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39 Cards in this Set
- Front
- Back
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Antigen |
Any substance capable of triggering an immune response |
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Epitopes |
An antigen announces its foreigners by means of intricate and characteristic shapes called epitopes Polysaccharides Protein |
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Characteristics of the skin |
Tough
Thick Dry Salty Oily High in fatty acid Low in nutrients |
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Innate Immune Response (Inbuilt immunity to resist infection) |
Not antigen-specific
Not enhanced by second exposure Has no memory Uses cellular and humoral components Poorly effective without adaptive immunity Triggers & amplifies the adaptive immune responses |
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Innate Immune response 2 |
Line of defences that the body uses no matter what the invader may be Responses need to be rapid Defences include Inflammation Phagocytosis |
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Adaptive Immune Response (Immunity established to adapt to infection) |
Learnt by experience Confers pathogen-specific immunity Enhanced by second exposure Has memory Uses cellular and humoral components Poorly effective without innate immunity |
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Inflammation |
Heat Swelling Redness Pain Loss of function |
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Function of Inflammation |
Destroy and remove pathogens If destruction is not possible , to limit effects by confining the pathogen and its products Repair and replace tissue damaged by pathogen and its products |
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Chemotaxis of Phagocytes |
Phagocytic neutrophils respond to soluble factors Chemotactic signal molecules are generated at or near the source of infection Cells migrate from the blood into the tissue underlying the infection along a concentration gradient towards the area of highest concentration |
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General scheme of an immune response |
Pathogen with non-elf proteins damages the epithelium to break through the epithelial barrier Epithelial cell 'activated ' upon contact with microorganism Soluble proteins (chemokines, cytokines: chemical alarm system) are made by activated epithelial cells |
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Innate Immunity |
Pathogen recognised by receptors encoded in the germline Receptors ave broad specificity (recognise PAMPs) Immediate response No memory of prior exposure |
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Adaptive Immunity |
Pathogen recognised by receptors generated randomly (BCR and TCR) Receptors have very narrow specificity Slow response Memory of prior exposure |
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PAMPs |
Lipopolysaccharide Lipoteichoic acid Peptidoglycan Bacterial flagellin Baterial DNA Viral DNA or RNA Viral capsids / proteins |
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Antibodies (Immunoglobulins) |
Y-shaped protein molecule Produced by B-lymphocytes Heavy and light chains Disulfide bridge Variable regions Constant regions |
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Cytokines and Chemokines |
Diverse collection of soluble proteins made by cells that affect the behaviour of other cells |
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Cell - cell contact |
Peripheral lymphoid tissues trap antigen - containing phagocytic cells and concentrate cells together to promote cell-cell contact |
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Phases of an adaptive immune response |
Recognition Activation Effector Decline homeostasis Memory |
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Acute Inflammation |
Fast onset Short response Main cellular component: Neutrophils Tissue injury in mild Prominent local and systemic symptoms |
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Chronic inflammation |
Slow onset Prolonged response Main cellular component: Monocytes/ macrophages, lymphocytes Often accompanied by severe tissue injury Attempts to repair the damage |
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Inflammation |
A protective physiological response aiming to eliminate harmful agents restore normal tissue function |
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The main cellular participants in inflammation |
Macrophage Neutrophil Mast cells |
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Phagocytosis |
Recognition and attachment Engulment Microbe ingested in pahgosome |
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The inflammatory response |
Bacteria trigger macrophages to release cytokines and chemokines Vasodilation and increased vascular permeability cause redness, heat and swelling Inflammatory cells migrate into tissue releasing inflammatory mediators that cause pain |
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Cytokines |
Small secreted proteins Released by different cells in response to activating stimuli Bind to transmembrane cytokine receptros on the target cells Act in autocrine, paracrine and endocrine manner Orchestrate and mediate immune responses IL-1beta, IL-6, IL-12 and TNF-alpha |
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Chemokines |
Chemotactic cytokines Induce directed chemotaxis in responsive cells in a paracrine manner First chemokine cloned and characterised was CXCL8 CXCL8 is associated with inflammation, secreted by macrophages Chemokines released by phagocytes |
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Neutrophil extravasation |
Neutrophils rolling Integrin activation Stable adhesion of neutrophils to endothelial cells Diapedesis through the vascular endothelium |
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What causes cancer? |
Hereditary cancers - Germline mutation Sporadic cancer -Somatic mutation |
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Cancer risk factors |
Smoking Lack of physical activity Alcohol High fat diet High percentage of processed meat and burnt food Obesity Oral contraceptives |
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The hallmarks of cancer |
Tissue invasion & metastasis An inflammatory microenvironment Insensitivity to growth inhibitors Self sufficiency in growth signals Limitless replicative potential Sustained angiogenesis Evasion of apoptosis |
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Transformation of normal cells |
Altered morphology Loss of contact inhibition Ability to grow without attachment to solid substrate Ability to proliferate indefinitely Reduced requirement for mitogenic growth factors High saturation density |
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Proto-oncogenes |
Regulate the proliferation pathways in normal cells |
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Tumour supressor genes |
Induce cell cycle arrest and apoptosis in response to exposure to harmful agents |
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C-MYC Oncogene |
Insertional mutagenesis ALV provirus is inserted into c-myc which is transcribed to produced myc mRNA Translation of this protein induces uncontrolled proliferation |
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HER2 Oncogene |
Epidermal growth factor receptor Gene amplification of the HER2 gene occurs due to protein overexpression of the HER2 receptor this leads to uncontrolled proliferation |
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RAS Oncogene |
Point mutation G-T, Gly-Val Prevents GTP in the protein cycle from being released which results in the protein being continuously active and uncontrolled proliferation take place |
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BCR-ABL Oncogene |
Chromosomal translocation t (9.22) abl and bcr become juxtaposed and upon transcription the bcrabl fusion protein becomes stuck in the chromosome this activates a nuclear kinase which results in cell proliferation |
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Tumour supressor genes + Tumour supressor proteins |
RB RB1) APC PT53 |
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From primary tumour to metastasis |
Primary tumour formation Localised invasion Intravasation Transport through circulation Arrest in microvessels of various organs Extravasation Formation of a micrometastasis Colonisation |
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Carcinoma progression |
Hyperproliferation Adenomatous polyps Severe dysplasia Adenocarcinoma Cancer |
