased Th1 response. IFN-gamma isn't secreted by Th1 and NK cells. However, if it still secreted and granulomas can still form
|
leads to disseminated mycobacterial infections, as well as salmonella infections
|
|
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SCID etiologies and labs
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Etiologies: defective IL-2 receptor (x-linked, MC), adenosine deaminase deficiency, failure to synthesize MHC II antigens
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Labs: decreased IL-2R, increased adenine (toxic to B and T cells), absent thymic shadow
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SCID has increased incidence of...
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malignant lymphoma
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Ataxia telangiectasia etiology and Triad
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Etiology: defective DNA repair enzymes
|
Triad: cerebellar defects (ataxia) spider angiomas, IgA deficiency
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|
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Wiskott-Aldrich etiology and Triad
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Etiology: X-linked recessive deletion of WASP gene (normally actin polyerizes and anchors membrane bound receptors to actin cytoskeleton). Leads to progressive deletion of B and T cells
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Triad: Thrombocytopenic purpura, Infections, Eczema
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Wiskott-Aldrich labs
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increased IgE, IgA; decreased IgM
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Leukocyte adhesion deficiency
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Defect in LFA-1 integrin (CD18) so phagocytes can't migrate out of bloodstream, leads to neutrophilia
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Recurrent bacterial infections, absent pus formation, delayed separation of umbilicus
|
|
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Chediak-Higashi
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autosomal recessive defect in mcrotubular function w/ inability to fuse phagosome and lysosome
|
|
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Chediak-Higashi clinical and labs
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BALIN: bleeding/bruising, partial albinism, leukopenia, recurrent staph/strep infections, peripheral neuropathy
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Labs: platelets and neutrophils w/ giant granules
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Acute vs. chronic rejection
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Acute: cell mediated, weeks, reversible
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Chronic: T-cell and antibody mediated, vascular damage, months to years, irreversible
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Classic example of Graft-v-host disease
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Child recipient, parent donor: parent cells recognize the child's "other-half" and attack it. The child, however, can't recognize the parents cells and can't mount and immune response to it
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Cyclosporine MOA
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binds cyclophilins, inhibits calcineurin. Prevents production of IL-2 and its receptor, blocking T-cells
|
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Cyclosporine S/E
|
nephrotoxicity (prevented w/ mannitol diuresis), gingival hyperplasia, excreted via biliary system
|
|
|
|
Tacrolimus S/E
|
nephrotoxicity, peripheral neuropathy, hypertension, pleural effusion, hyperglycemia, excreted via feces
|
|
|
|
Azathioprine MOA and S/E
|
MOA:precursor of 6-mercaptopurine that interferes w/ DNA synthesis
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S/E: bone marrow suppression, increased w/ allopurinol
|
|
|
Muromonab MOA and S/E
|
MOA: binds CD3, blocks signal transduction of T cells
|
S/E: cytokine release syndrome (anywhere from flu to shock), hypersensitivity, contraindicated in seizures, HF, prego
|
|
|
Sirolimus MOA and S/E
|
MOA: binds mTOR (which complexes w/ FK-binding protein) and inhibits response to IL-2
|
S/E: hyperlipidemia, thrombocytopenia, NO nephrotoxicity
|
|
|
Daclizumab
|
antibody w/ high affinity for IL-2 receptor, great for kidney transplant
|
|
|
|
Paracortex
|
hosues T cells, contains high endothelial venule, through which T and B cells enter from blood
|
|
|
|
Lymph drainage of anal canal above pectinate line
|
Internal iliac
|
|
|
|
Lymph drainage of bladder
|
external iliac (for superior portion), and internal iliac (for posterior portion)
|
|
|
|
Lymph drainage of prostate
|
internal iliac
|
|
|
|
Red pulp of spleen
|
contains splenic sinusoids and cords of billroth. The cords consist of reticular cells, RBCs, and macrophages that extend their processes through the discontinuous sinusoids to sample blood
|
|
|
|
Splenic dysfunction
|
decreased IgM leads to decreased complement activation, which leads to decreased C3b opsonization and susceptibility to encapsulated organisms
|
|
|
|
Differentiation of Th2 cells
|
constitutive IL-4 secretion
|
|
|
|
Differentiation of Th1 cells
|
IL-12 by macrophages and IFN-gamma by NK cells
|
|
|
|
B2-microglobulin
|
pairs w/ alpha chain of MHC I and aids in transport to the cell surface
|
not expressed on RBCs
|
|
|
MHC III
|
encodes for complement, TNF
|
|
|
|
HLA B8
|
Graves' disease
|
|
|
|
HLA DR2
|
MS, hay fever, SLE, Goodpasture's
|
|
|
|
HLA DR5
|
Hashimoto's thyroiditis, Pernicious anemia
|
|
|
|
HLA DR7
|
steroid-responsive nephrotic syndrome
|
|
|
|
T-cells kill...
|
tumor cells, virus-infected cells, donor graft cells
|
|
|
|
Natural killer cell enzymes
|
perforin and granzymes. induce apoptosis of virally infected cells or tumor cells
|
|
|
|
Cytokines that enhance NK cells
|
IL-12, IFN-beta, IFN-alpha
|
|
|
|
SUperantigens
|
cross-link beta-region of TCR to MHC class II, resulting in uncoordinated release of IFN-gamma from Th1 cells and IL-1, IL-6, and TNF-alpha from macrophages
|
|
|
|
Endotoxins/LPS
|
directly stimulate macrophages by binding to endotoxin receptor CD14
|
|
|
|
2 step activation of Th cells by APC
|
Signal 1: MHC II and TCR interaction
|
Signal 2: B7 on APC and CD28 on T-cell
|
|
|
2 step activation of Tc cell by virus infected cell
|
Signal 1: MHC I and TCR interaction
|
Signal 2: IL-2 release from a Th cells activates Tc cell to kill virus-infected cell
|
|
|
B and T cell coactivation
|
CD28 on T-cell binds B7 on B-cell, leading to activation of T-helper cell
|
CD40 on B-cell binds CD40L on T-cell, leading to activation of B-cell
|
|
|
T-cell independent activation of B-cells
|
Non-protein antigens and Mitogens
|
|
|
|
Papain
|
proteolytic enzyme used in experiments that cleaves antibodies at the hinge region, resulting in 2 identical Fab fragments and 1 Fc fragment
|
|
|
|
Where are carbohydrate side chains located on an antibody
|
On the Fc region
|
|
|
|
Terminal deoxynucleotidyl transferase
|
addition of nucleotides to DNA during recombination. Active only during B-cell heavy chain recombination and all of T-cell rearrangement
|
|
|
|
IL-1
|
secreted by macrophages. Causes acute inflammation, chemokine production, recruitment of leukocytes, expression of adhesion molecules, fever
|
|
|
|
IL-2
|
secreted by Th1 cells. Stimulates growth of helper and cytotoxic T-cells
|
|
|
|
IL-3
|
Secreted by activated T cells. Supports growth and differentiation of bone marrow cells (similar to GM-CSF)
|
|
|
|
IL-4
|
Secreted by Th2 cells. Promotes growth of B cells and enhances class switching to IgE and IgG
|
|
|
|
IL-5
|
Secreted by Th2 cells. Promotes differentiation of B-cells, enhances class switch to IgA, stimulates eosinophils
|
|
|
|
IL-6
|
Secreted by Th cells and macrophages. Stimulates production of acute-phase reactants from the liver and immunoglobulins from plasma cells
|
|
|
|
IL-8
|
Secreted by macrophages. Chemotactic factor for neutrophils
|
|
|
|
IL-10
|
secreted by Th2 cells. Activates Th2, inhibits Th1, inhibits IFN-gamma
|
|
|
|
IL-12
|
Secreted by B-cells and macrophages. Activates NK and Th1 cells
|
|
|
|
IFN-gamma
|
secreted by Th1 cells. Stimulates macrophages. Activates Th1, inhibits Th2
|
|
|
|
TNF
|
Secreted by macrophages. Mediates septic shock, causes leukocyte recruitment, vascular leak, cachexia
|
|
|
|
IL-12 deficiency
|
means that Th1 cells can't be made, which means that there will be an IFN-gamma deficiency
|
|
|
|
Helper T-cell markers
|
CD4, TCR, CD3, CD28, CD40L
|
|
|
|
Cytotoxic T-cell markers
|
CD8, TCR, CD3
|
|
|
|
NK cell markers
|
receptors for MHC 1, CD16, CD56
|
|
|
|
Alternate pathway
|
activated by microbial surfaces and cell surface components such as LPS or teichoic acid
|
initiates early, innate response that doesn't require antibody for activation
|
|
|
Lectin pathway
|
interacts w/ mannose on bacterial, viral, and fungal surfaces
|
|
|
|
Classical pathway
|
activated by antigen-antibody complexes (IgG, IgM)
|
Major effector mechanism of humoral immunity
|
|
|
Passive immunity given after infection with...
|
tetanus, botulinum, rabies, HBV
|
|
|
|
Organisms w/ antigen variation
|
salmonella (2 flagellar variants), Borrelia, Neisseria, Influenza, trypanosomes
|
|
|
|
Mark of B-cell anergy
|
decreased surface IgM
|
|
|
|
Serum sickness
|
caused by drugs, fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days after antigen exposure
|
|
|
|
Scleroderma (diffuse) autoantibodies
|
Anti-RNA polymerase III, anti-SCL-70 (topoisomerase I)
|
|
|
|
CVID defect
|
B-cell maturation, many causes
|
|
|
|
CVID clinical and labs
|
Clinical: usually seen in 20s and 30s, increased risk of autoimmune disease, lymphoma, sinopulmonary infections
|
Labs: normal number of B-cells, decreased plasma cells, decreased immunoglobulins
|
|
|
Hyper-IgE syndrome (Job's)
|
cells can't produce IFN-gamma
|
FATED: course Facies, cold (noninflamed) staph Abscesses, retained primary Teeth, increased IgE, Dermatologic problems (eczema)
|
|
|
IL-12 receptor deficiency
|
decreased Th1 response. IFN-gamma isn't secreted by Th1 and NK cells. However, if it still secreted and granulomas can still form
|
leads to disseminated mycobacterial infections, as well as salmonella infections
|
|
|
SCID etiologies and labs
|
Etiologies: defective IL-2 receptor (x-linked, MC), adenosine deaminase deficiency, failure to synthesize MHC II antigens
|
Labs: decreased IL-2R, increased adenine (toxic to B and T cells), absent thymic shadow
|
|
|
SCID has increased incidence of...
|
malignant lymphoma
|
|
|
|
Ataxia telangiectasia etiology and Triad
|
Etiology: defective DNA repair enzymes
|
Triad: cerebellar defects (ataxia) spider angiomas, IgA deficiency
|
|
|
Wiskott-Aldrich etiology and Triad
|
Etiology: X-linked recessive deletion of WASP gene (normally actin polyerizes and anchors membrane bound receptors to actin cytoskeleton). Leads to progressive deletion of B and T cells
|
Triad: Thrombocytopenic purpura, Infections, Eczema
|
|
|
Wiskott-Aldrich labs
|
increased IgE, IgA; decreased IgM
|
|
|
|
Leukocyte adhesion deficiency
|
Defect in LFA-1 integrin (CD18) so phagocytes can't migrate out of bloodstream, leads to neutrophilia
|
Recurrent bacterial infections, absent pus formation, delayed separation of umbilicus
|
|
|
Chediak-Higashi
|
autosomal recessive defect in mcrotubular function w/ inability to fuse phagosome and lysosome
|
|
|
|
Chediak-Higashi clinical and labs
|
BALIN: bleeding/bruising, partial albinism, leukopenia, recurrent staph/strep infections, peripheral neuropathy
|
Labs: platelets and neutrophils w/ giant granules
|
|
|
Acute vs. chronic rejection
|
Acute: cell mediated, weeks, reversible
|
Chronic: T-cell and antibody mediated, vascular damage, months to years, irreversible
|
|
|
Classic example of Graft-v-host disease
|
Child recipient, parent donor: parent cells recognize the child's "other-half" and attack it. The child, however, can't recognize the parents cells and can't mount and immune response to it
|
|
|
|
Cyclosporine MOA
|
binds cyclophilins, inhibits calcineurin. Prevents production of IL-2 and its receptor, blocking T-cells
|
|
|
|
Cyclosporine S/E
|
nephrotoxicity (prevented w/ mannitol diuresis), gingival hyperplasia, excreted via biliary system
|
|
|
|
Tacrolimus S/E
|
nephrotoxicity, peripheral neuropathy, hypertension, pleural effusion, hyperglycemia, excreted via feces
|
|
|
|
Azathioprine MOA and S/E
|
MOA:precursor of 6-mercaptopurine that interferes w/ DNA synthesis
|
S/E: bone marrow suppression, increased w/ allopurinol
|
|
|
Muromonab MOA and S/E
|
MOA: binds CD3, blocks signal transduction of T cells
|
S/E: cytokine release syndrome (anywhere from flu to shock), hypersensitivity, contraindicated in seizures, HF, prego
|
|
|
Sirolimus MOA and S/E
|
MOA: binds mTOR (which complexes w/ FK-binding protein) and inhibits response to IL-2
|
S/E: hyperlipidemia, thrombocytopenia, NO nephrotoxicity
|
|
|
Daclizumab
|
antibody w/ high affinity for IL-2 receptor, great for kidney transplant
|
|
