Celbiologie en Immunologie
Belangrijke info voorafgaand aan cursus
- Colleges zijn niet verplicht
- Practicum is verplicht
- Werkgroepen zijn verplicht
- BELANGRIJK: hou alles goed bij, het is namelijk veel.
Toetsing
- Tentamens zijn met meerkeuze vragen
- DT1 en DT2 gelden samen voor 80% van cijfer (het gemiddelde hiervan moet samen een 5.5
zijn, een herexamen is 1 toets van alle leerstof)
- Cmap opdracht is 20%
- DT1: 14-11
- DT2: 02-12
- DT3: 23-12 (IN HET ENGELS)
Inhoud Celbiologie
- Hoe worden processen in gezonde cellen gereguleerd?
- Hoe verloopt transformatie van gewone cel tot kankercel?
- Welke moleculaire processen zijn belangrijk bij deze transformatie?
- Hoe onderscheiden normale cellen zich van darmkankercellen?
- Hoe kan darmkanker vroegtijdig worden ontdekt?
Inhoud Immunologie
- Hoe is ons immuunsysteem opgebouwd en hoe werkt het?
- Hoe werkt adaptieve immuniteit en welke cellen zijn hierbij betrokken?
- Hoe beschermt ons immuunsysteem ons tegen infecties en op welke mechanismen berust
vaccinatie?
Werkgroep opdracht
- Concept mapping van celbiologische processen samen in een groepje van 4-6 studenten
- Maak hiervoor een werkplan, verdeel de taken, doe dit na je eerste werkgroep.
- Je doet eerst kennis op in 7 deelopdrachten (elke opdracht wordt gemaakt door twee
personen), deze kennis draag je over aan elkaar
- Deze kennis ga je vervolgens bundelen en integreren in een celmodel (CMap)
- Hiervoor lever je de PowerPoints in over alle deelopdrachten en daarnaast de CMap.
,Introduction and innate immunity
IMM1 – H1 tm H3
Hst 1: 1.3-1.7, 1.10-1.12; Hst 2: 2.2-2.3, 2.6, 2.7 (MAC functie), 2.8
Hst 3: 3.1-3.2 (t/m Fig 3.3), 3.4, 3.7 (niet RLR en signalering), 3.12, 3.14 (Fig. 3.26/28), 3.15-3.17
Elements of the immune system and their role in defense: Complement proteins, Cells & Receptors
Your immune system needs to see the difference between self and non-self and harmless and
harmful cells and removes and renews old/infected cells.
Self-harmless: our own cells and organs that act normally.
Self-harmful: cancer cells, they multiply too fast.
Non self-harmless: microbiome, animals. → if you do react you are allergic
Non self-harmful: pathogens
There is a delicate balance between immune-activation (inflammation) and -inhibition (tolerance). A
disbalance in immunity can cause disease:
When your immune system attacks self-harmless cells you speak of auto immune disease.
When your immune system does not attack self-harmful cells you develop cancer.
No reaction to non self-harmful cells can lead to death/
A reaction to non self-harmless cells can lead to allergy.
1.3 Physical Barrier
Physical barriers form the first line of defense against pathogens (you do not need to learn the
specifics).
Skin is an epithelium (line of cells) that protects from infections. Epitheilia that are in line with the
respiratory tracts are impermeable and is covered in mucus. It leads the way to specialized tissues
that communicate with the environment. These surfaces also secrete antimicrobial substances that
kill bacteria, fungi and viruses by perforating their membrane.
1.4 Innate immune response and inflammation
The innate immune system forms the second line of defense. When you have inflammation, your
innate immunity is working. Some properties of the innate immune system are:
- Rapid response
- Fixed (gebeurt op een bepaalde manier en niet anders)
- Limited number of specificities
- Constant during the response
Examples of the innate immune system are:
- macrophages
- neutrophils
- Complement proteins
- NK cells
,Cytokine: signaling molecule for activation of immune system
Chemokine: signaling molecule for migration (google maps of immune system)
The complement system plays an important role during inflammation through bacterial infection.
Your complement system complements ongoing inflammation and consists of plasma proteins with
enzymatic activity. The innate immune response consists of 2 phases: recognition and response.
1. Proteins on cell-surface receptors present that the pathogen is ready.
2. Once recognized, effector mechanisms are recruited to kill the pathogen.
You do not have to know all complement proteins; one you do need is C3. Complement proteins
guide the effector cells. They do this by tagging pathogens.
The 3 ways to activate C3 are important to know. It is splitted into:
C3a: immune cell recruitment
C3b: pathogen binding for phagocytosis and lysis (it marks the pathogen)
C3a can enhance inflammation within minutes through activation of endothelium and immune cell
recruitment. It can increase the permeability of the blood vessel; this has the following
consequences:
- Complement proteins and other plasma proteins enter infected tissue.
- Leukocytes (white blood cells) enter the infected tissue. Resident macrophages are activated.
, 1.5: The adaptive immune response builds on the innate immune response
Some infections outrun the innate immune response. The innate immune response will then still
minimize spread of infection while enlisting lymphocytes (white blood cells). These are active in the
adaptive immune response.
The adaptive immune system forms the third line of defense. It works when your body encounters
cells it has never seen before. Some properties are:
- Slow response
- Variable
- Numerous highly selective specificities
- Improve during course of response
The important difference between innate and adaptive immunity is in the receptors that
lymphocytes use to recognize pathogens.
The receptors of innate immunity are structurally of many different types. Each receptor recognizes
molecular features shared by groups of pathogens, and none is specific for a particular pathogen. On
the other hand, the lymphocytes of adaptive immunity recognize pathogens using only one type of
cell-surface receptor, but this is made in billions of different versions.
The adaptive immune response becomes specific for a particular pathogen by including only
lymphocytes expressing a receptor that recognizes the pathogen. Lymphocyte receptors are not
encoded by conventional genes, but by genes that are cut, spliced, and modified during lymphocyte
development.
Because activation and proliferation of pathogen specific lymphocytes (white blood cells) takes long,
the reaction of the adaptive immune system takes long. They clone to expand, one become many.
There are different kind of lymphocytes:
- T-lymphocytes: involved in the cellular immune response
- B-lymphocytes: involved in humoral immune response
- NK-cells: part of innate immunity, will be further explained
Primary lymfe organs: development of adaptive immune cells.
- Bone marrow: B-cells IMM6
- Thymus: T-cells IMM2
Secondary lymfe organs: activation of adaptive immune cells
- Lymfe nodes IMM3
- Spleen
- Gut associated Lymphoid tissues GALT cells form the cellular defense, B cells produce
antibodies: the humoral defense. Differentiation and growth of cells to T cells (IMM2/3) B
cells (IMM5-7).
The difference between humeral and cellular is that within the cellular defense there are white
blood cells that kill pathogens through fagocytose, and within the humoral defense antibodies in the
blood can bind to antigens on the pathogen so the cell will be killed.
