Evolution of adaptive immunity I–Phylogeny

This is posted specifically in response to Chapter Six of Darwin’s Black Box, which claims that our adaptive immune system is irreducibly complex.

Defense against pathogens has a very long evolutionary history, going back at least to bacteria and archea.  Adaptive (or “acquired”) immunity is the tip of the iceberg, very effective, yet built upon and integrated with the earlier “innate immune system.”  Indeed, it should be mentioned at the outset that there is no inherent reason to split up “adaptive immunity” and “innate immunity,” as they are both “parts” of an integrated system.  Evolution and convenience are the reasons for splitting the “two systems” up, for only gnathostomes (jawed vertebrates) and agnathans (jawless vertebrates–now down to only hagfish and lampreys) have full adaptive function added onto the immune system that we share (not without considerable evolved differences, of course) with the rest of multicellular eukaryotic life. It is an interesting and meaningful phenomenon–unless one subscribes to ID/creationism, in which case it is meaningless–that gnathostomes and agnathans have very different, evolutionarily distinct, systems of adaptive immunity.

As I have previously noted, immune functions have emerged in the familiar cladistic patterns, adding complexity to the immune systems as evolution continues–in essentially the way that evolutionary theory predicts. It would be well, though, to lay out some of the details of the evolution of immunity, and not only with respect to adaptive immunity, but as immunity has evolved roughly since before the Cambrian “explosion”.   To start out, phylogeny is very important in demonstrating that (unguided) evolution occurred, and it sets out the framework for understanding the particulars of the evolution of adaptive immunity.

Scroll past the sequence data below to “part C,” which shows the phylogeny of Toll and Toll-like receptors, not only of “higher animals,” but of a plant, a nematode, and a sponge.  There, an abbreviation for each organism is used, so here is the key to the abbreviations:  MEDTRU=Barrel medic, a legume plant, CAEL=C. elegans, a nemotode worm, SUBDO=a sponge, DROME=a fruit fly, TRICAS=the red flour beetle, DANIO=zebrafish, HOMO=human, MUS=mouse, GALLUS=chicken.

In the link above, MEDTRU=Barrel medic, a legume plant, CAEL=C. elegans, a nemotode worm, SUBDO=a sponge, DROME=a fruit fly, TRICAS=the red flour beetle, DANIO=zebrafish, HOMO=human, MUS=mouse, GALLUS=chicken.

 Here is the source for the above illustration, and this is the article it illustrates.

While not all of the Toll-like receptors (TLRs) give exactly the same relationships, clearly the expected relationships hold in general, with only fairly slight deviations. Mouse and human TLRs are rather closely related, chicken somewhat less, zebrafish is less related, the sponge and the nematode are even less related, and so is the plant. IDists such as Behe like to claim that the Cambrian “explosion” does not fit with “Darwinian evolution” because it appears discontinuous in the fossil record, yet genomes tend to show a reasonably steady progression of divergence of immunity genes, as well as all of the other genes–within our ability to resolve details, of course. That is, on the level of “punctuated equilibrium” evolution may not be especially slow and gradual (based on our resolution of genome sequencing), but immune system evolution across hundreds of millions of years is slow and gradual compared with any design expectations, even if it speeds up and slows down due to “punctuated equilibrium.”

For purposes of discussing Behe’s claims, even more important phylogeny appears right at Behe’s “irreducibly complex” adaptive immunity, for not only do we have excellent evidence that one adaptive immune system evolved, we have excellent evidence that two adaptive immune systems evolved from basically the same “physical precursors” that Behe rightly tells us are predicated of “Darwinian evolution.”  The old familiar accidental character of evolution is thereby evident, for no “design reason” can be adduced (or considered to be at all likely) for two different complex supplemental adaptive systems to be grafted onto the inherited innate immune systems of agnathans (jawless vertebrates) and gnathostomes  (literally “jaw-mouth” vertebrates–the vertebrates other than hagfishes and lampreys), while the inheritance, mutational, and environmental, accidents expected of evolution account quite nicely for the separate agnathan and gnathostome adaptive immune systems.

Here is another phylogenetic tree, this time not going quite so far back, and not based upon Toll and Toll-like receptors. For copyright reasons I do not think that I should reproduce it here, hence the link.  The main point presently of that linked illustration of phylogeny is the rather striking split of apparently unrelated adaptive immune systems in the two vertebrate groups, the aforementioned agnathans (represented by the lamprey) and gnathostomes.  The fact that molecules other than Toll and Toll-like receptors produce essentially the same phylogenies is not unimportant, either.

My purpose is never to get too much into the details, although future posts will do so more than this one does.  My objective is to show that biomolecules definitely do reveal a whole lot about evolution, and especially the patterns of splitting and of independent development of systems in organisms lacking in much horizontal (lateral) gene transfer possibilities (all of the organisms mentioned or linked in this post typically transfer genes only “vertically,” and only rarely undergo horizontal gene transfer).  Likewise, by no means do sequences only indicate “relatedness” as Behe wants us to believe, for the relatedness of agnathans and gnathostomes only explains why only certain biomolecules were available for the evolution (not true for design, certainly) of adaptive immunity in their respective cases, and not why a similar set of biomolecules gave rise to very different immune systems.  Only accident explains the latter phenomenon, while design not only provides no answers, it yields no leads to any research possibilities for discovering “design answers” to such questions.

So the phylogenetic tree of the immune system–including both the innate and adaptive parts–indicates the same thing happening through time, the splitting of the “bloodlines” and the fixing of quite different solutions to immune problems independently of whatever “designs” were occurring in genetically separate species.  A seeming paradox (to uninitiates) is that the accidents of evolution, which are predicted by theory and also borne out by the evidence, actually generate the kind of order that anything we can mean by “design” would not create, for only the constraints of evolution will split up agnathans and gnathostomes in the observed precise and unalterable fashion, while design (like horizontal gene transfer among prokaryotes) would mix up the “bloodlines.”

How odd it is for someone like Behe to claim that the evidence for “microevolution” (scare quotes are because he obviously is not using the scientific definition for that term), which is genetically impossible to differentiate from the evidence for “macroevolution,” came from a very different process.  Of course, in real science similar effects are accepted as having similar causes, unless a cause can be shown to cause the same effects, which the IDists know better than to even attempt to do.

Furthermore, it is evolution which produces the tremendous complexity found across life, for only evolution is predicted or expected to very often come up with different solutions to the same problem (convergence also occurs, though its different sources leave their marks).  Not only the level of complexity found in the tree of life, but the sort of complexity found there in which different “bloodlines” produce independent solutions dependent upon accidents of inheritance, environment, and of mutation, is predicted by unguided evolutionary processes alone.

The phylogenetic evidence is unmistakable:  It reeks of accident plus the refinements of natural selection, and it yields no evidence at all of the rationality, purpose, and “conceptual precursors,” which would be expected of design.  Behe has certainly not told us why two very different adaptive immune systems arose “by design” out of a common set of biochemicals in the agnathans and the gnathostomes.  Evolution uses accident to explain the patterns of phylogeny, as both the order and the complexity of life’s branching “bloodlines” can only come by accident,* and not at all by anything (other than a Loki-type god playing a joke on the universe) meant by the word “design.”

*This actually holds fairly well with language evolution as well, although a kind of “design” is able to cause horizontal language “borrowing.”  But essentially, while many of the constraints upon language are at least not wholly accidental (and even intelligence and design can play roles), language is not understandable except as involving a great deal of “inherited” and ongoing accidents.

This is part of a series of posts that I am combining into one long post, which may be found at Darwin’s Black Box.

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2 Comments on “Evolution of adaptive immunity I–Phylogeny”


  1. […] In my last post in this category, I pointed out that Toll and “Toll-like receptors” (TLR… The fact that other molecules of the immune system (adaptive and innate) reveal essentially the same patterns was also pointed out. But the fact is that Toll and the other “innate immune system” proteins are not simply to be found in the “innate” systems of vertebrates as well as in, for instance, fruit flies, they continue to utilize basically the same pathways–and they regulate and inform the adaptive response.  All except the last part is borne out in the following quote: In fruit flies, there is a very strict order of Toll pathway gene products starting with Toll and going on to dMyD88, Pelle, Cactus, and Dif/Relish, all of which are cytoplasmic proteins involved in the transmission of the signal from Toll, a cell-surface receptor, to the nucleus to induce the activation of specific sets of genes. The same order is found in the homologues of the Toll pathway found in the innate immune system in vertebrates(Fig. 1). The plant genes do not seem to be arranged in the same order. However, if one examines the plant genome carefully, there are signs of all these signaling elements.  Evolution of the innate immune system […]


  2. […] In my last post in this category, I pointed out that Toll and “Toll-like receptors” (TLR… The fact that other molecules of the immune system (adaptive and innate) reveal essentially the same patterns was also pointed out. But the fact is that Toll and the other “innate immune system” proteins are not simply to be found in the “innate” systems of vertebrates as well as in, for instance, fruit flies, they continue to utilize basically the same pathways–and they regulate and inform the adaptive response. All except the last part is borne out in the following quote: In fruit flies, there is a very strict order of Toll pathway gene products starting with Toll and going on to dMyD88, Pelle, Cactus, and Dif/Relish, all of which are cytoplasmic proteins involved in the transmission of the signal from Toll, a cell-surface receptor, to the nucleus to induce the activation of specific sets of genes. The same order is found in the homologues of the Toll pathway found in the innate immune system in vertebrates(Fig. 1). The plant genes do not seem to be arranged in the same order. However, if one examines the plant genome carefully, there are signs of all these signaling elements. Evolution of the innate immune system […]


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