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Lecture 11

BIOL442 - Lecture 11 - Immune.pdf

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Department
Biology
Course
BIOL 442
Professor
Christine Dupont
Semester
Winter

Description
Set 11 ImmuneInnate DefensesFirst line of defenseMost are based on recognition of broad molecular motifs found commonly in pathogensPAMPs pathogenassociated molecular patternseg bacterial cell envelope molecules eg peptidoglycan mannose foreign nucleic acid unmethylated CpG dinucleotides dsRNACan act quickly to rid the infection before adaptive response occursInnate mechanisms signal the adaptive response to beginThe Inflammatory ResponseA sequence of physiologic events triggered by an invading microbe andor damage to tissueInvolves the followVasodilationIncrease in the diameter of the capillariesBrings more blood to site and thus more defense cells and moleculesRedness and increase in temperatureProstaglandins and histamine are important effector molecules of vasodilation mast cellsIncrease in permeability of the vessel wallsAllows extravasation or movement of cells with immune function out of the blood vessels and into affected tissues Accompanied by fluid movement into the local tissueEvidenced by edema swelling of the local areaCarries serum components such as antibodies and complement factors into the areaProduction of cell adhesion molecules CAMsVasodilationsincreased permeability passively bring in cells and serum to site Inflammation induces the vessel walls endothelium to produce surface cell adhesion molecules CAMsCAMs bind to leukocytes mostly phagocytes from the blood allowing them to adhere to the interior vessel walls to facilitate extravasation activeBegin to clean up the foreign bodies and damaged cellsAs immune cell concentration increases they produce more mediators of inflammationviruses that do not cause a lot of cell death noncytolytic do not cause significant inflammationMolecules Complement Type I Interferons alpha betaComplementGroup of more than 30 secreted serum proteins involved in the binding and disruption of microbial membranesExist as inactive precursor proteins in the bloodWhen activated one complement factor acts on another in a sequential manner resulting in cleavageEnd result is formation of the membrane attack complex MAC which leads to disruption of the membrane envelopeComplement factors also influence inflammatory and immune responses eg C5a3 pathways classical alternative lectinbindingC3 inactive gets spontaneously hydrolyzed in serum to form C3z and C3bBinds to membranes cells have counteractive measures bacteria and enveloped viruses do notTLRsRecently discovered 1990sCell receptors that bind a variety of PAMPs New Section 1 Page 1
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