Evolution of Adaptive Immunity III–It Has the Marks of Irreducible Randomness*

As previously mentioned, adaptive immunity did not appear at the beginning of the Cambrian.  Of course, none of the basic biochemical pathways can be pinned down to the Cambrian “explosion,” nor did they appear at the same time as each other, so far as anyone can demonstrate.

Not only does adaptive immunity fail to break any kind of evolutionary patterns, or to come up with anything truly novel, it happened well after the IDists’ favorite “creation event,” the Cambrian “explosion.”  Perhaps this does not directly contradict ID or Behe, given how much they refuse to make definite claims, let alone to predict any of the expected effects of design.  However, as stated beforehand, the Cambrian “explosion” is one of the events that supposedly could not happen “gradualistically,” thus the IDists imply that some special design event occurred then.

All evidence tends to suggest that most of Behe’s “irreducibly complex” pathways actually appeared well before the Cambrian, from the bacterial flagella and eukaryotic cilia, to photosynthesis, and on to the clotting cascade and the biochemistry of vision.  Adaptive immunity is interesting by contrast for appearing around 430 million years ago, about 85 million years after the Cambrian began.

The timing of this, and of the appearance of other biochemical pathways, seems therefore to follow the expectations of evolutionary theory yet again.  Obviously, the IDists have no design reason for adaptive immunity appearing when it did, since it likely would have been of use well before the Cambrian period.  Combinations of accidents of heredity, environment, and mutation, plus natural selection, are evidently behind two very different forms of adaptive immunity appearing when they did, and evolutionary theory readily accounts for such accidents of timing and of divergence, while “intelligent design” has no accounting for it at all.  For, how is design supposed to explain irreducibly random* (in many, but not all, aspects) evolutionary events?

And while evolution is marked by appearances of biochemical pathways according to combinations of fortuity, accident, need, and the ordering principle of selection, it is not as if these causes ended with the appearance of these pathways–especially not in the case of immunity, adaptive or innate.  You really would not know that if you read The Edge of Evolution, since Behe there suggests that the immune system does not change (other than for a few point mutations) significantly in response to parasitism.  This gets to another of his fundamental misunderstandings, for he operates from a notion that “Darwinian evolution” should specifically adapt the immune system to malarial infection, as if the immune system is a specific defense against malaria, and not a general defense against a huge number of parasites.

Nevertheless, this general defense system has substantially evolved since adaptive immunity itself evolved.  One of the reasons for my previous post on adaptive immunity was to show that not only is adaptive immunity “built” as evolution predicts (integrated with what came previously), but that innate and adaptive immunity are not separately acting systems.  Toll-like receptors are as important to adaptive immunity as to innate immunity, and the same would go for nearly all of the components of “innate immunity” in organisms having adaptive immunity.  In light of that, what is important is that the immune system has evolved enormously in various gnathostomes (jawed vertebrates), which now differ a great deal in the numbers of genes per family, as may be seen in the table below:

Table 1. Comparison of gene family numbers in human, mouse,

opossum, and chicken genomes

                                  Human     Mouse     Opossum      Chicken

Cathelicidin                   1                1               12                  3

Beta-defensin             39              52              32                13

Alpha-defensin           10               6                 1                   0

Theta-defensin          1ps              0                 0                   0

Chemokine                  47             45              31                 24

KLRA1 (Ly49)            1ps              16                0                   0

NKG2D/KLRK1              1                1                1                   0

CD69                            1                1                1                   0

KLRC                            4                3                0                   0

Ig-like receptor          30              10           45              103

Source: Genome Research
 

With such a range in the numbers of molecules involved in various aspects of the immune function in different members of the gnathostomes, there is no excuse for writing as if the immune system does not evolve.  To be sure, Behe would almost certainly claim that such differences were not random in the aspects I have mentioned (except for heredity, which he seems to think the “designer” could not or would not overcome–clearly an assumption made merely to save his “hypothesis,” and having nothing to do with what we know of design principles), but he has no evidence for that claim, and anyway, the evidence for the evolution of gene families involved in immunity is basically of the same type as what he accepts as evidence that human and P. falciparum responses to each other are due to unguided evolution.

The facts I emphasize in this post are that adaptive immune systems have appeared and evolved as expected in normal evolutionary processes.  There is no coordination of evolutionary changes according to design principles, so that while the Cambrian “explosion” appears to have substantially involved an arms and armor race among the evolving phyla (among other likely factors), biochemical pathways appeared independently of that event, and subsequently evolved in accordance with accident, need, and natural selection.  Adaptive immunity appeared relatively late, compared with the most basic biochemical pathways, and the two versions of it appear to be as unrelated as, say, bats wings and bird wings are (which is to say, that accidents of heredity are found behind both, but the specific changes to the vertebrate forelimb which made wings in both cases are wholly unrelated).  Later evolution has dramatically altered the gene components of divergent jawed vertebrate taxa, quite unlike the stasis that Behe implies in both Darwin’s Black Box and in The Edge of Evolution.

The IDists are correct about one thing, which is that randomness could never produce systems like our immune system.  What is at least as certain is that randomness is the only causal factor able to account for the timing, most divergences, uncorrelated adaptations, and the sorts of new information (mutations) appearing through time in the genetic record.  By no means is randomness the whole story, yet the whole story includes so much irreducible randomness behind the selective pressures of competition that there is nothing to be concluded other than that design was not responsible for life’s biochemical pathways.  Only a theory which accounts for the lack of planning, rationality, and purpose, like our evolutionary theory, is able to explain the timing, patterns, and unrelated adaptational radiations of immune systems, as well as the rest of the biochemical pathways of life.

*By “irreducible randomness” and its variations I am using “irreducible” akin to the manner that IDists use “irreducible complexity,” and even more properly, as something that simply does not resolve into something else (especially not design).  It has nothing to do with the “irreducible randomness” of quantum mechanics, of course.

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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One Comment on “Evolution of Adaptive Immunity III–It Has the Marks of Irreducible Randomness*”


  1. […] in “innate immunity” and “adaptive immunity” since adaptive immunity arose, mentioned here. However, mostly that evolutionary evidence is not specific to adaptive immunity, and even though I […]


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