MIMM 214 Lecture Notes - Lecture 5: Basophil, Complement Component 5A, Lectin
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Lecture 5 – January 13, 2017
Regulation & Memory
Downregulation of T cells and immunological memory
MOUSE QUESTION
Memory is hallmark of adaptive immunity
- Primary response to first exposure to Ag:
o Takes time to develop
o Eventually tapers off
- Secondary exposure to the same Ag:
o Quicker response
o Stronger response
- Why?
o Memory lymphocytes
o Reactivation yields faster, more significant, better response
- Note
o Response to Ag B is a primary response
o Memory is not present in innate immunity
Summary
- Two broad mechanisms of immunity
o Innate (aka natural) Immunity:
▪ Immediately available and does not get better with exposure
▪ Mostly mediated by leukocytes other than lymphocytes (eg macrophages,
dendritic cells)
▪ No fine specificity
o Link make by DCs (or other APC) which activates adaptive cells in lymphoid tissues
o Adaptive (aka acquired) immunity
▪ Ag specific
▪ Mediated by lymphocytes (eg T and B cells)
• These cells express specific receptors
• Clonal selection
▪ Humoral and cell mediated
▪ Improves with exposure = faster and stronger
▪ Leading to immunological memory – long lasting protection
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Innate Immunity
Breach of epithelial cell layer
Local inflammation
Humoral immunity
Complement system
- Group of soluble proteins
- (mostly) proteases (>30) in blood and other fluids
o Protease: an enzyme that performs proteolysis → can break down proteins
o Mostly alled y C followed y a uer
o “oe alled fator followed y a letter
o Do’t eorize the all fro ook
- Complement proteins mostly produced by liver
- Set off a chain reaction that helps to amplify infalmmationa and clear pathogens
- Key mechanisms
o Increase vascular permeability and chemotaxis
o Destroy pathogen cell membranes
o Increasing recognition of pathogens and facilitating phagocytosis (opsonisation)
Opsonisation & Phagocytosis
- Opsonisation: the coating of the surface of the pathogen by antibody and or complement that
makes it more easily ingested by phagocytes
- Phagocytosis: internalization of particular matter by cells by a process of engulfment, in which
the cell membrane surrounds the material, eventually forming an intracellular vesicle
(phagosome) containing the ingested material
How does complement get activated?
- Initially, components are inactive pro-proteases (aka zymogens)
- Activated in 3 ways
o Classical pathway
o Alternative pathway
o Lectin pathway
- Acting as a cascade
o Proteolytic cleavage generating two fragments
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Document Summary
Primary response to first exposure to ag: takes time to develop, eventually tapers off. Secondary exposure to the same ag: quicker response, stronger response. Why: memory lymphocytes, reactivation yields faster, more significant, better response. Note: response to ag b is a primary response, memory is not present in innate immunity. Leading to immunological memory long lasting protection. Set off a chain reaction that helps to amplify infalmmationa and clear pathogens. Increase vascular permeability and chemotaxis: destroy pathogen cell membranes. Increasing recognition of pathogens and facilitating phagocytosis (opsonisation) Opsonisation: the coating of the surface of the pathogen by antibody and or complement that makes it more easily ingested by phagocytes. Phagocytosis: internalization of particular matter by cells by a process of engulfment, in which the cell membrane surrounds the material, eventually forming an intracellular vesicle (phagosome) containing the ingested material. Activated in 3 ways: classical pathway, alternative pathway, lectin pathway. Acting as a cascade: proteolytic cleavage generating two fragments, one small.