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Printable Handouts
Navigable Slide Index
- Introduction
- Manifestations of inherited complement deficiency
- Pathway-specific differences in presentation
- Typical infections in complement deficient patients
- Elimination of pathogens by complement
- Risk of lupus in complement deficient patients
- C4 gene copy number and risk of lupus
- Disposal of apoptotic debris mediated by C1q and C4
- Disposal of circulating immune complexes via erythrocyte receptor for C3b
- C3 deficiency reversed by liver-kidney transplantation
- Pathogen evasion of complement
- Renal tubule cell infected by uropathogenic E.coli
- Methods of complement evasion (1)
- Methods of complement evasion (2)
- Diseases Mediated by complement
- Diseases involving complement overactivity (1)
- Diseases involving complement overactivity (2)
- SARS-CoV-2 and hyperinflammatory syndrome
- Transplant rejection
- Locally synthesised complement and graft survival
- Effect of local C3 synthesis on post-ischaemic injury
- Complement enhances anti-donor T cell response
- Complement essential for antibody-induced rejection
- Link between complement and coagulation
- Cross-talk between complement and coagulation
- Defects in complement regulation
- Hereditary angioedema
- Age-related macular degeneration (AMD)
- Atypical haemolytic uraemic syndrome (aHUS)
- C3 glomerulopathy (C3G)
- Paroxysmal nocturnal haemoglobinuria (PNH)
- Regulation by complement factor H
- Therapeutic regulator based on CR1
- Donor kidney treated with tailed CR1 analogue
- Tissue lectin, organ development and inflammation
- Learning points
- Thank you
Topics Covered
- Complement deficiency
- Organ transplantation
- Methods of pathogen evasion of complement
- Diseases mediated by complement
- SARS-CoV-2 and hyperinflammatory syndrome
- Complement and coagulation
- Defects in complement regulation
- Therapy in complement deficiency
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Talk Citation
Sacks, S. (2021, November 30). The complement system in innate and adaptive immunity: diseases mediated by the complement system [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 11, 2024, from https://doi.org/10.69645/YZKB3579.Export Citation (RIS)
Publication History
Financial Disclosures
- Consultancies for industry currently including Alexion, Omeros, and UCB.
The complement system in innate and adaptive immunity: diseases mediated by the complement system
Published on November 30, 2021
46 min
Other Talks in the Series: The Immune System - Key Concepts and Questions
Transcript
Please wait while the transcript is being prepared...
0:00
Hello, I'm Steven Sacks, back again to introduce the second part of my talk on complement.
The first part, you will remember, was on the normal function of the complement system
in defence against infection.
I'm back with the second part of the talk, to talk about diseases mediated by complement,
which are either due to underactivity of the complement system in complement-deficient
individuals, or overactivity of the complement system, which is the more common
source of tissue injury.
0:36
Let me begin with complement-deficient states, which fortunately are rare though instructive,
because they tell us an awful lot more about normal functions of complement.
In particular the relevance and how important that is, both for the host and also
for the successful elimination of pathogens.
In this slide I've represented the cardinal manifestations of inherited complete
(so homozygous) complement deficiency, which is fortunately rare.
There are two manifestations, in the first (on the left), these individuals get recurrent infections
and repeated immune responses, in the second they form immune complexes.
In this instance in the kidney glomerulus, which when cumulative, develops as renal disease.
This particular example shown is the diffuse form of lupus nephritis.
On the left, you see the aftermath of a meningococcal infection
to which complement-deficient individuals are susceptible,
particularly those with terminal pathway deficiencies.
The lesions are teeming with macrophages and leukocytes,
and those cells are teeming with microorganisms - the diplococci which cause meningococcal sepsis -
a really unpleasant killing disease, often associated with complement deficiency.
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