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193 Cards in this Set
- Front
- Back
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Lymph node - functions
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Non-specific filtration by Macs
Storage and activation B/T cells Antibody production |
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Lymph node follicle
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Site of B-cell localization and proliferation
Located in outer cortex Primary follicle: Dense and dormant Secondary follicle: pale central germinal centers and are active |
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Lymph node medulla
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Medullary cords: Plasma cells
Medullary sinuses: Macs and reticular cells |
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Lymph node paracortex
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Houses T-cells
Region of cortex between follicles and medulla Paracortical hyperplasia in extreme cellular immune response (i.e. viral--EBV) Not well developed in DiGeorge's syndrome |
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Lymph node drainage
Upper limb, lateral breast |
Axillary
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Lymph node drainage
Stomach |
Celiac
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Lymph node drainage
duodenum, jejunum |
Superior mesenteric
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Lymph node drainage
Sigmoid colon |
Colic --> Inferior Mesenteric
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Lymph node drainage
Rectum (lower part) Anal canal (above pectinate line) |
Internal Iliac
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Lymph node drainage
Anal canal below pectinate line |
Superficial inguinal
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Lymph node drainage
Testes |
Superficial and deep plexus --> para-aortic
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Lymph node drainage
Scrotum |
Superficial inguinal
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Lymph node drainage
Superficial Thigh |
Superficial inguinal
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Lymph node drainage
Lateral side of dorsum of foot |
Popliteal
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Lymph node drainage
Right arm and right half of head |
Right lymphatic duct
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Thoracic duct drainage
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collects most of the lymph in the body
drains into the systemic (blood) circulation at the left brachiocephalic vein, between where the left subclavian vein and left internal jugular connect |
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Sinusoids of the spleen
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Long, vascular channels in red pulp with fenestrated "barrel hoop" BM.
Macs found nearby. |
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T-cells in the spleen
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Found in the PALS (periarterial lymphatic sheath) and red pulp
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B-cells in the spleen - location
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Follicles within the white pulp
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Red pulp of the spleen - function
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Mechanical filtration of RBCs
Reserve of monocytes |
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White pulp of the spleen - function
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Active immune response through humoral and cellular pathways
Antibody production |
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What removes encapsulated bacteria in the spleen?
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Macrophages
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Mechanism of infxn susceptibility in splenic dysfunction/asplenia
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Decreased IgM --> decreased C3b opsonization --> increased susceptibility to encapsulated organisms
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Organisms of concern in splenectomized patients
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S. pneumoniae
H. influenzae Salmonella N. Meningitidis |
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Blood smear results post-splenectomy
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Howell-Jolly bodies
Target cells Thrombocytosis |
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Sites of T and B-cell maturation
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T: thymus
B: bone marrow |
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Thymus: Structural Organization and Function
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Encapsulated. Cortex and medulla.
Site of T-cell differentiation and maturation. |
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Where is the thymus embryologically derived from?
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3rd branchial pouch.
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Thymus: cortex and medulla
Cellular histology |
Cortex: dense with immature T-cells
Medulla: pale with mature T-cells and epithelial reticular cells, contains Hassall's corpuscles Corticomedullary junction: where + and - selection occur |
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Thymocyte maturation process:
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Occurs at corticomedullary junction
1. Immature thymocytes from BM make T-cell receptors by gene rearrangement 2. + selection (MHC restriction) for functional T-cells occurs in the cortex 3. - selection for autoreactive T-cells occurs in the medulla |
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Innate Immunity
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Receptors that recognize pathogens are germline encoded.
Response to pathogens is fast and non-specific. PMNs, Macs, Dendritic cells, NK cells and complement |
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Adaptive Immunity
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Receptors that recognize pathogens undergo VDJ recombination during development.
Response is slow on 1st exposure, but memory response is faster and more robust. T-cells, B-cells, and circulating Ab |
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Cytotoxic T-cell: function
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CD8+
kills virus infected, neoplastic and donor graft cells |
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Helper T-cell:
Types and functions |
CD4+
IL-12 --> Th1 Cell (cell-mediated response) IL-4 --> Th2 Cell (humoral response) |
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Th1 cell function
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CD4+ --> Cell mediated response
Make IL-2, IFN-g Activate Macs and CD8+ cells Inhibited by IL-10 |
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Th2 Cell function
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CD4+ --> Humoral response
Make IL-4, IL-5, IL-10 Helps B-cells make Abs Inhibited by IFN-g |
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MHC
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Encoded by HLA genes
Present Ag fragments to T-cells and binds TCR |
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MHC I
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HLA-A, HLA-B, HLA-C
Expressed on almost all nucleated cells. Ag is loaded on RER of most intracellular peptides. Mediates viral immunity. Pairs with B2-microglobulin (aids in transport to cell surface) |
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MHC II
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HLA-DR, HLA-DP, HLA-DQ
Expressed only on APCs. Ag is loaded following release of invariant chain in an acidified endosome. |
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HLA-A3
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Hemochromatosis
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HLA-B27
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PAIR
Psoriatic arthritis Ankylosing spondylitis IBD Reiter syndrome |
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HLA-B8
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Grave's Disease
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HLA-DR2
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MS
Hay fever SLE Goodpasture's |
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HLA-DR3
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DM Type 1
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HLA-DR4
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RA
DM Type 1 |
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HLA-DR5
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Pernicious anemia (B12 deficiency)
Hashimoto's thyroiditis |
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HLA-DR7
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Steroid-responsive nephrotic syndrome
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B-cell functions
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Make Ab
IgG: opsonize bacteria, neutralize viruses Hypersensitivity rxns: Type I: IgE, allergy Type II: IgG/IgM, cytotoxic and Ab dependant Type III: IgG, immune complex deposition Preformed Abs can cause hyperacute organ rejection |
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T-cell functions
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CD4+: T-cells help B-cells make Ab and produce gamma interferon (activates Macs)
CD8+: Directly kills virus infected cells Type 4 Hypersensitivity: delayed cell-mediated Acute and chronic organ (allograft) rejection |
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NK Cells
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Only lymphocyte member of innate immunity
Uses perforin and granzymes to induce apoptosis of virally infected cells and tumor cells Activity is enhanced by IL-12, IFN-B, IFN-a |
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What induces NK cells to kill?
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When exposed to:
1) Non-specific activation signal on target cell 2) absence of MHC I on target cell surface |
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T-cell glycoproteins
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CD4: binds MHC II
CD8: binds MHC I CD3 complex: cluster associated with T-cell receptor Important in signal transduction |
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3 Antigen Presenting Cells
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Macs
B-cells Dendritic cells |
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Macrophage-lymphocyte interactions
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Activated lymphocytes and macrophages stimulate one another
Lymphocytes secrete IFN-g --> Macs Macs secrete IL-1, TNFa --> lymphocytes |
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Effect of superantigens (S.pyogenes and S.aureus)
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cross-link B-region of TCR to MHC II on APCs
results in uncoordinated release of IFN-g from Th1 cells and subsequent release of IL-1, IL-6 and TNF-a from Macs |
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Effects of endotoxin/LPS from gram(-) bacteria
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directly stimulate Macs by binding to endotoxin receptor CD14
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Th cell activation
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Signal 1: foreign antigen (phagocytosed by APC) is presented on MHC II and recognized by TCR on Th cell
Signal 2: "Costimulatory signal" is given by interaction of B27 (APC) and CD28 (Th) Th cell is now activated to produce cytokines |
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Tc cell activation
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Signal 1: Endogenously synthesized (viral or self) proteins presented on MHC I and recognized by TCR on Tc cell
Signal 2: IL-2 from Th cell activates Tc cell to kill virus infected cell |
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B-cell class switching
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Signal 1: IL-4, IL-5, IL-6 from Th2 cell
Signal 2: CD40 receptor activation by binding CD40L on Th cell |
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Antibody structure
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Variable part of L and H chains recognize Ag
Fc portion of IgM and IgG fixes complement Heavy chain: Contributes to Fc and Fab fractions Light chain: Contributes only to Fab fraction Chains held together by disulfide bonds |
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Fab
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Ag binding fragment
Determines idiotype: only 1 antigenic specificity expressed per B-cell type |
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Fc
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Constant
Carboxy terminal Complement binding (IgG and IgM) Carbohydrate side chains Determines Isotype (IgM, IgD, etc) |
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Functions of Abs
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Opsonization: promotes phagocytosis
Neutralization: prevents bacterial adherence Complement activation: activates complement, enhancing opsonization and lysis |
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Ab diversity is generated by:
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1. random recombination of VJ (light-chain) or V(D)J (heavy) chain genes
2. Random combination of heavy chains with light chains 3. Somatic hypermutation (following stimulation) 4. Addition of nucleotides to DNA during recombination by terminal deoxynucleotide transferase |
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B-cell isotype switching
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Alternative splicing of mRNA, mediated by cytokines and CD40L
Mature B-cells express IgM and IgD on surfaces Can differentiate by isotype switching into plasma cells that secrete IgA, IgE or IgG |
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IgG
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Main Ab in secondary (delayed) response to Ag.
Most abundant. Fixes complement Crosses placenta (provides passive immunity in infants) Opsonizes bacteria Neutralizes bacterial toxins and viruses |
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IgA
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Prevents attachment of bacteria and viruses to mucous membranes.
Does not fix complement. Found in secretions (saliva, tears, mucus) and breast milk (colostrum) |
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IgM
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Produced in the primary (immediate) response to an antigen.
Fixes complement Does not cross the placenta |
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Antigen receptors on the surface of B-cells
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IgM and IgG
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IgD
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Unclear function.
Found on surface on many B cells and in serum. |
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IgE
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Binds mast cells and basophils.
Cross links when exposed to allergen, mediating Type I (immediate) hypersensitivity through release of histamine. Mediates immunity to worms by activating eosinophils. Lowest concentration in serum. |
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Ig Allotype
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Polymorphism - Ig epitope that differers among members of the same species.
Can be on light or heavy chain. ALLotypes represent different ALLeles. |
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Ig Isotype
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Ig epitope common to a single Ig class.
Ig MADGE |
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Ig Idiotype
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Specific for a given antigen. Ig epitope determined by Ag-binding sites.
Hypervariable region is unique. |
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Thymus-independent Ag
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Antigens lacking a peptide component.
Cannot be presented by MHC to T-cells. Stimulate release of IgM Abs only and do not result in immunologic memory. Ex: LPS from cell envelope of gram (-) bacteria and polysaccharide |
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Thymus-dependent Ag
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Ag containing a peptide component.
Class switching and immunologic memory occur as a result of direct contact with Th cells (CD40-CD40L interaction). Release of IL-4, IL-5, IL-6. Ex: H.influenzae vaccine |
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IL-1
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Secreted by Macs --> acute inflammation.
Recruit leukocytes Activates endothelium to express adhesion molecules Endogenous pyrogen |
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IL-2
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Secreted by Th cells.
Stimulates growth of helper and cytotoxic T-cells. |
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IL-3
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Secreted by activated T-cells.
Growth and differentiation of bone marrow stem cells. (Similar to GM-CSF) |
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IL-4
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Secreted by Th2 cells.
Growth of B-cells. Enhances class switching to IgE and IgG. |
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IL-5
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Secreted by Th2 cells.
Differentiation of B-cells. Class switching to IgA. Production/activation of IgE. |
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IL-6
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Secreted by Th cells and Macs.
Production of acute phase reactants and Ig's. |
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IL-8
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Secreted by Macs.
Major chemotactic factor for PMNs. Help clear infxns. "Clean up on aisle 8" |
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IL-10
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Secreted by regulatory T-cells.
Inhibits actions of activated T-cells. Activates Th-2, inhibit Th-1. |
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IL-12
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Secreted by B-cells and Macs.
Activates NK cells and Th1 cells. |
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Gamma interferon
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Secreted by Th1 cells.
Stimulates Macs. Activates Th1, inhibits Th2. |
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TNF
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Secreted by Macs.
Septic shock. Leukocyte recruitment, vascular leak. |
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Hot T-Bone stEAk
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IL-1: hot (fever)
IL-2: stimulate T-cells IL-3: stimulate bone marrow IL-4: stimulate IgE production IL-5: stimulate IgA production |
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Helper T-cells - cell surface proteins
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CD4
CD3 CD40L CD28 TCR |
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Cytotoxic T-cells - cell surface proteins
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CD8
CD3 TCR |
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B-cells
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IgM
MHC II CD40 CD19 CD20 CD21 (receptor for EBV) B7 |
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Macrophages - cell surface proteins
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MHC II
CD40 B7 CD14 Receptors for Fc, C3b |
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NK cells
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Receptors for MHC I
Receptor for Fc of IgG CD56 |
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All cells except mature RBCs
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MHC I
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Interferon mechanism
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Proteins that place uninfected cells in anti-viral state.
Induce production of a ribonuclease that inhibits viral protein synthesis by degrading viral mRNA. "Interferes with viruses" |
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Interferon functions
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1. alpha and beta: inhibit viral protein synthesis.
2. gamma: increase MHC I and II expression and Ag presentation in all cells 3. activates NK cells to kill virus-infected cells |
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Active immunity
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Induced after exposure to a foreign antigen.
Slow onset. Long acting protection -- memory. |
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Passive immunity
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Receiving pre-formed Abs from another host.
Rapid onset. Short life-span of Abs (3 weeks). Ex: IgA in breast milk. |
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Which toxins require the administration of preformed (passive) Abs?
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Tetanus
Botulinum HBV Rabies "After exposure to Tetanus, Botulinum, HBV, Rabies, patients are given pre-formed Abs To Be Healed Rapidly" |
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Complement system
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System of proteins that interact to play a role in humoral immunity and inflammation.
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MAC defends against what type of bacteria?
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Gram negative
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Classic pathway (complement)
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Activated by complement proteins binding antigen-Ab complexes
IgM or IgG |
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Alternative pathway (complement)
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Activated by complement binding to molecules on microbial surfaces (non-specific activators, i.e. endotoxin)
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Mannose-lectin pathway
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Activated by mannose-binding lectin binding microbial surfaces
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C3b
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Main function is opsonization.
Aids in clearance of immune complexes. Increases internalization by phagocytic cells by opsonization. |
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2 primary opsonins in bacterial defense
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C3b and IgG
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Which 2 molecules help prevent complement activation on self-cells?
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DAF (decay-accelerating factor)
C1 esterase |
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Complement proteins involved in viral neutralization
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C1 - C4
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Complement proteins involved in anaphylaxis
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C3a and C5a
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C5a
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Anaphylaxis and PMN chemotaxis
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Membrane Attack Complex is comprised of which complement proteins?
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C5b - C9
Function: Lysis and Cytotoxicity |
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Deficiency of C1 esterase
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hereditary angioedema
C1 esterase inhibits C1, F12, kallikrein --> increased vasoactive substances |
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Hereditary angioedema
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C1 esterase deficiency
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Deficiency of C3
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Severe, recurrent pyogenic sinus and respiratory infxns
Increases susceptibility to type III hypersensitivity rxns |
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Deficiency of C5-C8
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Neisseria bacteremia
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Susceptibility to Neisseria bacteremia
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Deficiency of C5-C8
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Deficiency of DAF
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Complement-mediated lysis of RBCs and PNH
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Complement mediated lysis of RBCs and PNH
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Deficiency of DAF
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Antigenic variation in Influenza virus
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Major = shift --> "shit"
Minor = drift |
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Some mechanisms for antigenic variation:
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DNA rearrangement
RNA segment reassortment (influenza major shift) |
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Examples of antigenic variation in bacteria:
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Salmonella (2 flagellar variants)
Borellia (relapsing fever) Parasites (trypanasomes --> programmed rearrangement) |
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Anergy
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Self-reactive T-cells become non-reactive without co-stimulatory molecule.
B-cells also become anergic, but tolerance is less complete than in T-cells. |
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Granulomatous diseases (8)
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1. TB
2. Fungal infxns 3. Syphillis 4. Leprosy 5. Cat scratch fever 6. Sarcoidosis 7. Chron's 8. Berylliosis |
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Granulomatous disease process
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APC induces Th cell to release IFN-g
IFN-g induces monocyte --> Mac --> epithelioid cell --> giant cell |
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granuloma
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giant cell
epithelioid cell fibroblasts lymphocytes |
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Type I Hypersensitivity
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Anaphylactic and atopic - First and fast
Free Ag cross-links IgE on presensitized mast cells and basophils --> trigger release of vasoactive amines that act at post-capillary venules Rapid rxn after Ag exposure due to preformed Ab Test: Scratch test and radioimmunoabsorbent assay |
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Type II Hypersensitivity
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Antibody mediated.
IgM, IgG bind to fixed Ag on cell --> lysis (via complement) or phagocytosis Ab and complement lead to MAC Test: Direct and indirect Coomb's |
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3 mechanisms of Type II hypersensitivity rxn
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1. Opsonize cell or activate complement
2. Ab recruits PMNs and macs that incite tissue damage 3. Bind to normal cellular receptors and interfere with functioning |
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Type III Hypersensitivity
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Immune Complex
Ag-Ab (IgG) complexes activate complement --> attracts PMNs to release lysosomal enzymes. Immune complex = Ab-Ag-complement Ex: serum sickness and arthus rxn |
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Which hypersensitivity types are Ab mediated?
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Type I, II, III
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Serum Sickness
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Type III hypersensitivity
Abs to foreign proteins are produced (5 days). Immune complexes form and are deposited in membranes, where they fix complement --> tissue damage Now caused mostly by drugs --> fever urticaria, arthalgias, proteinuria, lymphadenopathy 5-10 days after Ag exposure. |
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Arthus rxn
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Type III hypersensitivity
local subacute Ab-mediated rxn Intradermal injection of Ag induces Ab --> form Ag-Ab complexes in skin Sx: edema, necrosis, and activation of complement Test: Immunofluorescent staining |
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Type IV Hypersensitivity
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Delayed (T-cell mediated) type
Sensitized T-cells encounter antigen and release lymphokines --> Mac activation (no Ab involved) Not transferable by serum. 4 T's : T-cells Transplant rejection TB skin test Touching (contact dermatitis) Test: patch test (i.e. PPD) |
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4 Hypersensitivity Rxns:
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ACID
Anaphylactic and Atopic (I) Cytotoxic (Ab-mediated) (II) Immune Complex (III) Delayed (cell-mediated) (IV) |
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Type I Hypersensitivity: Disorders
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Anaphylaxis (bee sting, food/drug allergies)
Allergies and atopic disorders (i.e. rhinitis, hay fever, eczema, hives, asthma) |
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Type I Hypersensitivity: Presentation
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Immediate, anaphylactic, atopic
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Type II Hypersensitivity: Disorders
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Hemolytic anemia
Pernicious anemia ITP Erythroblastosis fetalis Acute hemolytic transfusion rxns Rheumatic fever Goodpasture's syndrome Bullous pemphigoid Pemphigus vulgaris Grave's disease Myesthenia gravis |
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Type III Hypersensitivity: Disorders
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SLE
RA Polyarteritis nodosa Post-streptococcal glomerulonephritis Serum sickness Arthus rxn (i.e. after tetanus vaccine) Hypersensitivity pneumonitis (i.e. farmer's lung) |
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Type IV Hypersensitivity: Disorders
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DM Type I
MS Guillan-Barre syndrome Hashimoto's thyroditis GVHD PPD (test for TB) Contact dermatitis (poison, nickel) |
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ANA, anti-dsDNA, anti-Smith
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SLE
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Anti-histone
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drug induced lupus
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Anti-IgG
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aka rheumatoid factor
RA |
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Anti-centromere
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CREST/Sceleroderma
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Anti-Scl-70 / anti-DNA topo I
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Diffuse scleroderma
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Anti-mitochondrial
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Primary Biliary Sclerosis
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Anti-gliadin, anti-endomysial
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Celiac disease
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Anti-basement membrane
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Goodpasture's syndrome
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Anti-desmoglein
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Pemphigus vulgaris
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Anti-microsomal, anti-thyroglobulin
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Hashimoto's thyroiditis
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Anti-Jo-1
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Polymyositis
Dermatomyositis |
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Anti-SS-A / anti-Ro
Anti-SS-B/ anti-La |
Sjogren's syndrome
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Anti-U1 RNP
(ribonucleoprotein) |
Mixed connective tissue disease
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Anti-smooth muscle
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Autoimmune hepatitis
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Anti-glutamate decarboxylase
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Type I DM
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c-ANCA
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Wegener's granulomatosis
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p-ANCA
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other vasculitides
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Bruton's aggamaglobulinemia
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X-linked recessive
Defect in BTK (tyrosine kinase gene) Defect in B-cell differentiation/maturation Recurrent bacterial infxns after 6 mo (decreased maternal IgG) Opsonization defect Labs: Normal pro-B Decreased B-cells, Ab (all classes) |
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Hyper-IgM syndrome
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Defective CD40L on Thelper cells --> unable to class switch B-cells
Severe pyogenic infxns early in life Labs: Increased IgM Decreased all other Ig's |
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Selective Ig deficiency
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Defect in isotype switching --> specific class of Ig deficiency
Sinus and lung infxns Milk allergies and diarrhea Anaphylaxis (after exposure to blood products with IgA) Labs: IgA deficiency most common |
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Thymic aplasia
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22q11 deletion --> DiGeorge's
failure to develop 3rd and 4th pharyngeal pouches tetany (hypocalcemia) recurrent viral/fungal infxns (T-cell deficient) congenital heart and great vessel defects Labs: Absent thymic shadow in CXR Decreased T-cells, PTH, Ca |
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Di George's Symptoms
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CATCH
Cardiac anomalies (Tetralogy of Fallot) Abnormal facies Thymic aplasia Cleft palate Hypocalcemia |
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IL-12 receptor deficiency
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Decreased Th1 response
Disseminated mycobacterial infxns Labs: Decreased IFN-g |
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Hyper-IgE syndrome
(Job's syndrome) |
Th cells fail to produce IFN-g
PMNs unable to respond to chemotactic stimuli FATED course Facies cold, non-inflamed staph Abscesses retained primary Teeth increased IgE Dermatologic problems (eczema) Labs: Increased IgE |
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Chronic mucocutaneous candidiasis
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T-cell dysfunction
Candida albicans infxns of skin and mucous membranes. |
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SCID
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Several types --> B and T-cell deficiency
Defective IL-2 receptor (most common, X-linked) Adenosine deaminase deficiency Failure to synthesize MHC II Ag Recurrent viral, bacterial, fungal and protozoal infxns Tx: Bone marrow transplant (no allograft rejection) |
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Ataxia-telangiectasia
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Defect in DNA repair enzymes
Triad: cerebellar defects (ataxia) spider angiomas (telangiectasia) IgA deficiency |
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Wiskott-Aldrich syndrome
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X-linked recessive defect.
Progressive deletion of B and T-cells. Triad - TIE: Thrombocytopenic purpura Infections Eczema Labs: Decreased IgM |
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Leukocyte adhesion deficiency (type I)
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Defect in LFA-1 integrin (CD18) protein on phagocytes
Recurrent bacterial infxns Absent pus formation Delayed separation of umbilicus Labs: Neutrophilia |
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Chediak-Higashi syndrome
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AR inheritance
Defect in microtubular function with decreased phagocytosis Recurrent pyogenic infxns Staph and strep Partial albinism Peripheral neuropathy |
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Origin of Systolic murmur that Increases in intensity with Squatting to Standing (rapidly for 30 sec)
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Hypertrophic cardiomyopathy
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Syngeneic graft
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From identical twin or clone.
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Allograft
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From non-identical individual of same species.
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Xenograft
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From different species
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Hyperacute rejection
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Ab mediated (type II)
Preformed anti-donor Abs in recipient Occurs in minutes after transplantation |
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Acute rejection
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Cel mediated - cytotoxic T-cells against foreign MHCs
Weeks after transplantation. Reversible with cyclosporin and OKT3 |
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Chronic rejection
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T-cell and Ab mediated vascular damage (obliterative vascular fibrosis)
Occurs months to years after transplantation. Irreversible. CTL perceives as Class I-MHCself presenting non-self antigen. |
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GVHD
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Grafted T-cells proliferate in irradiated ICH and rejects cells with foreign proteins
Severe organ dysfunction. Maculopapular rash, jaundice, hepatosplenomegaly, diarrhea |
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Cyclosporine
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Calcineurin inhibitor --> prevents IL-2 and receptor production. Block differentiation and activation of T-cells
Use: Transplant, AI disorders Toxicity: Viral Infxns Lymphoma Nephrotoxic (prevent with mannitol diuresis) |
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Tacrolimus
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Similar to cyclosporine. Binds FK-binding protein --> Inhibits IL-2 and other cytokine secretion.
Use: Potent, used in transplant Toxicity: Significant Nephrotoxicity Peripheral Neuropathy HTN Pleural effusion Hyperglycemia |
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Azathioprine
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Antimetabolite precursor of 6-MP.
Interferes with metabolism/synthesis of nucleic acids. Toxic to proliferating lymphocytes. Use: Kidney transplant, AI disorders (glomerulonephritis, hemolytic anemia) Toxicity: BM suppression Toxic effects of increased allopurinol |
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OKT3 (muromonab-CD3)
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Monoclonal Ab that binds CD3 on T-cell surface
Blocks T-cell signal transduction. Use: kidney transplant Toxicity: Cytokine release syndrome Hypersensitivity rxn |
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Sirolimus / Rapamycin
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Binds to mTOR.
Inhibits T-cell proliferation in response to IL-2 Use: Kidney transplant used in combo with cyclosporine and corticosteroids Toxicity: Hyperlipidemia, Thrombocytopenia, Leukopenia |
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Mycophenolate mofetil (CellCept)
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Inhibits de novo guanine synthesis and block lymphocyte production
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Daclizumab
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Monoclonal ab with high affinity for IL-2 receptor on activated T-cells
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Aldesleukin (IL-2)
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Recombinant cytokine
RCC, metastatic melanoma |
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Erythropoietin (epoetin)
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Anemias (esp. in renal failure)
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Filgrastim (G-CSF)
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Recovery of bone marrow
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Sargramostim (GM-CSF)
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Recovery of bone marrow
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Alpha interferon
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Hep B, C
Kaposi sarcoma Leukemias Malignant melanoma |
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Beta interferon
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MS
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Gamma interferon
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CGD
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Oprelvekin (IL-11)
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Thrombocytopenia
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Thrombopoietin
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Thrombocytopenia
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