Talk:Complement system

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To-do list for Complement system:
  • Create complement system graphic (possibly like this, or this, or even this) showing the interrelationships and differences between the three pathway types.

Contents

[edit] Overhaul of Alternative Pathway

I'm going through the complement system and comparing it to an Immunology text book (specifically, Immunology, Infection, and Infection by Pier, Lyczak, and Wetzler, copyright 2004) and the Alternative pathway could use some work, both for clarity and accuracy.

Major Points: C3 spontaneously breaks and activates because of a breakdown in a thioester bond via a condensation reaction. In short, it's mildly unstable in water. This results in C3(H20). C3(H20) is then capable of covalently binding to a membrane surface if it is near enough. Upon binding with a cellular membrane C3(H20) is capable of being bound by Factor B. Upon being bound, Factor B is then cleaved by Factor D into components Bb and Ba, Bb is the larger of the two components and stays attached to C3(H20) to form C3(H20)Bb, a C3 convertase which cleaves further C3 molecules to amplify the effect. Ba diffuses away. C3 convertase cleaves C3 molecules into C3b and C3a, of which C3b is the larger of the two and can bind to C3(H20)Bb to form C3(H20)Bb3b, which has C5 convertase activity.

Protection/Dissociation of C3(H20): Since C3(H20) formation is spontaneous, there is a greater chance of it causing a Membrane Attack Complex (MAC for short) to form on a host cell. This is prevented by several ways. First, Factor H in the blood causes the dissociation of C3(H20)Bb. Second, C3(H20)Bb is inherently unstable and eventually will dissociate on its own. Furthermore, mammalian cell membranes have both sialic acid and heparin, which promote binding of factor H. Factor H, in addition to destabilizing the C3(H20)Bb molecule, acts as a cofactor to allow Factor I to cleave C3(H20)Bb and inactivate it. In addition to this, mammalian cells also have structurally homologous proteins to Factor H embedded in their membranes, which have the same effect.

Stabilization of C3(H20): C3(H20) can be stabilized by the protein properdin, which is present in the blood stream.

That's enough on the alternative pathway for now, I'll also work on a more detailed diagram of the 3 pathways and how they intertwine. Let me know if I should go ahead and work these changes into the page. ~Richard, e-mail Kinnin@gmail.com —Preceding unsigned comment added by 157.62.190.17 (talk) 21:39, 22 October 2007 (UTC)


[edit] Spelling

Typo in "This binding leads to *cnformational* changes in C1q molecule..."

I assume it should read conformational but I'm savvy enough on this matter to be sure... someone else please correct it and delete this.--nunocordeiro

Be bold! JFW | T@lk 22:20, 19 January 2006 (UTC)
But don't be reckless Your right though... I'll be a little bolder in the future. :) --nunocordeiro 03:14, 28 March 2006 (UTC)

[edit] Categories

There is need for this article to be both in Category:Complement system and its parent Category:Immune system - parent/grandparent conflict (P/G-C). So i removed the grandparent link. I also added Category:Complement system to Category:Acute phase proteins b/c it doesn't make sence to have the article "Complement system" in the "Acute phase proteins" tree structure and not have Category:Complement system, as a result of that change i had to remove the direct link from here to "Acute phase proteins" b/c of another P/G-C. -- Boris 17:12, 9 February 2006 (UTC)

[edit] Complement system diagram

I came across the diagram I have inserted into the article while looking for diagrams for the Immune system. I added the detailed information to the diagram, hopefully it suits your needs. If more info is needed I can add it, relatively easily, to the existing diagram, let me know.--DO11.10 21:19, 5 September 2006 (UTC)

Where is Factor D on the Alternative Pathway diagram? I think the diagrams really need replacing by an english version, though these are quite clear, to their credit. Philbradley 11:31, 12 May 2007 (UTC)

[edit] Other organisms?

I can't work out from reading the article if the complement system is only found in mammals such as humans, or if it is present in other organisms. TimVickers 23:32, 30 December 2006 (UTC)

Complement definatly exists in organisms outside of Chordates like Echinoderms, Arthropods, Urochordates, and possibly Annilids. Maybe someone more knowledgable in this could add a small section on non-mammalian complement? This should at least be mentioned somewhere in the page. JosephJP (talk) 19:21, 15 March 2008 (UTC)

[edit] The Caption on the MAC Complex

Caption currently reads, "A complement protein attacking an invader", which is incorrect - it is a Membrane attack complex, causing cell lysis. It is made of several different complement protein and you cannot tell if it is a host cell or a foreign cell. —Preceding unsigned comment added by 82.16.95.94 (talk) 21:47, 3 December 2007 (UTC)

[edit] differnt names in "Classical" and "alternative"

In the paragrapf about the classical pathway, it is explained that the C3 convertase complex should now correctly be called C4b2b. But in the paragraph "Alternative pathway", it still says that C4b and C2a combine to make C3 convertase. I think this should be changed to "C4b and C2b etc. ..." 85.127.84.16 (talk) 14:04, 7 February 2008 (UTC)

You're right that it's confusing and that if all complement proteins followed the regular nomenclature, then the fragment in question would be C2b; however, the scientific community seems to be just as confused about it as we are. The newest version of the Janeway textbook (7th edition) reverts to calling it C2a even after explaining that the nomenclature would call it C2b. I don't have my old text, but I'm fairly certain the 6th edition did call it C2b, so it's a confused protein fragment. I'm in favor of calling it C2b, but that does put Wikipedia at odds with what's widely considered the premier immunology text. JosephJP (talk) 19:15, 15 March 2008 (UTC)