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Author
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Topic: Intelligently Designing Immunity
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gedanken
Member
Member # 594
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posted 09. April 2003 18:33
Alonso, I’ll respond to this post more fully in the “Sequence of tests” thread, since most of your post is regarding subjects of that thread. Briefly:
You claim that all the definitions are equivalent. If so, you can show that logical equivalence (in the “Sequence” thread). And by that I mean show it in generic terms, not just a claim of equivalence with a specific case. I’ll repeat that if two tests are equivalent, then they should have the same test -- and we can examine the test itself to see if it meets the terms of each definition. And if it is claimed that this is equivalent because of some property of nature and not because the definitions are directly equivalent, then you can specify that aspect of nature and show logically why they are equivalent. (This is not a scientific level discussion in this, I am speaking of direct logical equivalence.). If however you claim that they have the same effect, then you can demonstrate that logically in the “Sequence” thread, or operationally for a particular case in the thread that is discussing the specific case. (And refer to the specific definitions and tests and show how they operate in the specific cases).
Also you said that definitions change, and that is a normal part of science. Of course this is correct, which is precisely why I want you to specify which definition you are using.
You said specifically:
quote:
Secondly I keep challenging you to randomly pick any definition of IC that you see out there defined by ID theorists (Dembski, Behe) and show that it somehow does not apply to any of the systems I discuss (ATP synthase; combinatorial immunity - antibody diversity, clonal selection, complement cascade; bacterial flagellum). You have never accepted this challenge. …
I don’t at all deny that some definitions or tests will “apply” to the systems you discuss. I’m quite convinced that there are definitions of IC for which the test will come up positive for many individual cases. What I don’t believe follows from those results is any problem for evolution. Some tests may pass -- but the definitions they test for don’t mean any problem for evolution. Other tests may not pass or may not be demonstrable (because they depend on the form of an “argument from ignorance” for example), and thus the definition may inherently be designed to pose a problem for evolutionary theory if it were met, but then the test can never actually be completed to make a demonstration that it is met.
As to equivalence -- once again be my guest (in that thread) in showing logically how they are equivalent. (“Logically” however means that you show logical properties in a logical domain, as in a nearly mathematical proof of equivalence.) If you want to show operationally that they are equivalent by examples, please show that in a thread where biologists are discussing the specific case, as I am not a biologist and will simply refer the case to others in an appropriate thread. If you want to show a logical equivalence that depends on specific properties of nature (e.g. that there are further premises for an argument that is strictly on logial grounds after that point), then please show your premises clearly in generic terms. We can then analyze those premises for correctness in individual cases in the respective thread in which the specific case occurs. And we can label those premises specifically so they are clearly and exactly identified for such analysis.
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Nel
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Member # 614
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posted 09. April 2003 19:18
Once again, these replies are short, so I'll do it in one post, in this post I resepond to Ged and Charlie :
Charlie,
Luckily, all I have to do is copy and paste (again). I don't mind continuing to show you how I have pinned down the ICness of antibody-diversity. When you decide to respond to the argument I'll wake up and respond to your points.
quote:
The antigen receptor/VDJ recombinase truly does not work unless you have one with the other. And if you don't have the signals the system is functionless. And if you don't have the Rag machine the system is functionless. If you don't have the receptors the whole thing is pointless. Thus it is IC.
Thus resulting in a large repetoire of antigen-specific antibodies.
and
quote:
I think Behe's point here is that there is a dangerous gap between the jump from innate immunity to acquired immunity, acquired immunity is largely successful because it can generate specificity for any kind of foreign substance. Innate immunity cannot. And then there's the fact that if innate immunity consisted of receptors with single specificities, then the likelihood of a foreign substance being recognized diminishes. Even if there are some innate receptors or something like them, with single specificities, a handful of them wouldn't be enough. Which is why Behe says that a system with only a few antibodies are "not sufficient to make a difference".
Ged,
Showing it with a specific case is just like showing it in generic terms. In fact, showing it in generic terms is worse, especially for a sequence test, since with letters and/or numbers, the interactions are invisible. I realize that ID critics don't like discussing the specific cases but they're just gonna have to deal with it. In a testable model, you usually are presented with concrete specific examples so that you can repeat the test.
You write:
quote:
Also you said that definitions change, and that is a normal part of science. Of course this is correct, which is precisely why I want you to specify which definition you are using.
Of course, you completely ignored what I wrote. I wrote specifically that I don't think that the IC definition has changed, but that it might and that there is nothing wrong with this.
I find it interesting that you decided not to accept my challenge concerning the functional equivalence of all IC definitions. Again if you think that the definition has changed, and that one is completely different from the other, why won't you accept my challenge?
With respect to showing how they are functionally equivalent through sequence tests, I have already done this in your thread. And when I say they are all equivalent I don't mean just the effect, I mean the whole kit and kabootle, from well-matchness, to functionally indivisible parts to showing how they are a problem for Darwinian evolution and support for ID. This is getting off-topic, so I'll see you in your thread.
[ 09. April 2003, 19:34: Message edited by: Nelson_Alonso ]
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charlie d.
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Member # 159
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posted 09. April 2003 19:57
quote:
The antigen receptor/VDJ recombinase truly does not work unless you have one with the other. And if you don't have the signals the system is functionless. And if you don't have the Rag machine the system is functionless. If you don't have the receptors the whole thing is pointless. Thus it is IC.
LOL, Nelson.
I have to concede, finally, that if you define your IC system as "antigen receptor/VDJ recombinase", it sure does need antigen receptors and VDJ recombinase (intended as RAGs and RSSs) to fit the definition, and it couldn't be otherwise. Of course, it's just a big useless tautology, but anyway....
Since you started it, let see how many system s like that one can come up with. Here's one: the "my ears/nose and my glasses" system is IC, because without my ears, or my nose or my glasses, it wouldn't be the "my ears/nose and my glasses" system. The "Sun/Earth/Moon" system is IC because it needs all three. So is the "pimple on by big nose" system, because without my big nose, or the pimple, the system disappears. Gee, why didn't I think of it earlier.
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Nel
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posted 09. April 2003 20:20
Charlie:
The antibody-diveristy is a function of the VDJ recombinase/receptors. How the heck is this a tautology? The VDJ recombinase/receptor system is not a large repetoire of antibodies, it's how you make them.
You write:
quote:
Since you started it, let see how many system s like that one can come up with. Here's one: the "my ears/nose and my glasses" system is IC, because without my ears, or my nose or my glasses, it wouldn't be the "my ears/nose and my glasses" system. The "Sun/Earth/Moon" system is IC because it needs all three. So is the "pimple on by big nose" system, because without my big nose, or the pimple, the system disappears. Gee, why didn't I think of it earlier.
That would be a pretty insightful statement if it wasn't completely wrong. I never said that the VDJ recombinase/receptor system is IC because it is a VDJ recombinase/receptor system. I said that the VDJ recombinase/receptor system is IC because you need a large repetoire of antigen-specific antibodies. And an immune system with one or two specific antibodies are like a propeller on your boat that only goes turns 1 revolution per hour when you are being chased by pirates.
[ 09. April 2003, 20:30: Message edited by: Nelson_Alonso ]
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yersinia
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Member # 324
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posted 09. April 2003 20:59
Nelson...
quote:
I said that the VDJ recombinase/receptor system is IC because you need a large repetoire of antigen-specific antibodies.
What didn't you understand about charlie's posts the last time we went around the merry-go-round on the specificity question?
Over here, charlie wrote,
quote:
Now, let's look at "ancestral" adaptive imune systems. In cartilagineous fishes, antibodies are generated by RAG-mediated gene recombination, thus "diverse" (by Nelson's definition). However, sharks have neither effective affinity maturation, nor memory. The vast majority of their circulating antibodies, both early and late during an immune response, are low affinity and thus polyspecific. In this respect, they look much like innate immunity receptor, with the added bonus of randomly generated diversity. Yet they allow sharks as a group to grow bigger than any but a few mammals. If size matters, it's not becasue of antibody affinity/specificity.
Clonal selection mechanisms for antibody specificity and affinity in fact appear gradually in vertebrates, but full-fledged affinity maturation, with its dramatic increase in antigen specificity (which seem to be so essential for Nelson), is pretty much an invention of endothermic vertebrates and it has nothing to do with RAG proteins or their somatically generated diversity. If we are looking at IC system components for these functional properties, the RAGs ain't them.
But you, Nelson, have been repeating ad nauseum that the step between
(1) non-rearranging receptors and
(2) the high-specificity antibodies of modern endotherms
wouldn't be selectable. But the sharks prove you wrong, because they have exactly what you claim can't exist -- functional rearranging antibodies but not high specificity.
(There is also a massive lack of precision in this discussion about what constitutes "high" specificity (is a flagellin receptor specific or general?), what the border between "high" and "low" is (there is no border, it's gradual), etc. But I digress)
Super-high specificity is a late addition to an already functioning recombining receptor system. Recombination is an addition to already functioning non-recombining receptors. Both intermediate stages are known to be functional, because many organisms thrive with them.
Modern mammalian adaptive immunity may well be IC, in that we die without it. But phylogenetically basal organisms get by just fine with varying subsets of this system. This guts Behe/Nelson's argument that the intermediate stages are unworkable and therefore unselectable.
Where's that gap you're trying to wedge your designer into, again?
[ 09. April 2003, 21:00: Message edited by: yersinia ]
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charlie d.
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Member # 159
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posted 09. April 2003 21:06
quote:
Charlie:
if you define your IC system as "antigen receptor/VDJ recombinase", it sure does need antigen receptors and VDJ recombinase (intended as RAGs and RSSs) to fit the definition, and it couldn't be otherwise.
Nelson:
I never said that the VDJ recombinase/receptor system is IC because it is a VDJ recombinase/receptor system.
Actually, that is precisely what you said. Here it is again: quote:
The antigen receptor/VDJ recombinase truly does not work unless you have one with the other. And if you don't have the signals the system is functionless. And if you don't have the Rag machine the system is functionless. If you don't have the receptors the whole thing is pointless. Thus it is IC.
Unless I am mistaken, "it" in the last sentence refers to the "antigen receptor/VDJ recombinase" in the first, which is therefore your purported IC system. In the first sentence, you specifically say "one cannot work without the other" (i.e, the system defined by the 2 components "antigen receptor" and "VDJ recombinase" is not the same if one of the components is missing - duh). Then, like I said, you further distinguish the VDJ recombinase sub-components (the signals sequences and the RAGs). Thus, your statement can be fairly paraphrased as:
"The antigen receptor/VDJ recombinase [RSS and RAGs] truly does not work unless you have both antigen receptor and VDJ recombinase [RSSs and RAGs]. ... Thus, it is IC."
Your problem is, again, that until you define your system without reference to what its supposed IC components are, and its function in an objective way (which you still haven't), you can't even start to work out whether it's IC or not. Of course, it seems that if you do so, the ICness of the system becomes essentially impossible to support (or, in alternative, that one must conclude that an IC system can evolve through a direct darwinian pathway). That's a quandary, alright.
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yersinia
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posted 09. April 2003 21:18
quote:
quote:
yersinia wrote:
Regarding the complement system, you didn't actually read Inlay's article because you couldn't answer charlie d's question. There are plenty of invertebrates with only parts of the complement cascade. This is why Poenie (one of your quotes in the opening post was from him, you should add his name) admitted that this "IC" system had originated gradually.
Again, which "IC steps" were shown to evolve with regard to the complement system? As I showed with the complement cascade, each cascade still has switches, which is what Behe was pointing to that is IC about the complement cascade. In fact, all the cascades are analogous to eachother. Lastly, I don't think you ever answered me as to where Dr. Peonie stated that the complement cascade evolved gradually. You probably did asnwer me but I probably didn't get to it. But this is the best time to quote him as I couldn't find it. I do remember you saying something to the effect that you said something and "Dr. Peonie didn't reply". If that is what you are going to respond with, I gotta laugh.
Here you go, Nelson:
quote:
[from page 1, in reply to yersinia]
There is much continuity between the innate immunity of lower eukaryotes and vertebrates but to say that there “are numerous extant organisms getting by with only pieces of this irreducibly complex system” seems to confuse the two systems
(innate versus adaptive immunity) one of which seems to have a long evolutionary history and the other that arises dramatically and suddenly in an event appropriately dubbed the “Immunological Big Bang” (Schluter et al., 1999).
(bold added)
In other words, Poenie specifically chose not to contest the evolutionary origin of the complement system, because he knew that it emerged gradually. So, if you're going to cite him as an authority, then your authority already concedes that IC can evolve, in which case the IC-->ID inference is sunk.
The bit about Poenie "not replying" is that various discussants immediately commented along the lines of "Hey, Poenie conceeds that the complement system originated gradually" and Poenie, in several subsequent posts, never took the opportunity to deny that that is what he meant.
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yersinia
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posted 09. April 2003 21:28
Charlie d. points out that a possible conclusion here is that recombining receptors arose via "a direct darwinian pathway".
I think this is a significant point. "Direct darwinian pathway" has no well-defined meaning in biology, but to Behe it meant basically "improving the intial function" (paraphrase).
Which is what we see with adaptive immunity -- improvements on pre-existing immune function. Non-rearranging receptors have useful immune system function, low-specificity rearranging receptors have immune function, etc. In many ways, then, the origin of mammalian immunity is much more like the origin of the eye from an eyespot (massive expansion of an intially very simple system with "the same basic function" [more or less]) than, say, the origin of middle-ear bones, which underwent a radical change in function.
The RAG insertion is perhaps "indirect" in that it "changed function" (not that it had much of one beforehand, mostly self-propagation) -- but the basic function of the system, antigen recognition, remains the same throughout.
Main point: if this interpretation is correct, then Behe's IC argument would not only have failed by failing to rule out indirect pathways, it would have failed by failing to rule out direct pathways as well.
yersinia
[ 09. April 2003, 21:37: Message edited by: yersinia ]
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yersinia
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posted 09. April 2003 21:36
Hmm, I just realized that Poenie also contradicted another of Nelson's recent claims.
Nelson said:
quote:
As I stated sharks are only relevant if you can show that their immune system was the ancestral state to the mammalian state. Furthermore, shark antibodies are already arranged. It looks absolutely nothing like the mammalian system
But Poenie said, regarding the combinatorial immune system:
quote:
This is not to say that there are no developments after the initial emergence of the combinatorial immune system but the basic system is all present in sharks.
yersinia
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Nel
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posted 10. April 2003 12:21
Yersina,
There is no "merry-go-round" with respect to the specificity question. I have outlined why I think that innate receptors with single specificities are useless to the immune system, they are useful because they do not have single specificities. Our antibodies do.
With respect to Charlie's comments, again, they are irrelevant. Sharks do undergo recombination, and thus they do have a good deal of antibody-diversity, but their antibodies are non-specific, and it's a lot smaller than ours, probably because they do it in clusters. This is advantageous to them because they can bind to a wide array of bacteria. They grow large because they make a lot of these things. Again, polyspecific receptors are effective, and here we have a large diversity of them. Again, as I have always said weeks ago and in my opening post, the problem is getting from generic binders to specific binders. Although with sharks, we see that the Rag machine, the signals, antigen receptors appear abruptly, thus the stage is already set for the highly specific large amount of antibodies that we have. Thus, the "Big Bang of immunity.
But again, the transition is difficult here. We have large arrays of Vs Ds and Js that can rearrange. However, sharks do it in clusters. In other words, although we have long strings of Vs and Ds and Js, sharks have V1-D1-J1-C V2-D2-J2-C,etc. When you try to get something like what humans have, you'll probably end up with something like a V1-V2-J2-C which is garbage. Also, as Julie Thomas also mentioned, fusing these segments has a chance of a frameshift. By the way, all of this suggests that antibodies themselves are IC in that they need all three segments to be a useful antibody. But I digress. This is why shark immune system would be relevant if we can show that their system is ancestral to ours.
Secondly, I never said that clonal selection mechanisms need the Rag genes. You need them for antibody diversity, but then once you have that, the other IC system here is as I already discussed:
All immunoglobins recognize and bind specifically to a an epitope on an antigen.B cells are initially activated to secrete antibodies after the binding of antigens to specific membrane Ig's. After that, the B cell gets the signal to make a secreted form of Ig, which activates the response to attack the foreign invader. No I don't agree that they appear gradually.
The required components are:
quote:
(1)the membrane-bound form of the antibody;(2) the messenger; and (3) the exported form of the antibody.
Yersinia also writes:
quote:
But you, Nelson, have been repeating ad nauseum that the step between
(1) non-rearranging receptors and
(2) the high-specificity antibodies of modern endotherms
wouldn't be selectable. But the sharks prove you wrong, because they have exactly what you claim can't exist -- functional rearranging antibodies but not high specificity.
Nic, where exactly do I say that either of those things can't happen? This is important because you say that I am repeating this "ad nauseum" and yet I cannot find a single instance. I never said that non-rearranging receptors are useless. Sharks don't prove me wrong just because they don't have high specificity. In fact, that they don't have high specificity proves me right --- a few antibodies with high specificity is useless to the immune system.
The mammalian system has antibodies of high specificity, but they make quite a few. If you had 50 V, 20D, and 6 J regions able to code for a heavy chain, and 40 V and 5 J region genes able to code for a light chain, you would have a repertoire of 1,200,000 specificities. And thats what you would need to make antibodies with single specificities work.
There is a preciseness in my discussion of antibodies with single specificities. Each lymphocyte carries on its surface receptor molecules of only a single specificity. Innate receptors are generic, and unlikely to have single specificities. The area between high specificity and high generality is an unselectable step.
By the way Yersinia, I'm still laughing at your Peonie discussions. You quote:
quote:
There is much continuity between the innate immunity of lower eukaryotes and vertebrates but to say that there “are numerous extant organisms getting by with only pieces of this irreducibly complex system” seems to confuse the two systems
(innate versus adaptive immunity) one of which seems to have a long evolutionary history and the other that arises dramatically and suddenly in an event appropriately dubbed the “Immunological Big Bang” (Schluter et al., 1999).
The "one of which" here is referring to "innate immunity".Long evolutionary history, sure, maybe not Darwinian. Nothing here describes Peonie's thoughts about the complement system. Did the complement system evolve step by step? Poenie doesn't say. However, Dr. Poenie may think that it did evolve, he doesn't say. By the way, I could justify your attempts at putting words into Dr. Poenie's mouth if I was simply quoting his words, without any back-up to the literature or evidence that he discussed, and simply agreed with Poenie. However, I agree with Poenie and quoted him because he talked about the data, and referenced the literature and that convinced me. If Dr. Poenie decided to contribute to this discussion by explaining the data pertaining to the evolution of the complement cascade with refence to the the literature, and described how natural selection and random mutation built the cascade while bypassing the irreducible complexity of the switches, then I would be just as convinced as his abrupt arguments about the rest of acquired immunity. Telling me that Dr. Poenie didn't reply because you said the complement system evolved is telling me nothing at all.
You also write:
quote:
Hmm, I just realized that Poenie also contradicted another of Nelson's recent claims.
But Poenie said, regarding the combinatorial immune system:
and then you quote Dr. Poenie:
quote:
This is not to say that there are no developments after the initial emergence of the combinatorial immune system but the basic system is all present in sharks.
But again, you are wrong. It would help you not make so many mistakes if you would just read my posts. Here is what I wrote in my OP:
quote:
The fact that Rag1 and Rag2 was acting as a transposase before jumping into an organism, interacting with Ig and TCR molecules, and at roughly the same time we get MHC, the jaw, and thymus suggests strongly that what we are seeing is an intelligently designed event which can be called "The Big Bang" of acquired immunity.
In jawed fish and all "higher" vertebrates, adaptive immunity is possible because of what I like to think of as the immunological "Big Bang," which occurred in some ancestor of the jawed fish.
Janeway: Immunobiology, 2001
As mentioned already, this is true for sharks and rays as well, in that it appears all at once.
[EDIT: Took out some heated comments]
[ 10. April 2003, 15:13: Message edited by: Nelson_Alonso ]
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Nel
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posted 10. April 2003 12:28
Charlie,
I wrote:
quote:
Nelson:
I never said that the VDJ recombinase/receptor system is IC because it is a VDJ recombinase/receptor system.
You reply that "that is precisely what you said" and then you only quote part of my post in my response to you. So lets restore context of this quote:
quote:
The antigen receptor/VDJ recombinase truly does not work unless you have one with the other. And if you don't have the signals the system is functionless. And if you don't have the Rag machine the system is functionless. If you don't have the receptors the whole thing is pointless. Thus it is IC.
What did I say after that?
quote:
Thus resulting in a large repetoire of antigen-specific antibodies.
And it's consequences for specificity of the combinatorial immunity:
quote:
I think Behe's point here is that there is a dangerous gap between the jump from innate immunity to acquired immunity, acquired immunity is largely successful because it can generate specificity for any kind of foreign substance. Innate immunity cannot. And then there's the fact that if innate immunity consisted of receptors with single specificities, then the likelihood of a foreign substance being recognized diminishes. Even if there are some innate receptors or something like them, with single specificities, a handful of them wouldn't be enough. Which is why Behe says that a system with only a few antibodies are "not sufficient to make a difference".
Again, the antibody-diveristy is a function of the VDJ recombinase/receptors. How the heck is this a tautology? This is true even in Sharks. The VDJ recombinase/receptor system is not a large repetoire of antibodies, it's how you make them.
[EDIT to out some heated comments]
[ 10. April 2003, 15:47: Message edited by: Nelson_Alonso ]
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Moderator
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posted 10. April 2003 12:47
The participants in this thread need to improve the discussion on two fronts.
1. Stop the "Nuff Said" "in your face" attitudes - stop heating the fire
2. More content and less quotations.
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charlie d.
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posted 10. April 2003 18:29
Nelson:
what's "antibody-diversity"? Why is it a function? One could perhaps say that the function of somatic recombination is the generation of diverse antigen receptors.
And again, if you define your system as "VDJ recombinase/antigen receptor" of course any other system that uses a method different from VDJ recombinase to generate diversity would be a different system by definition (there it is, once more, your tautology problem: you define the system on the basis of the components that supposedly make it IC, then if you take away one component, of course your system ain't there anymore).
For instance, as I mentioned before, chickens generate antibody diversity not through VDJ recombination, but through gene conversion. VDJ recombination only takes place on a single gene segment, probably as an evolutionary remnant of a more "antiquated" system, like ours, and generates no significant diversity. Do chickens use VDJ recombinase to make antibodies? You bet. Do they need it to generate diversity? No.
Similarly, I would argue that the only way "diversity" is meaningful is in a true functional sense. Counting abstract potential antigen specificities, or setting arbitrary specificity or affinity limits, has no value to the organism. The only thing that matters to an organism is to be able to recognize the vast majority of potential pathogens it can be exposed to. Whether this is done through 10^10 individual receptors, or 100 pattern-recognizing receptors, it matters not a bit, as long as immunity is successful.
And this brings me to the last point, ie that your insistence that the non-rearranging precursors of adaptive immunity receptors must have had single specificities. This is just also an artifical restriction, an attempt to set a constraint that is logical, not biological. The original proto-antibody could well have been an innate immune system polyreactive receptor, whose diversity a transposon insertion somehow augmented, and that would have been perfectly fine from an adaptive and evolutionary and adaptive point of view. Indeed, that the protoantibodies were likely low affinity and polyreactive, is strongly suggested by the fact that antibodies in cartilagineous fishes, despite RAG-mediated somatic recombination, still are polyreactive and of low affinity.
Two conclusions follow: VDJ recombination per se is neither absolutely sufficient (sharks) nor necessary (chickens) to generate antigen receptor diversity. Of course, it is required and sufficient (well, almost, but let's forget about details right now) within the contingent situation of our own immune system, but that's but one example amongst a wide array of evolutionary solutions to the immunity problem.
So, IC fails here as a basic heuristic tool, focusing on the wrong, static characteristic of a system, and entirely disregarding the meaningful biological concepts of adaptation, selective advantage, plasticity, phylogenetic relationships etc. It seems to me that by looking at nature from the peephole of IC and related "artificial" constructs, one runs the serious risk of missing the big picture of the biological world.
[ 10. April 2003, 18:30: Message edited by: charlie d. ]
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gedanken
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posted 10. April 2003 19:44
Here is something to consider with respect to "antigens receptors". [Thanks to Yersinia]
They are a means to ward off invading bacteria or the like. But that bacteria is in general a parasite in the sense that it requires the host in order to multiply, and doesn't exist without the hosts.
So if a host type has little resistance, it will die back where it comes in contact with the invading organism. But that must be in concentrated groups of the very host itself.
Therefore the assumption that one needs to fight off the invader in order for the species to survive is incorrect. What that ability to do (fight off invader) appears to allow for an increase in the density of the host in the environment, not allow for the life of the host itself.
This appears to be an argument that ability to fight off the invader is an improvement in fitness that is a matter of degree. This is consistent with Darwinian evolution. Degree of specificity or degree of ability to fight off such invader is also a matter of degree. And greater specificity allows for greater ability to fight off the invader.
Though not directly relevant, this is another example where the conditions for the “No Free Lunch” theorems are not applicable in the sense that the invading hosts and the ability to repel them evolves simultaneously. The “fitness functions” are not a constant of the environment, rather are changing as the co-evolution of the various organisms occurs. Any parasite that completely kills off its required host will itself immediately die.
I would like to hear some biologist comment on this, as I am posing it from a “gut” level of knowledge and would like for a biologist to correct any inaccuracies or misinterpretations.
[ 11. April 2003, 00:35: Message edited by: gedanken ]
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yersinia
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posted 10. April 2003 23:46
Hey gedanken,
...I think you mean "antigen receptors" (like antibodies) instead of "antigens", yes? Antigens are things that the immune system responds to.
A great summary is online at Kimball's biology page on antigen receptors.
PS: Regarding your main point I basically agree, in that specialized diseases require hosts, lots of them, in order to persist. There is AFAIK actually no such thing as a disease that causes 100% mortality for any typically large population of hosts -- some will always escape through isolation, lucky genetic variants, etc.
There is also an entire interesting field about how disease virulence evolves under different evolutionary conditions -- high virulence can only persist under conditions where transmission is rapid, or else the virulent strain will "burn out" and be extinct.
However, I should mention that focusing on the Yersinias of the world (bubonic plague etc.) is probably not the best way to look at the immune system biologically. What the immune system's real function is is shown in people with highly compromised immune systems (AIDS etc.). They get attacked by all kinds of mundane bugs that most of us could roll in a vat of without trouble. Without your immune system the local soil fungus will eat you alive.
PPS: It suddenly occurs to me that perhaps one reason for the super-duper immune systems of mammals is simply warm-bloodedness. Things can replicate alot faster when they are warm.
yersinia
[ 11. April 2003, 02:20: Message edited by: yersinia ]
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