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138 Cards in this Set
- Front
- Back
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What are 3 functions of a lymph node?
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1) store & proliferate B & T-cells
2) make antibodies 3) place for macrophages to filter through |
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Where are B-cells localized in a lymph node?
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follicle - in the outer cortex, 2ndary follicles are pale with active germinal centers
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Lymph node medullary CORDS contain:
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plasma cells, lymphocytes
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Lymph node medullary SINUSES contain:
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macrophages, reticular cells - communicate with efferent lymphatics
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Where are the T-cells located in a lymph node?
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paracortex, which is between the follicles & medulla - contains High Endothelial Venules where lymphocytes enter the node from the blood
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Which part of the lymph node gets huge during, say, a viral infection?
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PARACORTEX - where the T-cells are!
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A patient with DiGeorge's syndrome is going to have a very poorly developed ___ of his lymph node.
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paracortex - deficient T-cells
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The thoracic duct drains which parts of the body?
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everything except R arm and R half of head (drained by right lymphatic duct)
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The spleen consists of scattered nodules of ___ pulp in extensive ___ pulp.
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white; red
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Where would you find B-cells in the spleen?
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germinal centers of white pulp
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Where would you find T-cells in the spleen?
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Periarterial Lymphatic Sheath (PALS) of the white pulp; also in RED PULP!
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What is the function of spleen red pulp?
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remove old RBCs from circulation
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What is the thymus derived from, embryologically?
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epithelium of 3rd branchial pouches (ugh...branchial pouches)
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Where are mature T-cells located in the thymus?
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medulla - pale, also has Hassal's corpuscles
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Where in the thymus do positive & negative T-cell selection occur?
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corticomedullary junction
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Positive selection of T-cells is where they must demonstrate the ability to bind to ___ in order to keep maturing.
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peptide:MHC complex
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Negative selection of T-cells is where those that ___ are apoptosed, because otherwise they might be autoreactive.
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bind too strongly to self-peptide:MHC complexes
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Macrophages secrete IL-___ which induces naive T helper cells to become Th___ cells.
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IL-12, Th1
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Th1 helper cells secrete ___ & ___ which do what?
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gamma-IFN & IL-2: activate macrophages and CD8 T-cells, respectively
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Which interleukin induces naive helper T-cells to become Th2 cells?
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IL-4 (cell source unknown)
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Which interleukins help B-cells make antibody (turn them into plasma cells)?
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IL-4, 5
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Which line of lymphocytes is responsible for autoimmunity?
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B-cells
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Which line of lymphocytes is responsible for hay fever and other type 1 hypersensitivity?
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B-cells
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Which line of lymphocytes defends against infection by opsonizing bacteria and neutralizing toxins and viruses?
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B-cells
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Which line of lymphocytes defends you against tuberculosis, virus-infected cells, and fungi?
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T-cells
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Which line of lymphocytes is responsible for graft rejections?
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T-cells
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Which line of lymphocytes is responsible for poison ivy allergies?
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T-cells
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Which line of lymphocytes regulates the antibody response, either by helping or suppressing?
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T-cells
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All NUCLEATED cells have MHC class ___ proteins.
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MHC class I
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Which type of MHC do antigen presenting cells have?
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both MHC I & II
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MHC class I genes: (3)
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A, B, C
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MHC class II genes (3):
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DP, DQ, DR
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MHC class I proteins consist of ___ polypeptide(s):
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1 transmembrane polypeptide: alpha chain + beta-2 microglobulin
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Where does MHC I pick up its antigen to present?
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RER - presents intracellular antigens like viruses
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Where does MHC II pick up its antigen to present?
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acidified endosome - picks up extracellular antigens that have been phagocytosed
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___ T-cells have CD4 which binds to MHC class ___.
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helper; MHC II
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Cytotoxic T-cells have CD___ which binds to MHC class ___.
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CD8; MHC I
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What is the CD3 complex?
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proteins associated with T-cell receptor complex that transduce signals to the cell interior after Ag has been recognized
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What are the 3 kinds of antigen presenting cells?
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1) dendritic cells
2) macrophages 3) B-cells |
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Steps in T helper cell activation: start with Ag being phagocytosed
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1) Ag phagocytosed by APC
2) Ag presented on MHC II 3) CD4 T helper cell binds 4) B7:CD28 costimulate Th cell 5) Th cell makes IL-2 and gamma IFN |
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How is a Tc cell activated?
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1) recognizes protein presented on MHC I
2) IL-2 from Th cell activates Tc cell to kill virus-infected cell |
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An antigen presenting cell has which half of the B7:CD28 costimultory signal?
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B7
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Which part of the antibody fixes complement?
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constant part of the heavy chain, of IgG and IgM only
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What are 4 characteristics of the Fc portion of an antibody?
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1) constant
2) complement binding (IgG, M) 3) carboxy terminal 4) carbohydrate side chains |
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Which part of the antibody binds antigen?
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variable regions of light and heavy chains (Fab fragment)
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What are 3 things that antibodies do to bacteria?
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1) opsonization to promote phagocytosis
2) neutralization to prevent their adherence to cells 3) complement activation to enhance opsonization & lysis |
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What are 4 ways to generate antibody diversity?
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1) random recombination of VJ (light chain) or VDJ (heavy chain) genes
2) random recombination of heavy chains w/light chains 3) somatic hypermutation (only in B-cells) 4) addition of nucleotides to DNA during genetic recombination by terminal deoxynucleotidyl transferase |
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What is somatic hypermutation?
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nucleotide substitutions into immunoglobulin light and heavy chain genes --> some variant immunoglobulins produced may bind the antigen better
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Mature B-cells express ___ and ___ on their surface.
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IgM, IgD
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What is the process where mature B-cells turn into plasma cells and secrete immunoglobulins other than IgM and IgD?
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isotype switching
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What is IgG and what does it do?
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1) main Ab in 2ndary response
2) most abundant Ig 3) crosses placenta 4) fixes complement (Fc frag) 5) opsonizes bacteria 6) neutralizes toxins & viruses |
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Which immunoglobulin prevents bacterial attachment to mucous membranes?
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secretory IgA (picks up the secretory component from epithelial cells before secretion)
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Which immunoglobulin is produced in the primary response to an antigen?
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IgM - fixes complement, monomer or pentamer
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Which immunoglobulin is found in LOWEST concentration in the serum?
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IgE
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What is IgE responsible for?
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type 1 hypersensitivity - induce release of mediators from mast cells & basophils in response to allergen binding (recall: IgE crosslinking and cell degranulation)
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What is an isotype?
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Ig epitope common to a single class of Ig, like IgG, IgA... (there are 5 classes, each determined by its heavy chain)
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What is an allotype?
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the encoded proteins of alleles, which are different forms of a gene
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What is the cytokine that is:
- secreted by macrophages - causes fever - stimulates T-cells, B-cells, PMN, fibroblasts, epithelial cells |
IL-1 (hot)
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Which cytokine is secreted by Th1 cells that activates Tc cells as well as Th cells?
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IL-2 (T-cells)
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Which cytokine has a function similar to that of GM-CSF, which is to stimulate bone marrow stem cell growth and differentiation?
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IL-3
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This cytokine stimulates B-cells to class switch to IgE and IgG.
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IL-4
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Which interleukin enhances B-cell class switching to IgA?
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IL-5
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Which cytokine stimulates production and activation of eosinophils?
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IL-5
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IL-6 is produced by _____ and stimulates production of _____.
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Th cells & macrophages; acute phase reactants
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Which interleukin is a major neutrophil chemoattractant?
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IL-8
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Which cytokine stimulates Th2 cells and inhibits Th1 cells?
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IL-10 - made by Th2 cells
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Which cytokine activates NK cells and Th1 cells? Which cells make it?
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IL-12; made by macrophages and B-cells
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Which cytokine activates macrophages?
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gamma-IFN (made by Th1 cells in addition to IL-2)
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TNFa is made by ___ and acts to:
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macrophages
1) IL-2 receptor synthesis by Th cells 2) B-cell proliferation 3) attracts neutrophils 4) stimulates DCs to go to LN |
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Cell surface proteins on Th cells: (5)
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1) CD4
2) TCR 3) CD3 4) CD28 5) CD40L |
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Cell surface proteins on Tc cells: (3)
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1) CD8
2) TCR 3) CD3 |
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What kind of cell expresses the following on its surface: IgM, B7, CD19, CD20, CD40, MHC II
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B-cells!
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What cell surface proteins does a macrophage express?
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MHC II, CD14 (both of which are receptors for Fc and C3b)
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What do NK cells express on the surface?
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MHC I, CD16, CD56 (major marker)
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How is complement activated in the classic pathway?
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IgM, IgG (bind complement with their constant heavy chain portions)
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How is complement activated in the alternate pathway?
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by molecules on the surface of microbes, especially ENDOTOXIN!!!
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Complement defends the host against infection by what kind of bacteria?
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gram negative
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C1, 2, 3, 4 do what?
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neutralize viruses
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C3b does what?
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opsonization (recall: macrophages have Fc and CD14 surface proteins which are receptors for C3b), also clears immune complexes from serum!
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What complements are responsible for anaphylaxis?
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C3a, C5a (C5a is also neutrophil chemoattractant, like IL-8 and LTB4)
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Which complements mediate cytolysis by forming MAC?
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C5b, 6, 7, 8, 9
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What happens if you don't have C1 esterase inhibitor?
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hereditary angioedema from overactive complement
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What happens if you don't have C3?
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severe recurrent pyogenic sinus and respiratory tract infections
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Deficiency of C6-C8 causes bacteremia by which species?
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Neisseria
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Deficiency of Decay Accelerating Factor causes:
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paroxysmal nocturnal hemoglobinuria
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What do interferons do to uninfected cells when there is a viral infection going on?
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puts them in an anti-viral state; activate NK cells to kill virus-infected cells
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How do gamma interferons help in a viral infected state?
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increase MHC I & II expression, upregulate antigen presentation in all cells
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What kind of immunity is getting antibodies premade by another host?
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passive - rapid onset immunity but short lived
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What kind of immunity is induced after personal exposure to foreign antigens?
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active - slow onset but memory forming (long lasting)
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Exposure to what 4 toxins call for passive immunity for quick action?
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- rabies
- HBV - tetanus - botulinum |
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Which protozoan has antigen variation?
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trypanosomes
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Which bacteria can have antigen variation?
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- Salmonella (flagella)
- Borrelia (relapsing fever) - N.gonorrhea (pilus) |
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Which virus is famous for antigenic variation by shifting or drifting?
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influenza virus
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What happens to T-cells that bind to self molecules but don't have a costimulatory signal?
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anergy - become nonreactive
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Anaphylaxis, asthma, hives, local wheal and flare are all examples of what kind of hypersensitivity?
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type 1 - antigen crosslinks IgE on presensitized mast cells & basophils --> release vasoactive amines like histamine
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How does type 2 hypersensitivity work?
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IgM, IgG bind to antigen on cell; can --> lysis or phagocytosis
(examples: autoimmune hemolytic anemia, Rh disease, Goodpasture's, rheumatic fever, Grave's, bullous pemphigoid, myasthenia gravis, ITP) |
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What are the 3 components of type 3 hypersensitivity?
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antigen: antibody: complement
attracts neutrophils which release enzymes and cause tissue damage (PAN, SLE, RA, immune complex glomerulonephritis) |
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Describe what happens in serum sickness:
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1) inject forein proteins
2) make Abs against them 3) Ag:Ab complexes deposit in membranes (systemic) 4) fix complement --> tissue damage |
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How does serum sickness manifest clinically?
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5-10 days after antigen exposure, patient will present with fever, urticaria, arthralgia, proteinuria, lymphadenopathy
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What is the Arthus reaction?
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intradermal injection of foreign Ag --> Ag:Ab complexes in skin with LOCAL inflammation & necrosis, edema, complement activation (example: farmer's lung)
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Wot is type 4 hypersensitivity? (I'm so bored...)
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SENSITIZED T-cells bind antigen and release cytokines that activate macrophages --> transplant rejection, positive PPD skin test, contact dermatitis
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Bruton's agammaglobulinemia =
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XR defect in tyrosine kinase gene, low B-cells and ALL immunoglobulins! Recurrent bacterial infections after 6 mo of age when Mom's IgG wears out
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DiGeorge's syndrome =
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failed development of 3rd & 4th pharyngeal pouches --> no thymus (so no T-cells) or parathyroids, tetany, recurrent viral & fungal infections, 22q11 del, congenital heart defects (truncus, tetralogy)
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SCID =
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low B & T-cells, defect in stem cell differentiation, recurrent bacterial, viral, fungal, protozoal infections (many causes like ADA deficiency, defective IL-2 receptors, no MHC II antigens)
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Disseminated mycobacterial infections. Due to low activation of:
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Th1 cells (IL-12 receptor deficiency)
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Super high levels of IgM and very low levels of IgG, IgA, IgE suggest:
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hyper-IgM syndrome where defective CD40L on Th cells leads to inability to help B-cells class switch
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Elevated IgA, normal IgE, and low IgM levels along with recurrent pyogenic infections, thrombocytopenic purpura, and eczema suggest:
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Wiskott-Aldrich syndrome (XR), can't mount IgM response to encapsulated bacteria (polysaccharide antigen)!
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Job's syndrome =
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Th1 cells don't make gamma-IFN so can't activate macrophages --> no TNFa to attract neutrophils --> recurrent staph abscesses, eczema, coarse facies, retained primary teeth (odd), and HIGH IgE!
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Leukocyte adhesion deficiency syndrome =
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defective LFA-1 adhesion proteins on phagocytes (early severe pyogenic & fungal infections, delayed separation of umbilicus)
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What do you suspect in a patient who gets recurrent infections by staph & strep, is partially albino, and has peripheral neuropathies?
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Chediak-Higashi (AR) - microtubule dysfunction --> impaired phagocytosis and melanin distribution
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Some who gets a lot of infections with S.aureus, E.coli, and aspergillus, and a negative nitroblue tetrazolium dye reduction test has:
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chronic granulomatous disease - NADPH oxidase deficiency
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Chronic mucocutaneous candidiasis =
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T-cell dysfunction specifically against Candida albicans
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Selective immunoglobulin deficiency =
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usually selective IgA deficiency due to defect in class switching (get sinus and lung infections, milk allergies, diarrhea)
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Ataxia-telangiectasia =
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defect in DNA repair against x-rays, presents with progressive cerebellar ataxia and spider angiomas, associated with IgA deficiency
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anti-dsDNA, anti-Smith antibodies =
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SLE
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anti-histone antibodies =
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drug-induced lupus
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anti-IgG antibodies =
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rheumatoid arthritis (anti-IgG is rheumatoid factor)
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anti-centromere antibodies =
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CREST scleroderma
(calcinosis, Raynaud's, esophageal dysmotility, sclerodactyly, telangiectasia, limited skin involvement to face and fingers) |
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anti-scl-70 antibodies =
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diffuse scleroderma
(widespread skin involvement, rapid progression, early organ involvement) |
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anti-mitochondrial antibodies =
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primary biliary cirrhosis
(intrahepatic, obstructive jaundice, steatorrhea, pruritus, xanthoma, high ALP) |
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anti-epithelial cell antibodies =
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pemphigus vulgaris
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anti-microsomal antibodies =
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Hashimoto's thyroiditis
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anti-thyroglobulin antibodies =
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Hashimoto's thyroiditis
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anti-Jo-1 antibodies =
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1) dermatomyositis (skin rash, inc. risk malignancy, progressive proximal muscle weakness)
2) polymyositis (progressive proximal muscle weakness) |
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anti-U1RNP antibodies =
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mixed connective tissue disease (FA p319)
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anti-gliaden antibodies =
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celiac sprue
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anti-basement membrane antibodies (collage type 4)
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Goodpasture's
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HLA B27 =
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psoriasis, ankylosing spondylitis, IBD, Reiter's syndrome
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HLA B8 =
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Grave's, celiac sprue
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HLA DR2 =
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multiple sclerosis, hay fever, SLE, Goodpasture's
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HLA DR3 =
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diabetes mellitus type 1 (and lupus?)
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HLA DR4 =
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diabetes mellitus type 1, rheumatoid arthritis
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HLA DR5 =
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Hashimoto's thyroiditis, pernicious anemia --> B12 deficiency
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HLA DR7 =
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steroid-responsive nephrotic syndrome
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Presence of preformed, anti-donor antibodies leads to which type of transplant rejection?
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hyperacute - occurs w/in minutes after transplant
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Tc cells reacting to foreign MHCs is what kind of transplant rejection?
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acute rejection - weeks after transplant, reversible with immunosuppressants like cyclosporin & OKT3
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Describe a chronic transplant rejection:
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occurs months to years later, irreversible, antibody-mediated vascular damage (fibrinoid necrosis)
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Explain graft vs. host disease:
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immunocompetent T-cells grafted along with the transplanted tissue starts attacking "foreign" proteins --> severe organ dysfunction, maculopapular rash, jaundice, hepatosplenomegaly, diarrhea
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