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97 Cards in this Set
- Front
- Back
cold agglutinin
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- aka cryoagglutinin
- an IgM antibody - produced by 60% of patients infected with Mycoplasma pneumoniae - reversibly agglutinates human erythrocyte antigen I positive RBCs at low temperatures - cause of cold agglutinin disease (autoimmune hemolytic anemia) |
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DiGeorge syndrome
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- impaired thymic development (affects T-cells)
- small deletions in chromosome 22 - also spontaneous |
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Chronic granulomatous disease
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- X-linked ressive or
- autosomal recessive - NADPH oxidase defficiency in neutrophils |
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Follicle of Lymph Node
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- Site of B-cell localization and proliferation.
- located in outer cortex of node - primary follicles are dense/dormant - secondary follicles have pale central germinal centers, active. |
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Medulla of Lymph node
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- cords -> closely packed lomphocytes and plasma cells
- sinuses -> reticular cells and macrophages - communicate with efferent lymphatics |
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Paracortex
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- Houses T cells.
- between follicles and medulla - contains high endothelial venules -> allow T and B cells to enter from blood - enlarged in extreme cellular immune response - undeveloped in DiGeorge syndrome |
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Location of T-cells in Spleen
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- Periarterial lymphatic sheath
- red pulp |
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Location of B-cells in spleen
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- follicles within the white pulp
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Sinusoids of spleen
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- long vascular channels in red pulp
- fenestrated "barrel hoop" basement membrane - Machrophages found nearby |
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Thymus develops from what?
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- 3rd Branchial pouches
- Lymphocytes originate from mesenchyme |
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Hassall's corpuscles
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- found in medulla of thymus
- formed from type VI epithelial reticular cells - source of cytokine TSLP (unknown function) |
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Components of innate immunity
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- neutrophils
- macrophages - dendritic cells - complement |
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Components of Adaptive immunity
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- T cells
- B cells - circulating antibody |
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Differentiation of T cells
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- T cell precursor from bone marrow
- in thymus, aquires T cell receptor, CD8 and CD4 (becomes CD4+ and CD8+) - One cluster of differentiation becomes dominant - in lymph node, CD4+ become cytotoxic T cells - CD8+ become T helper cells (1 and 2) |
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Th1 cells
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- produce IL-2 and IFN-gamma
- activate macrophages and cytotoxic CD8+ T cells. |
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Th2 cells
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- produce IL-2, IL4 and IL-5
- help B cells make antibody |
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MHC I
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- encoded by Human Leukocyte Antigen (HLA) A, B and C
- expressed on almost all nucleated cells - antigen loaded in RER - mediates viral immunity - pairs with beta 2- microglobulin |
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MHC II
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- encoded by Human Leukocyte Antigen (HLA) DR, DP and DQ
- expressed only on antigen presenting cells (APCs) - antigen loaded in an acidified endosome - main determinants of organ rejection |
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B cells
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- make antibody
- IgG antibodies opsonize bacteria and viruses - IgE responsible for Allergy from type I hypersensitivity - Antibodies cause organ rejection (fast) |
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T cells
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- CD4+ T cells help B cells make antibody and produce gamma-interferon that activates macrophages
- kills virus-infected cells directly (CD8+ T cells) - produces allergy through type IV hypersensitivity - organ rejection (slow) |
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Antigen-presenting cells
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- Macrophages
- B cells - Dendritic cells |
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Th activation
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- Foreign body is phagocytosed by APC
- Foreign antigen is presented on MHC II and recognized by TCR on Th cell (first signal) - Costimulatory signal given by B7 of APC binding with CD28 of Th - Th cell activated -> produces cytokines |
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Tc activation
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- Endogenously synthesized (viral or self) proteins presented on MHC I
- recognized by TCR on Tc cell (signal one) - IL-2 from Th cell activates Tc cell to kill virus-infected cell (signal 2) |
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Antibody structure
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- VL and VH chains recognize antigens
- CH of IgM and IgG fixes complement - Heavy chain contributes to Fc and Fab fractions - Light chain contributes only to Fab fraction |
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Antibody diversity generaged by:
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- random recombination of VJ (light chain) and VDJ (heavy-chain) genes
- random combination of heavy chains with light chains - somatic hypermutation - Addition of nucleotides to DNA during genetic recombination by terminal deoxynucleotidyl transferase |
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Mature B lymphocytes express what?
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- IgM and IgD
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Isotype switching
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- mediated by cytokines and CD40 ligand
- causes mature B lymphocytes to differentiate into plasma cells that secrete IgA, IgE or IgG |
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IgG
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- Main antibody in secondary response
- most abundant - fixes complement - crosses the placenta - 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 - monomer or dimer - found in secretions - picks up secretory component from epithelial cells before secretion |
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IgM
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- Produced in the primary response to antigen
- fixes complement - does not cross the placenta - antigen receptor on the surface of B cells - monomer or pentamer |
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IgD
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- Unclear function
- found on surface of B cells and in serum |
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IgE
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- Mediates immediate (type I) hypersensitivity by inducing the release of mediators from mast cells and basophils when exposed to allergen
- mediates immunity to worms - lowest concentration in serum |
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Ig allotype
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- Ig epitope that differs among members of same species
- on light or heavy chain |
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Ig Isotype
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- Ig epitope common to a single class of Ig
- determined by heavy chain (IgG, IgA, etc.) |
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Ig idiotype
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- Ig epitope determined by antigen-binding site
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IL-1
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- secreted by macrophages
- stimulates T cells, B cells, neutrophils, fibroblasts and epithelial cells to grow, differentiate or synthesize specific products - an 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
- supports the growth and differentiation of bone marrow stem cells - similar function to GM-CSF |
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GM-CSF
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- granulocyte macrophage colony-stimulating factor
- stimulates production of white blood cells - located on myeloblasts and mature neutrophils, not on any erythroid or megakaryocytic lineage cells |
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IL-4
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- Secreted by Th2 cells
- Promotes growth of B cells - enhances class switching if IgE and IgG |
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IL-5
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- Secreted by Th2 cells
- Promotes differentiation of B cells - enhances class switching of IgA - Stimulates production and activation of eosinophils |
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IL-6
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- Secreted by Th cells and macrophages
- Stimulates production of acute-phase reactants and immunoglobulins |
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IL-8
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- Major chemotactic factor for neutrophils
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IL-10
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- Secreted by Th2 cells
- Stimulates Th2 while inhibiting Th1 |
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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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gamma-interferon
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- secreted by Th1 cells
- Stimulates macrophages |
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TNF-alpha
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- Secreted by macrophages
- increases IL-2 receptor synthesis by Th cells - increases B-cell proliferation - Attracts and activates neutrophils - stimulates dendritic cell migration to lymph nodes |
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Helper T cell surface proteins
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- CD4
- TCR - CD3 - CD28 - CD40L |
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Cytotoxic T cell sufrace proteins
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- CD8
- TCR - CD3 |
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B cell surface proteins
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- IgM
- B7 - CD19 - CD20 - CD40 - MHC II |
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Macrophage surface proteins
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- MHC II
- CD14 - Receptors for Fc and C3b |
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NK cell surface proteins
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- Receptors for MHC I
- CD 16 - CD56 |
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Membrane attach complex
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- defends against gram-negative bacteria
- activated by IgG or IgM in the classic pathway - activated by molecules on the surface of microbes (endotoxin) in the alternate pathway - C3b and IgG primary opsonins in bacterial defense |
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Complement:
C1, C2, C3, C4 function |
- viral neutralizaion
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C3b
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opsonizaion
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C3a and C5a
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- anaphylaxis
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C5a
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- neutrophil chemotaxis
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C5b-9
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- cytolysis by MAC
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Deficiency of C1 esterase inhibitor
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- hereditary angioedema (overactive complement)
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Deficiency of C3 leads to
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- severe, recurrent pyogenic sinus and respiratory tract infections
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Deficiency of C6-C8
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- Neisseria bacteremia
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Deficiency of decay accelerating factor
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- paroxysmal nocturnal hemoglobinuria (PNH)
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Classic complement pathway
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- antigen/antibody complexes
(draw) |
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Lectin Complement pathway
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- microbial surfaces
(draw) |
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Alternative complement pathway
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- Microbial surfaces (nonspecific activators, endotoxin)
draw |
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Interferon mechanism
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- alpha, beta and gamma
- proteins that place unifected cells in an antiviral state - induce the production of a 2nd protein that inhibits viral protein synthesis by degrading viral mRNA - activate NK cells to kill virus-infected cells |
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Interferon alpha and beta
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- inhibit viral protein synthesis
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gamma-interferons
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- increase MHC I and II expression and antigen presentation in all cells
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Passive immunity given for:
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- preformed antibody injection
- Tetanus, botulinum, HBV or Rabies |
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Type I hypersensitivity
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- Anaphylactic and atopic
- antigen cross-links IgE on presensitized mast cells and basophils - triggers release of vasoactive amines (histamine) - develops rapidly due to preformed antibody |
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Antibody mediated hypersensitivities
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- type I, II and III
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Type II hypersensitivity
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- Antibody mediated (IgM, IgG
- binds to antigen on enemy cell - lysis by complement or phagocytosis |
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Type III hypersensitivity
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- Immune complex
- Serum sickness - Arthus reaction |
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Immune complex hypersensitivity
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- type III
- antigen-antibody complexes activate complement -> attracts neutrophils - neutrophils release lyosomal enzymes |
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Serum sickness
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- Type III hypersensitivity
- immune complex disease - antibodies to the foreign proteins are produced over 5 days - immune complexes formed and deposited in membranes - fix complement -> tissue damage |
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Arthus reaction
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- Type III hypersensitivity
- local subacute antibody-mediated hypersensitivity reaction - intradermal injection of antigen induces antibodies - andigen-antibody complexes form in skin - edema, necrosis, activation of complement |
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common problems of serum sickness
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- often caused by drugs instead of serum
- fever, urticaria, arthralgias, proteinuria, lymphadenopathy - occurs 5-10 days after exposure |
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Type IV hypersensitivity
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- Delayed (T-cell mediated)
- sensitized T lymphocytes encounter antigen - release lymphokines -> macrophage activation |
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complications of Type IV hypersensitivity
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- Transplant rejections,
- contact dermatitis - TB skin test uses this mechanism |
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Diseases of type I hypersensitivity
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- anaphylaxis
- allergic rhinitis (hay fever) |
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Diseases of type II hypersensitivity
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- Hemolytic anemia
- Idiopathic thrombocytopenic purpura - Erythroblastosis fetalis - Rheumatic fever - Goodpastures's syndrome - Bullous pemphigoid - Graves'disease - Myasthenia gravis |
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Diseases of Type III hypersensitivity
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- Lupus
- Rheumatoid arthritis - Polyarteritis nodosum - Post-streptococcal glomerulonephritis - Serum sickness - Arthus reaction - Hypersensitivity pneumonitis |
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Diseases of Type IV hypersensitivity
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- Type I diabetes mellitus
- Multiple sclerosis - Guillain-Barré syndrome - Hashimoto's thyroiditis - Graft-versus-host disease - PPD (test for M. tuberculosis) - Contact dermatitis |
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Immune deficiency causing a decrease in production of B cells
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- Bruton's agammaglobulinemia
- X-linked recessive defect in a tyrosine kinase gene associated with low levels of all classes of immunoglobulins - recurrent bacterial infections after 6 monts of age (declining maternal IgG - occurs in boys |
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Immune deficiency causing a decrease in production of T cells
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- Thymic aplasia (DiGeorge syndrome
- Thymus/parathroids fail to develop - failure of development of 3rd and 4th pharyngeal pouches - presents with Tetany owing to hypocalcemia - recurrent viral and fungal infections from T-cell deficiency - congenital defects of heart and great vessels - 22q11 deletion |
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Immune deficiency causing a decrease in production of B and T cells
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- Severe combined immunodeficiency (SCID)
- Defect in early stem-cell differentiation - presents with recurrent viral, bacterial, fungal and protozoal infections - can have multiple causes (failure to synthesize MHC II antigens, defective IL-2 receptors or adenosine deaminase deficiency. |
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Immune deficiency causing a decrease in activation of T cells
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- IL-12 receptor deficiency
- Presents with disseminated mycobacterial infections |
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Hyper IgM syndrome
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- decrease in the activation of B cells
- defect in CD40 ligand on CD4 T helper cells -> inability to class switch - Presents early in life with severe pyogenic infections - High levels of IgM - Very low levels of IgG, IgA and IgE |
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Wiskott-Aldrich syndrome
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- decrease in B cell activation
- X-linked defect in the ability to mount an IgM response to capsular polysaccharides of pacteria - elevated IgA levels, normal IgE levels, low IgM levels - Triad of symptoms includes recurrent pygenic infections, thrombocytopenic Purpura, Eczema |
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Job's syndrome
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- decreased activation of Macrophages
- failure of gamma-interferon production by helper T cells - Neutrophils fail to respond to chemotactic stimuli - presents with recurrent "cold" (noninflamed) staphylococcal abscesses, eczema, coarse facies, retained primary teeth, high levels of IgE |
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Leukocyte adhesion deficiency syndrome
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- Defect in LFA-1 adhesion proteins on phagocytes
- presents early with severe pyogenic and fungal infections - delayed separation of umbilicus |
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Chédiak-Higashi disease
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- Autosomal recessive
- defect in microtubular function and lysosomal emptying of phagocytic cells - presents with recurrent pyogenic infections by staphylococci and streptococci - partial albinism - peripheral neuropathy |
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chronic granulomatous disease
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- defect in phagocytosis of neutrophils owing to lack of NADPH oxidase activity or similar enxymes
- presents with marked susceptibility to opportunistic infections with bacteria, esp. S. aureus, E. coli and Aspergillus - diagnosis confirmed with negative nitroblue tetrazolium dye reduction test |
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Chronic mucocutaneous candidiasis
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- T-cell dysfunction specifically against Candida albicans
- presents with skin and mucous membrane Candida infections |
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Selective Immunoglobulin deficiency
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- Idiopathic dysfunction of B cells
- Deficiency in a specific class of immunoglobulins (possibly due to defect in isotype switching) - Selective IgA deficiency is most common selective immunoglobulin deficiency - presents with sinus and lung infections, milk allergies and diarrhea common |
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Ataxia-telangiectasia
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- Idiopathic dysfunction of B-cells
- Defect in DNA repair enzymes with associated IgA deficiency - Presents with cerebellar problems (ataxia) - spider angiomas (telangiectasia) |
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Common variable immunodeficiency
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- Idiopathic dysfunction of B cells
- Normal numbers of circulating B cells - decreased plasma cells - decreased Ig - can be acquired in 20's and 30's. |