College aantekeningen immunologie deeltoets 1 (AB_1132)
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Course
Celbiologie en immunologie (AB_1132)
Institution
Vrije Universiteit Amsterdam (VU)
Dit document bevat aantekeningen van alle college's voor deeltoets 1 van het vak celbiologie en immunologie, en kan dus gebruikt worden als samenvatting. Ik had een 7,4 voor het tentamen!
Celbiologie en immunologie
IMM 1
Intro: immune system & defense
Self vs non-self and harmless vs harmful
--> non-self harmful & self harmful
Balans tussen activation (inflammation) and inhibition (tolerance)
A sysbalance in immunity can cause disease
Need to know what the right balance is, how it's achieved and wat causes dysbalance
Aller eerste waar pathogeen mee moet dealen is huidbarrière --> pH van huid is zuur
Geen vragen over details huidbarrière
Innate immune system is tweede rang, ook bij ontsteking
Effector cell = macrofagen
--> produceren signaalmoleculen: cytokines (zetten een receptor aan) & chemokines (alleen
gebruikt om te zorgen dat cellen weten waar ze naartoe moeten, google maps --> hoe
dichter bij infectie hoe meer chemokines)
Cytokines zorgen dat epitheelcellen lek worden
Ontsteking wordt rood omdat vaten lek worden, en dik omdat de cellen bezig zijn
Innate iummunity:
Rapid response within hours
Fixed
Limited number of specifities
Constant during the course of response
Addaptieve immuunsysteem is derde rang (niet altijd: geheugencellen)
Hebben receptoren --> variabele regio: meerdere receptoren kunnen gemaakt worden
Clonal expansion: van één receptor naar heel veel, kost tijd
Addaptive immunity:
Slow response in days to weeks
Variable
Numerous highly selective specifities
Improve during the course of response
Development and activation occurs in lymphoid tissues
Rode deel = primaire --> development of adaptive immune cells --> ontstaan ook cellen
tegen eigen cellen
--> bone marrow: B cells, Thymus: T cells
, Gele deel = secondary --> activation of adaptive immune cells
--> lymph nodes, spleen, Gut Associated Lymphoid Tussues (GALT)
T cellen: altijd interactie met andere cellen
--> form cellular defense
B cellen: interactie met T cellen
--> producing antibodies (antilichamen: zorgt voor neutralisatie, neutraliseert effect van
pathogeen), the humoral defense
Kan niet leven zonder innate immunsysteem of adaptive immuunsysteem
Collaboration:
1. Activation of adaptive immunity by innate dentritic cells
2. Specific activation of innate immune cells by adaptive immunity: T cells and antibodies
Immune cells arise from two common progenitors during hematopoiesis:
Myeloid (monocyten: macrofagen, dendritische cellen) & lymphoid (B-cellen, CD8, NK cellen)
Lymphocytes include T cells, B cells and NK cells
Hematopoiesis is the development of immune cells --> two common precursors for
lymphocytes (adaptive, except NK cells) and myeloid cells (innate)
The complement system
Complements ongoing inflammation
Bestaat uit plasma eiwitten met enzym activiteit
Meest belangrijke factor is C3
Activated upon cleavage for tag & recruit (C3a & C3b, enzymatic reaction)
--> C3a: anaphylatoxin, immune cell recruitment (vaak inactief in plasma)
--> C3b: complement fixation, pathogen binding for phagocytosus and lysis
Phagocytis and destruction pathogen
Anaphylatoxins (C3a) werken als trigger voor endotheelcellen, en halen effector cellen van
bloed
Complement fixation:
Recruited immune cells express complement receptors (CR)
--> Efficiently bind opsonized C3b
CR-C3b binding induces pathogen uptake by phagocytes
--> Endo- or phagocytosis
Degradation via fusion with acidic lysosomes
Drie routes die kunnen lijden tot complement fixation:
1. Alternative pathway
First, a soluble C3 convertase is activated via C3 hydrolysis followed by binding and
cleavage of an additional complement factor
Next, opsonized C3b is used to form membrane bound C3 convertase
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