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An overview of the strategies of innate immunity in defending against intracellular and extracellular pathogens. It covers the roles of antimicrobial peptides, phagocytic cells, nk cells, exotoxins, endotoxins, tissue damage caused by infections, antimicrobial peptides like defensins, cathelicidins, and histatins, the complement system, and complement activation through the lectin, classical, and alternative pathways. The document also discusses the converging step of complement activations, complement activation products like c3a and c5a, complement membrane attack proteins, complement receptors, and complement regulatory proteins.
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destroy the pathogens before the infect cells - this uses antimicrobial peptides and phagocytic cells recognize and kill cells infected with the pathogen - this is done by NK cells TERM 2
DEFINITION 2 extracellular bacterial pathogens cause disease by releasing protein toxins.innate immune system has little defense against these. so highly specific antibodies produced by the adaptive immune system are required to neutralize their action TERM 3
DEFINITION 3 non-secreted constituents of bacterial structure that trigger phagocytes to release cytokines with local and systemic effects TERM 4
DEFINITION 4 Pathogens adhere to epitheliumnormal flora, local chemical factors, phagocyteslocal infection, penetration of epitheliumwound healing inducedantimicrobial proteins and peptides, phagocytes and complement destroy invading microorganismslocal infection of tissuescomplement, cytokines, chemokines, phagocytes, NK cellsactivation of macrophages. dendritic cells migrate to lymph nodes to initiate adaptive immunity TERM 5
DEFINITION 5 defensins, cathlicidins, histatins Cathelicins are made by neutrophils, macrophages and by keratinocytes in the skin and epithelium of the lungs in response to infection.in neutrophils they are in secondary granules Histatins - produced by parotid, submandibular, sublinqual glands. active agaisnt pathgoen fungi
when a pathogen breaches the host epithelial barriers and initial antimicrobial defenses, it next encounters the complement system.it uses opsonization, coating a pathogen by antibodies and/or complement proteins so that it is destroyed by phagocytic cells.In the absence of infection, the complment proteins circulate in an inactive form. TERM 7
DEFINITION 7 mannose binding lectin (MBL) and ficolins recognize and bind carbohydrates on pathogen surfaceuses soluble receptors that recognize microbial surfaces to activate the complement cascadeMBL/ficolin, MASP-2C4C TERM 8
DEFINITION 8 C1q interacts with pathogen surface or with antibodies bound to surfaceinitiated by activation of the C1 complex and is homologous to the lectin pathwayC1q, C1r, C1sC4C TERM 9
DEFINITION 9 C3 undergoes spontaneous hydrolysis to C3(H2O) to intiate eventual deposition of C3 convertase on microbial surfaceamplification loop for C3b formation that is accelerated by recognition of pathogens by properdinFactor DFactor BproperdinC TERM 10
DEFINITION 10 the most important step.All pathways generate a C convertase, which cleaves C3, leaving C3b bound to the microbial surface and releasing C3a
C1rC1sC2aBdDMASP- TERM 17
DEFINITION 17 C4bC3b TERM 18
DEFINITION 18 C5aC3aC4a TERM 19
DEFINITION 19 C5bC6C7C8C TERM 20
DEFINITION 20 CR1CR2CR3CR4CRig
TERM 22
DEFINITION 22 C1q - binds to pathogen surface or antibody allowing activa of C1rC1r - cleaves C1s to activate proteaseC1s - cleaves C4 to C2C4b - covalently binds pathogen and opsonizes it.C4a - peptide mediator of inflammationC2a - active enzyme C3/C5 convertase. Cleaves C3 and C5C2b - precursor of vasoactive C2 kininC3b - acts as opsonins. initiates amplification via alternative pathway and binds C5 for cleavage by C2aC3a - peptide mediator of inflammation TERM 23
DEFINITION 23 specificity - C5afunction - binding of C5a activates G proteincell types - endothelial cells, mast cells, phagocytes TERM 24
DEFINITION 24 specificity - C3afunction - binding of C3a activates G proteincell types - endothelial cells, mast cells, phagocytes TERM 25
DEFINITION 25 bacterium is coated with C3bwhen only C3b binds to Cr1, bacteria are not phagocytosedC5a can activate macrophages to phagocytose via CR