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56 Cards in this Set
- Front
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Innateor natural immunity |
Available quickly Not specific to the pathogen in question Prevents entry of pathogens Separates the inside of the human bodyfrom the outside (Structuralbarriers-Skin, Cough reflex, Sneeze, Mucus,associated cilia ,Ear wax) |
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Acquiredor Adaptive immunity |
Specific reaction to one pathogen doesn'tprotect from another Large scope- lots of invaders can be targeted,some that don't even exist yet Can discriminate from self Has memory |
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Leukocytes |
White blood cells. All have CD45+ Granulocytes, Monocytes, Natural Killer Cells, and Lymphocytes |
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Sentinel Cells |
Cells in the body's first line of defense, which embed themselves in tissues such as skin Macrophages, Mast cells, and Dendritic cells |
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Granulocytes |
Namedfor staining of granules using Wright’s stain All are CD15+ Neutrophils, Eosinophils, and Basophils |
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Neutrophils |
Neutral colored granulocytes 50-70% of leukocytes in blood Primary functions: Phagocytosis -first cell at an infection and antigen presentation |
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Eosinophils |
Red colored granulocytes 1-3% of leukocytes in blood Primary functions: Allergic and anti-parasitic responses |
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Basophils |
Blue colored granulocytes 0.4-1% of leukocytes in blood Primary function: Not completely defined but have a role in allergy and anti-parasitic responses |
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Monocytes |
4-6% of leukocytes found in blood CD14+ Phagocytosis and antigen presentation Macrophage when it's a sentinel cell |
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Mast Cells |
Sentinel cell primary cell in allergy and anti-parasitic responses receptor for IgE |
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Dendritic cells |
Sentinel cell Phagocytosis and antigen presentation CD11c+ |
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Natural killer (NK) cells |
2-3% of leukocytes and 10-15% of the lymphocytes Kills tumor cells, virally infected cells some bacteria and protozoan CD56+, CD16+, CD3-, and receptor for cytokineIL-2 |
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Lymphokine-activated killer (LAK) cells |
Present only when NK cells are activated Improved NK cells |
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Macrophages |
Monocytes found in tissues Innate functions include: microbialkilling, anti-tumor activity, intracellular parasite eradication, phagocytosisand secretion of cell mediators Life span can be several monthsD |
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Macrophage: Kupfer cells |
Found in Liver |
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Macrophage: microglialcells |
Found in Neuraltissue |
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Macrophage: histioccytes |
Found in Connective tissue |
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Macrophage: osteoclasts |
Found in Bone |
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Macrophage: mesangialcells |
Found in Kidney |
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Macrophage: alveolarmacrophage or dust cells |
Found in Lungs |
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Macrophage: foam cells |
Found in Heartdisease |
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NK cells kill by |
Make direct contact with their target (secrete perforins and granzymes) Antibody directed cellular cytotoxicity(ADCC) (surfaceCD 16 binds antibody coated target cells) |
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Molecules of innate immune system |
Patternrecognition receptors Themolecules produced in response to the infection (cytokines, antimicrobialpeptides, and acute phase reactants) Complementproteins |
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Pattern Recognition Receptors (PRRs) |
Recognize surface molecules expressed ingroups of microorganisms On cell surface or molecules in solution •Cellsurface •Involvedin phagocytosis and cytokine release •12types of Toll-like receptors (TLRs) -Each binds to a different PAMP -Binding causes inflammation, immunecell proliferation and chemotaxis in solution – acute phase proteins |
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Pathogen-associatedmolecular patterns (PAMPs) |
Molecules recognised by PRRs •Bacterialand viral unmethylated DNA containing increased levels ofCpG •Surfaceexpression of terminal sugar mannose •Fungalassociated saccharides•Lipopolysaccharides(LPS) of gram negative cell wall •Peptidoglycansand lipotechoic acids of gram-positive cell walls •Bacterialflagellin •Aminoacid N-formylmethionine found in bacteria •Doublestranded and single stranded viral RNA |
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Acute phase proteins |
Proteins whose concentrations change withinflammation May cause the inflammation associatedincrease in erythrocyte sedimentation rate (ESR) Production stimulated by cytokines Produced in response to infection |
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Effector molecule |
A small molecule that selectively binds to a protein and regulates its biological activity. Cytokines, Antimicrobial peptides, Acute phase proteins, and Complement |
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Antimicrobial Peptides |
Targets or recognizes bacterial cell walls of the microbe increase membrane permeability to kill pathogen. Producedby epithelial cells and phagocytes Protect at epithelial surface Ex. Defensins and cathelicidins |
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Acute phase protein: C-reactive protein |
Activates complement Is an opsonin Enhances cell-mediated cytotoxic effects on the pathogen |
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Acute phase protein: Alpha-1 acid glycoprotein |
Binds drugs and hormones and inhibits their function |
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Acute phase protein: Fibrinogen |
Forms clot |
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Acute phase protein: Serum amyloid A |
Binds cholesterol for clearance Recruits enzymes to digest the extracellular Chemotactic |
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Complement |
25 serum proteins involved ininflammation, opsonization, chemotaxis, lysis of cells Three pathways of activation Differ in formation of C3 convertase (Afterthis all pathways are the same) |
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Classical pathway |
Only functions with antibody bound toantigen so linked to the acquired immune system |
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Alternative pathway |
Begins with spontaneous hydrolysis ofsome of the C3 that is in the serum This C3 may bind to surfaces of bacteria,fungi, viruses, or tumor cells and subsequently bind the next molecules of thepathway |
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Lectin pathway |
Binds mannose on the surface of pathogens Cleaved C4 binds to C3 and thuscomplement is activatedm |
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Processes of innate immune system |
Inflammation, Chemotaxis, and Phagocytosis |
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Three pathways of Complement |
Classical, Alternative, and Lectin |
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Lymphocyte |
Tand B cells 20% of circulating white blood cells Almostall nucleus Arisefrom hematopoietic stem cells |
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B-cells |
Lymphocytes matured in bone marrow Produce antibody in response to theantigen specifically binding to the surface immunoglobulin on the B cell Characterized by this surfaceimmunoglobulin and by the presence of the surface molecules CD 19, 20, 21 Can respond to soluble antigen |
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T-cells |
Lymphocytes matured in thymus Respondto antigens bound to their TCR CD3+ |
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HelperT cells |
Products are cytokines that canupregulate the immune response Respond to a specific antigen bound totheir TCR and the MHC class II molecule of the APC CD4+ |
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Tcytotoxic cells |
Product is direct cytotoxicity of cellsbearing the antigen Respond to a specific antigen bound totheir TCR and the MHC class I moleculeof the APC CD8+ |
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RegulatoryT cells |
Product cytokines that downregulate theimmune response Bind to their specific antigen throughtheir TCR in MHC class II molecules of the APC or sometimes in MHC class I ofAPC usually CD4+ Maybe CD8+ FoxP3+ |
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Primarylymphoid organs |
Where lymphocytes mature into T and Bcells andNK cells Bone Marrow and Thymus Antigen contact results in cell death viaapoptosis |
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Secondarylymphoid organs |
Where lymphocytes meet antigens Bcells make antibody and Tcells making cytotoxic or helper response. Antigen brought to lymph nodes by phagocytic cells Lymph nodes, Spleen, Tonsils , Mucosal-associated lymphoid tissue (MALT), and Skin-associated lymphoid tissue (SALT) |
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Bone Marrow |
Contains: Hematopoietic stem cells—can be any bloodtype, Macrophages, Stromal cells, Connective tissue, Adipocytes |
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Thymus |
Lymphoidprogenitor cells enter from bone marrow at cortex. Become immature thymocytes, corticalepithelial cells, and macrophages Firststep in their maturation, T cell receptors develop that have either ab chains or g dchains |
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Disorders of Neutrophils |
Chediak-Higashi syndrome, Chronicgranulomatous disease (CGD), Complementreceptor 3 (CR3) deficiency, Myeloperoxidasedeficiency, and Specificgranule deficiency |
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Chediak-Higashi Syndrome |
•Giant lysosomes that stain gray green inneutrophils •Failure of lysosome and phagosome fusion•Impaired intracellular killing •Frequent pyogenic infections •Platelet dysfunction >> increasedbleeding•Partial albinism •Photophobia •Death at early age •rare autosomal recessive |
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Chronic Granulomatous Disease |
•Appear normal •Defective activation of membrane NADPHoxidase – unable to generate oxidative burst in phagosome to kill pathogen •Recurrent infections in lungs, bone,liver•Granuloma formation due to chronic T cellstimulation •Laboratory Diagnosis – both negative withCGD Nitroblue tetrazolium reduction test (NBT)-detects peroxide formation by reduction of the dye to a black formazan deposit |
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Myeloperoxidase Deficiency |
•Cellsappear normal •Absenceof myeloperoxidase •Defectiveintracellular killing •Increasedbacterial and fungal chronic infections in people with other underlying disease(diabetes) •Lesssevere than CGD |
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Leukocyte Adhesion Deficiency |
•Cellsappear normal•Absenceof LAD-1 (deficiency of β2-integrin subunit) and LAD-2(failure of transporter function) Failure of diapedesis •Frequentbacterial and fungal infections•Impairedwound healing •Autosomalrecessive |
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Abnormalities of macrophages |
Gaucher’sDisease and Niemman PickDisease |
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Gaucher’sDisease |
Qualitative abnormalities rareautosomal lipid storage diseases Deficiency of the enzyme glucocerebrosidaseleads to accumulation of lipid glucocerebrosidewithin lysosomes of macrophages Foundin bone marrow, spleen, other organs (not in circulating blood) |
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Niemman PickDisease |
Deficiency of one of catabolicenzymes (sphingomyelinase) involved in breakdown of sphingolipids Produces foamy macrophages |
