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134 Cards in this Set
- Front
- Back
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Humoral Immunity
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1. Antibodies
2. Defends against extracellular agents |
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Can B cells be stimulated if there are no functional T cells?
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Yes. Thymus-independent Antigens 1) Contain no peptides 2) Stimulate only IgM 3) Create no memory 4) Mitogens activate many clones of cells and are used to assess lymphocyte function
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Class (isotype) switching is able to occur...
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..with direct contact of B cells with Th cells (CD 40- CD40 Ligand interaction) and release of IL-4, IL-5, AND IL-6
Need: 1) T cell 2) CD-40 Ligand 3) Cytokines |
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What is ALWAYS the first antibody made in any reaction to any antigen?
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IgM!!!!
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Which antibody molecule has highest Avidity?
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IgM: avidity correlates with number of binding site. IgM is in the shape of pentamer and is most important in the entrapment of FREE ANTIGENS! Also along with IgG, IgM can also activate CLASSIC COMPLEMENT
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Which Antibody has highest affinity??
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IgG
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When and where does Class switching occur? What region "switches"?
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During an immune response. Occurs in Secondary Lymphoid tissues. Specifically in Germinal center (only formed during an immune response)! Change of constant region of antibody.
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Primary immune response is mainly which antibody?
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IgM
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Secondary immune response is mainly?
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IgG
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Germinal centers
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clones of proliferating Antigen specific B cells
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Somatic Hypermutation
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creates POINT mutations in antibody idiotype
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Clonal selection causes...?
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Affinity Maturation
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What kind of cytokines dictate SWITCH REGION ACTIVATION?
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TH2
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Hyper-IgM Syndrome
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--X- linked failure of T Cells to express CD40L
--IgM levels up to 10 times normal (none of the other Ab isotypes) --Deficiency of IgG, IgA, IgE --Fail to make germinal centers --Recurrent respiratory infections |
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Why would a pt with Hyper-IgM Syndrome suffer from reccurrent respiratory infections?
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--Missing IgA (predominant protector at the mucosal surfaces)
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What Antibody with 4 subisotypes, the ability to activate complement classic pathway, major mediator of ADCC (antibody dependent cellular cytotoxicity), is the only antibody that can OPSONIZE and CROSS THE PLACENTA?
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IgG
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IgA
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--secreted as a dimer with J chain
--produced in submucosa --Protector at the mucosal level! --important component in breast milk and colostrum --IL-5 and TGF-beta cause switch to IgA!!!!!! |
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MALT (mucosal-associated lymphoid tissues), contains TH2 cells that help the B cells CLASS SWITCH to IgA production. Why does IgA do so much better in mucosa then the rest?
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Secretory IgA has secretory component in its dimer formation
--Secretory component helps with transepithelial transport AND proteolytic cleavage |
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Secretory component on secretory IgA dimer helps with what 2 things?
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1. Transepithelial transport
2. Proteolytic cleavage |
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What binds to the Poly Ig Receptor (on basolateral side of epithelial cells which faces the submucosa)?
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The J-chain, on the IgA dimer (has just been released from plasma cell in submucosa) binds the Poly Ig Receptor.
--Poly Ig Receptor is transported across epithelial layer with IgA dimer into the mucoal layer and IS THE SECRETORY COMPONENT of secretory IgA!!! |
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Can IgM cross into the mucosa as well (IgA known for this)?
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YES! IgM also has a J-chain which is the part that binds the Poly Ig Receptor on the basolateral side of the epithelial cell in the submucosa layer. Thus, IgM can cross the mucosal layer, but not as readily as IgA.
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What 2 cytokines cause isotype (class switching) switching to IgE?
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IL-4 and IL-13
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What part of IgE binds to mast cells and basophils?
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Fc portion!!!
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IgE
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binds to mast cells and basophils
IL-4 and IL-13 cause isotype switching to IgE mediates type I (immediate) allergic responses protects against PARASITES!!!! |
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What 2 antibodies are on surface of naive B-cells?
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IgM and IgD
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In the Complement System: most important chemotaxin?
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C5a
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3 important Functions of Complement System...
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1. Recruitment of inflammatory cells (C3a, C4a, C5a)
2. Opsonization of pathogens (major complement protein C3b) 3. Killing of pathogens |
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Which chemotaxins function as anaphylatoxins?
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C3a AND C5a, can both bind directly to mast cells and basophils and cause degranulation WITHOUT IgE!
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What is the major Complement Protein that helps eliminate immune complexes and major part of opsonization process?
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C3b (without it pt will have Type III Hypersensitivity reactions)
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(T/F) Alternative Complement Pathway is completely Innate (does NOT need antibody).
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TRUE
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Innate Immunity
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-no memory (response doesn't get any better)
-present intrinsically -nonspecific -limited diversity |
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Two types of immunity?
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1. Innate Immunity
2. Adaptive Immunity |
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Adaptive Immune Response
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--composed of lymphocytes (B cells and T cells) and plasma (B cell at the end of the line) cells
--APC cells (help with adaptive immune response, but NOT PART OF a.i.r.) |
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APC's
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--e.g. Macrophages, B cells, and dendritic cells
--however, Macrophages and dendritic cells ARE PART OF INNATE IMMUNITY only help with adaptive immune responses |
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Adaptive Immunity
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--Inducible (can be turned on when needed, off when not)
--specific --memory --extensive diversity --self vs. non-self discrimination --self-limiting |
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Major membrane marker for macrophages (also have CD40) and monocytes?
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CD14
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Macrophage major duties...
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1. phagocytosis
2. antigen presenting and processing 3. make cytokines that help activate T cells |
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What type of dendritic cells are known for "maintaining memory"?
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Follicular Dendritic cells, they capture and hold antigens- antibody complexes with their long cytoplasmic arms on their surfaces. They hold them and constantly "aggitates" the immune system (memory)
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What type of dendritic cell is known for "antigen processing and presentation"?
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Antigen presenting dendritic cells
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2 types of dendritic cells....
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1. Follicular dendritic cells
2. APC's |
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What type of cell is most numerous cell at initial site of inflammation/infection?
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Neutrophils
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Major increase in what type of myeloid cell in PARASITIC INFECTION?
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Eosinophils!!!!! components w/in granules of eosinophils are very cytotoxic to parasites
--***Can also see a lot of eosinophils in the late stages of a Type I Hypersensitive reaction |
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Initiation of immediate type of Type I Hypersensitivity reaction causes an...
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Immediate degranulation (release of granules) of basophils
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What major proteins are on surface of B cells (produce antibody)?
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CD 19, CD 20, CD21
CD40, MHC II, B7 |
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What is the receptor of Epstein-Barr virus?
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CD-21
"you can drink Beer at the Bar when you're 21" |
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What are the major proteins on the surface of T-helper cells (regulate immune responses "mob boss")?
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CD3, CD4
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What are the major proteins on the surface of Cytotoxic T cells (kill altered cells)?
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CD3, CD8
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Where is the difference between the antibodies?
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Constant region, determines biological effects (function of the antibody-antigen complex s/p binding to one another)
Constant region determines isotype (IgM vs. IgG vs. IgE, etc.) |
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What part of antibody determines idiotype?
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Variable region
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Antibody (receptor) vs. TCR (T-cell receptor)
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Antibody--flexible at Hinge region; 2 light chains and 2 heavy chains, bivalent
TCR--can only bind peptides that have been processed and presented on an MHC, two beta (heavy), two (alpha) chains, not flexible, not secreted, monovalent |
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B-cell Receptor (BCR)
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works thru B-cell signal transduction s/p antigen binding to its antibody; heterodimer (Ig-alpha and Ig-beta)
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What is the component that is associated with TCR for signal transduction pathway (on T-Cell surface)?
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CD3! Initiates signal transduction s/p activation by TCR associated complex. Tyrosine kinases bind to and are activated by activated CD3 cytoplasmic tail
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Difference between lymph node and splenic white pulp?
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Difference--both pathogens and lymphoctyes enter and leave spleen in blood!!
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How are mucosal lymphoid tissues different from lymph nodes or spleen?
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Difference: M-CELLS (specialized cells of mucosal epithelium--thus, pathogens arrive at mucosa associated lymphoid tissues by direct delivery across mucosa via these M-cells) !!!
* Difference: Mainly in route of pathogen entry and migration patterns of lymphocytes |
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Lymphocytes that are activated in mucosal tissues stay within mucosal system and... (2 things)
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1. Once activated, can move out from lymphoid tissue into Lamina Propria and mucosal epithelium (perform effector actions there)
2. Once activated, can re-enter mucosal tissues from the blood as effector cells after being recirculated! |
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What do HRF (homologous restriction factor) and CD59 restrict?
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Restriction of formation of C9 pore on human cell.
Block C5b678 MAC complex recruitment of C9 to human cell surface! |
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Cause of Paroxysmal Nocturnal Hemoglobinuria
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Pt has episodes of complement-mediated lysis of RBCs that lack cell-surface DAF, HRF, or CD59.
-Impaired synthesis of DAF, HRF, and CD59 glycosylphosphatidylinositol lipid tail which adheres proteins to human plasma cell membrane nlly. |
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Children with asplenia are susceptible to encapsulated bacteria...Types?
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Streptococcus pneumoniae, Haemophilus influenzae
THEY NEED VACCINATION FOR PROTECTION |
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Adult with spleen removed (or who were vaccinated as children) have less risk of becoming infected with encapsulated bacteria, i.e. Strep. pneumoniae, Haemophilus influenzae
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May need vaccination against S. pneumoniae though!
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MHC Class I --Intracellular pathogens
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Endogenous (cytosolic) Ag processing pathway
Regcognized by cytotoxic T cell in TCR and CD8 coreceptor Expressed on almost all nucleated cells (not RBCs) |
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MHC Class II--Extracellular pathogens
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Exogenous (lysosomal) Ag processing path
Recognized by helper T cell in TCR and CD-4 coreceptor Expressed ONLY ON APC'S (macrophage, DC, B cells) |
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One type of Humoral Immunity: Complement system needs what protein most to be activated?
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C3--infection activation of complement always leads to C3 cleavage into C3a and C3b
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Functions of C3a and C3b in complement system?
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C3a recruits phagocytes
C3b fixated to bacterial surface--tag for destruction!!!! |
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s/p C3b fixation to bacterial surface, the bacteria is tagged for destruction. Name things that occur s/p C3b tag.
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1. Recruitment of inflammatory cells
2. Opsonization and phagocytosis--CR1 receptor on macrophages love C3b ligand!! 3. Perforation of pathogen membrane |
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Lack of Factor I (prevents uncontrolled numbers of C3 convertases from forming on MICROBIAL surfaces--nlly part of regulation of complement deposition)
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Increased numbers ear infections, abscesses caused by encapsulated bacteria
No factor I Too little C3b on bact. surface Less phagocytic clearance |
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DAF and MCP are regulators of complement activation. Prevent what?
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Prevent activation of complement on membranes of HUMAN cells
Some bacteria, i.e. Staph. aureus, Strep. pyogenes, cover surfaces with Sialic acid--inhibits Factor H and disrupts C3 convertase activity (blocks complement activation pathway like MCP DOES ON HUMAN CELL SURFACES :) |
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MAC
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C5-C9, form pore and lead to cell destruction
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C9 molecule of MAC blocked by
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CD 59 (protectin), HRF
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Complement-mediated lysis of RBCs
Paroxysmal Nocturnal Hemoglobinuria caused by? |
Lack of MAC formation regulators! impairment in glycosylphosphatidylinositol lipid tail formation leads to lack of DAF, CD59, HRF!!!!
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MAC formation problem in pt leads to susceptibility to ...
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Neisseria gonorrhoeae
Neisseria meningitidis |
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Anaphylatoxins , C3a and C5a..
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incr inflammation at site of Complement activation--cause blood vessels to be more "leaky"
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Lack of Factor D or Properdin (of Alternative and Lectin pathways of complement activation) makes pt susceptible to...
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Neisseria meningitidis and other neisserial infections!!
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Deficiency in C3 (of complement activation) leads to susceptibility to ..
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pyogenic infections (pus forming) think neutrophils
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Deficiency in MBL
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associated with recurrent infections
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Classical pathway of complement activation: Deficiencies of C1q,r,s, C4, or C2 leads to ..
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Susceptibility to immune complex diz's
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Formation of MAC:
Deficiency in C5-C9 (only one) |
Neisseria meningitidis and other neisserial infections
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Regulation of complement act. and MAC formation:
Lack of DAF and MCP |
Paroxymal nocturnal hemoglobinuria
Unregulated complement activation occurs on RBC Hemoglobinuria most pronounced in AM!! (morning) |
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Regulation of complement act. and MAC formation:
Lack of C1 INH |
Hereditary angioneurotic edema
uncontrolled, pathologic activation of C1 production of vasoactive protein frag.s leakage of fluid (edema) in larynx and other tissues (gut) |
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TLR 4-MD2-CD14-binds LPS (on gram negative bact.) causes what in macrophage?
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TLR 4 receptor binding (on macrophage) to LPS (on gram neg. bact) activates MyD88-->kinase cascade-->activation of transcription of NFkappaB factor--> gene transcription of Cytokines-->secretion of inflammatory cytokines (mainly TNF-ALPHA) from macrophage!
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TLR 4 activation leads to secretion of inflammatory cytokines (mainly TNF-ALPHA) from macrophage and what other route can it take?
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TLR4 bound to TRIF-TRAM -->IRF3-->syn. and secretion of type I interferons: IFN alpha and IFN beta!
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TNF-alpha (induced by LPS bound to TLR-4 then NFkappaB) secreted from macrophage, causes inflammation and...
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local effect leaky blood vessels
Systemic effect: Shock, fever!!! SEPTIC SHOCK if TNF-alpha gets into bloodstream (secreted into blood by liver and spleen macrophages!) |
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What 3 cytokines (syn.ed and secreted from macrophage via NFkappaB stimulation) cause the systemic effect, Fever?
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IL-6 (acute prod. of liver cells)
TNF-alpha IL-1beta |
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Chronic Mycobacterium avium infections and chronic viral infections, severe bact. infections despite vaccinations, see a blockade in transcription of genes activated by ...
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NFkappaB
all sx caused by mutation in NFkappaB essential modifier gene NEMO lack IKK Subunit! |
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Which cytokine induced for secretion from macrophage via NFkappaB attracts neutrophilic infiltrate into area?
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CXCL8
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Pt has Staph. aureus or Strept. pyogenes, large activity and concentration of what granulocyte seen?
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Neutrophils! they enter tissues by process of extravasation
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Acute inflammatory response
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bacteria enter CNS (meninges)
Macrophages and fibroblasts--secrete IL-1, IL-6, TNF-alpha, CXCL8, chemokines-->changes in endo. cells, expression of adhesion molecules-->influx of NEUTROPHILS! |
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Acute inflammatory response evidence seen in blood...
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1. Leukocytosis "Left shift" younger neutrophils mobilized from bone marrow to blood!
2. Exhaustion of bone marrow neutrophil precursors-->crash in WBC count ! |
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Chronic Granulomatous Diz (CGD)
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No functional NADPH oxidase made by phagocytes!!! No hydrogen peroxide or super oxide made! Pt unable to eradicate bacteria and fungus ASPERGILLUS
Formation of GRANULOMAS seen! Non-functional Respiratory Burst response to LPS on gram negative bacteria |
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Leukocyte Adhesion Deficiency (LAD)--EXTREME NEUTROPHILIA--CD18
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1. --genetic defect in CD18, common beta chain on 3 integrins that allows phagocyte migration out of blood vessels to site of infection (inflammation).
2. fail to express LFA-1, Mac-1, CR4 (all complement receptors on phagocytes) 3. Recurrent pyogenic infections, wound healing prob.s, early death 4. massive leukocytosis with NEUTROPHILIA 5. lymphoctye HOMING NOT affected; Tcell fxn seems to be NORMAL despite lack of LFA-1 |
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Chediak-Higashi Syndrome
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1. -defect in cytoplasmic vesicle formation and trafficking--a. neutrophil and macrophage defect (can't phatocytose and kill) b. defect in endocytosis and Ag processing c. defect in cytotoxic killing via CD8 Tcells and NKcells
2. Recurrent bacterial infections 3. ALBINISM 4. Excessive bleeding (platelet dysfunction) 5. adolescents: neurological defects |
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Acute phase proteins that opsonize and activate complement...(2)
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C-reactive protein (CRP)--Pentraxin binds PC of LPS and S.pneumoniae C-polysac.--CRP triggers classical path of complement activation!!
Mannose binding lectin (MBL): Ca++dependent lectin binds mannose (carbs) on bact. surfaces |
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Hemagglutination test
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Positive test: Positive seroconversion then RBCs are agglutinated and appear "puffy" or convalescent
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Hemagglutination Inhibition test
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opposite from Hemagglutination test; "puffy" RBCs are a negative test result; aka Acute
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Test used for "new diz" to assess whether a pt has a certain Ab to a certain Ag or not.
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Complement fixation Tests
1. get rid of all pt's complement 2. add Ab-Ag reaction and specific amt of complement (if Ab to Ag is present--Complement is "fixed" 3. Add Indicator System (RBC plus antibody to RBC) Positive Test: Indicator addition binds all leftover complement--RBCs DO NOT LYSE and AB-AG PRESENT!! Positive Test: no free Hemoglobin. s/p centrifugation PELLET SEEN (PELLET POSITIVE!) |
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Process to make surface or secreted forms of Ig heavy chain ?
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Alternative splicing
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Pt. has Streptococcus pneumoniae (encapsulated bacterium). Blood tests ELEVATED IgM, no IgA or IgG. Pt is deficient in which protein?
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AID (activation-induced cytidine deaminase), enzyme that becomes fxnal s/p B cell activated by Ag.
AID converts cytosine to uracil, uracil converted to any DNA base, acts in V regions of Heavy and Light chains, causes one mutation per cell division, changes are concentrated in CDR3 of H chain. Somatic Hypermutation: rearranged v-region sequences are diversified in B-cell (s/p B cell activation by antigen!!!) |
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B cell development: stimulated by bone marrow STROMAL CELLS
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Lymphoid progenitor cell binds to stromal cell via CAM and stromal cell secretes IL-7 (which is a growth factor). As Immature B cell exits to secondary lymph tissue it only has IgM on its surface :)
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Late Pro-B cell--VDJ gene rearrangement (in bone marrow)of H-chain locus needs which proteins?
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RAG 1/RAG 2, BTK (tyrosine kinase that works in signaling), Ig alpha and Ig beta, VpreB and gamma-5 (surrogate light chain)
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Pre-B cell monitors quality of Ig H chains and causes...
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ALLELIC EXCLUSION!!!! all other recomination is inhibited at this
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What would happen without Allelic Exclusion?
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Heterogenous B-cell receptors with low-avidity (number of binding sites per Ab that bind Ag) binding.
Normal Allelic exclusion gives homogenous BCRs with high avidity binding !!!! |
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Rearrangement of L chain loci is efficient and occurs at what stage of development of the B-cell?
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pre-B cell
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Diagnosis of problems of B cell development or type of B cell tumor needs what 2 tests to be ordered?
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Flow cytometry test OR Immunohistochemistry
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RAG1 and RAG2 are proteins found at what stage of B cell development?
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Early pro-Bcell and Small pre B cell
Function: ***lymphoid specific recombinase!!! |
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Gamma 5 and VpreB serve what function?
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proteins that act as surrogate light chain in early pro-B cell
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Ig alpha, Ig beta, Btk serve what function?
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Signal transduction
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PAX-5 serves what function?
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Transcription factor expressed in Early pro-B cell
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(Btk defect in formation) Bruton's Agammaglobulinemia?
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B cell formation will arrest at Pre-B cell stage; X-linked diz; caused by defect in B cell maturation Arrest at pre-B cell stage--no Ig's made
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Burkitt's lymphoma (IgH-MYC) &
Follicular lymphoma IgH-BCL-2, both ex.'s of ??? |
B cell tumors carry chromosomal translocation involving Ig genes; translocaiton fuse part of one chromo. with another, proto-oncogenes, genes that control cell growth, division, differentiation, are fused with Ig genes
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Failure of thymus to develop...
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DiGeorge syndrome--children have no thymus--failure of embryonic development. Child has B cell but no T cells and will suffer opportunistic infections
-involution of thymus at 1 year starts then cont.s thru life. still have T cell immunity as mature T cells have long lives in the periphery still. Possible mature T cells become self-renewing |
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Loss of the thymus thru aging...
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removal of thymus due to CA does NOT affect T cell immunity in adults
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Where does T cell commitment occur?
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Thymus--T cell precursor arrives in cortex of thymus as a double negative no expression of CD4 or CD8;
--Notch 1 signaling drives toward T cell differentiation |
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Failure of Autoimmune regulator (AIRE) transcription factor -- results in ?
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Autoimmune polyendocrine syndrome; normally AIRE acts in the medulla of the thymus in negative selection of T cells; extended repertoire of peptides displayed by special epi. cells in medulla of thymus --most peptides expressed here for endocrine organs (PTH glands, adrenal glands, pancreatic islets)
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Treg (regulatory T cells) function?
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suppression of autorxn T cells by regulatory T cells (Treg) requires them to interact with the same APCs
--have TCR specific for self Ag --express CD25 and FOXP3 --secrete inhibitory cytokines: TGF-beta, IL-10, IL-35 |
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Lack of FoxP3 leads to fatal autoimmunity leads to what 4 diz? thus regulatory CD4 T helper cell cannot function properly!!!
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Immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX)
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Autoimmune polyendocrine syndrome
Sx: recurrent infections of skin, oral mucosa infected with Candida, hypoparathyroidism (tetany, seizures, laryngospasm, and leg cramps). Serum endocrine autoantibody screening reveals presence of Ab's to PTH, thyroid peroxidase, and islet cells. |
Child missing AIRE
Failure of AIRE to kill auto-reactive T-cells (in corticomedullary junction) Failure of NEGATIVE SELECTION!!!! |
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Btk (Bruton's tyrosine kinase) Deficiency
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X-linked agammaglobinemia
requires life-long tx with IgG infusion!!! |
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CD40 ligand (CD40L) deficiency
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--males make only IgM and IgD--"hyper IgM syndrome"
--no IgA, IgE, IgG |
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Activation-induced cytidine deaminase (AID) deficiency
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males AND females --"hyper IgM syndrome"
no IgA, IgE, IgG |
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Severe Combined Immunodeficiency syndrome (SCID)
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lack of functional B and T cells
--Candida Albicans infection in mouth --rash due to chronic inflammation |
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Omenn syndrome
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genetic defect results in 80% loss of RAG activity; fatal without BMT
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What are the 3 components for TCR complex?
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1. TCR heterodimer (one alpha one beta chain)
2. four CD3 molecules 3. zeta chain homodimer |
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ITAM (immunoreceptor tyrosine based activation motif)
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a conserved sequence found on TCR complex and BCR!!!
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Zeta chain homodimer of TCR complex is also FcRIII on what cells?
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NK cells and T cells :)
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Tuberculoid leprosy (lest severe) --intracellular pathogen
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strong Th1 response
Th1 regulates cell-mediated response Secretes Th1 cytokines: IFN-gamma (activates macrophages) and IL-2 (activate CD8 T cell) Th1 cell inhibited by IL-10 from Th2 cell |
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Lepromatous Leprosy (most severe)
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Strong Th2 response and reciprocal inhibition of Th1
Th2 cell: regulates humoral response (Abs made!) Secretes Th2 cytokines: IL-4 (promotes class switching to IgG and IgE) and IL-5 (promotes class switching to IgA) and IL-10 Th2 is inhibited by IFN-gamma from Th1 cell |
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Polyclonal Abs
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from person to be tested and reacted with KNOWN antigen(s)
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Monoclonal Abs
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used to detect presence of SPECIFIC ANTIGENS on/in an individual's cells
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Test used to determine presence of Rh antigens...
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RBC Agglutination (same as ABO typing) AKA Coomb's test
--Indirect antiglobulin test (indirect Coomb's test)--use mother's serum and add Anti-Rh Ab's --Direct Coomb's test: use baby's serum add Ab's to blood cell Ag that are bound to RBCs in circulation |
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Indirect Coomb's test
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No RBC agglutination seen NEGATIVE TEST: mom's serum does not have antibodies to Rh factor!
Positive test: agglutination occurs! Mom's serum has Ab's as Antihuman globulin bound Fc portion of Ab's in mom's serum and caused agglutination of RBCs !!! |
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Direct Coomb's test (direct antiglobulin test)
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to determine if baby's RBC's are coated with Ab; Rh+ neonate whose mom is Rh-neg and has made Ab's to Rh+ neonate; Result: Positive agglutination! if neonate Rh+serum already has bound maternal Ab's to is Rh+ factor then s/p addition of Antihuman globulin, POSITIVE AGGLUTINATION WILL BE SEEN
Drug induced systemic lupus erythematosus also tested this way! |
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Flow cytometry
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analysis of individual cells by cell surface marker! has Histogram
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Natural Ab's made by ?
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B1 B cells in the intestine
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Pre- and post- vaccine levels determined by ?
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EIA
--protein vaccine (diphtheria-pertussis-tetanus) DPT --Polysaccharide vaccine (pneumococcal or Haemophilus influenzae type b) HiB --Ag-specific IgM and IgG or a 4 fold rise in specific Ab titer |
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Proliferation assay
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tells whethor or not the pt's T cells are capable of activation; use of pt's lymphocytes and add mitogen (pokeweed, phytohemagglutinin, concanavalin A) or specific Ag and culture. Lymphocyte proliferation can be analyzed by flow cytometry, to reveal cell cycle analysis and cell proliferation Ag's
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