Lecture 19: B Lymphocytes and Antibodies Flashcards
Features of cytokines?
- Small glycoproteins
- Synthesized de novo
- Affect target cells via specific membrane receptors
- Paracrine or autocrine, some endocrine
Properties of cytokines?
- Pleiotropic: Dont have specific site of action (multiple action)
- Redundant: Multiple cytokines do same shit
- Synergistic
- Antagonistic
Innate cytokines
-IFN alpha beta and gamma: Interfere with viral replication
A and B: transient virus resistance; on NK cells causes them to kill virus infected cells
-IL-1, IL-6 and TNK-a: pro inflammatory (esp bacterial). Wound healing and tissue repair (fibroblast proliferation, bone resorption, prostaglandin and collagenase synthesis)
Adaptive cytokines
Antigen specific responses (don’t learn details)
IL-1: T cell and B cell activation
IFN y: antiviral, macrophage activation, NK cell activation, MHC up regulation
IL-2: T cell prolif, NK cell activation
IL-4,5,6: B cell diff, antibody class switching
Chemokines
Direct cells around the body
IL-8: attracts neutrophils
Haematopoietic cytokines
Involved in signalling in bone marrow to create lineages of particular blood cells.
G-CSF, GM-CSF
IL-3 multi lineage
Antibody structure
See page 136 in BII course book
Antibodies at birth
Receive some IgG at birth and IgA from colostrum
IgG increases again after a few months
B cell clonal activation
- In secondary lymphoid organs
- Antigen binds to specific sIg
- B cell expressed antigen on class 2 MHC
- Th cell binds with co stimulator (CD40 and CD40-L)
- Cytokine release
- Differentiates and proliferates into plasma cells and memory cells
Antibody effects (4) elaborate
- Blocking and neutralisation: attachment and entry of virus/bacteria; mainprotective effect of IgA; toxins; immobilises bacterial flagella
- Agglutination: clumping to assist phagocytosis. Graph where antibody excess, then equivalence (large lattices) to antigen excess, smaller lattices
- Opsonisation: Fc regions binds to Fc receptor on phagocytic cell enhance phagocytosis (e.g IgG)
- Antibody dependent cellular cytotoxicity
- Complement activation Fc region binding also
Complement activation (classical)
Antibodies bid to bacterium
Early complement components bind to CH2
This causes enzymatic cleavage of C3 by C3 convertase
C3a causes vasodilation an chemotaxis
C3b opsonisation and s a part of late complement: part of assembly for membrane lysis with late complement (membraneattack complex) and C5a (chemotaxis also)
Alternative pathway
Complement components bind to pathogen surface, form C3 convertase
Cleaves C3 to C3a and C3b
C3a- vasodilation and chemotaxis
C3b- Opsonisation, focus for late complement components for membrane lysis
IgM and IgG in the primary and secondary responses
IgM: First antibody in primary(lower) response. Same height and less involved in secondary
IgG: Second in primary response, far higher and occurs first in secondary response
IgM features
\_\_\_\_\_ antibody molecule (pentamer) Mostly in blood and lymphatics First in \_\_\_\_ response Very effective \_\_\_\_\_\_ Efficient \_\_\_\_\_\_ activator Important defence against blood borne spread such as bacteria
Largest antibody molecule Mostly in blood and lymphatics First in primary response Very effective agglutinator Efficient complement activator Important defence against blood borne spread such as bacteria 10%
IgG features
\_\_\_\_ monomer 70-75% Diffuses to \_\_\_\_\_\_ spaces Potent \_\_\_\_\_ antibody (neutralisation) Good versus \_\_\_ infection Actively transported in \_\_\_\_ Good complement activator Strongly bound to \_\_\_\_ (opsonisation)
Small monomer 70-75% Diffuses to extravascular spaces Potent antitoxin antibody Good versus viral infection Actively transported in placenta Good complement activator Strongly bound to phagocytic
