2010

[Editor’s Note: This is part four of a six-part series from microbiologist Donald L. Ewert responding to Kathryn Applegate, of the BioLogos Foundation, in her arguments that the vertebrate adaptive immune system illustrates the claimed creative the Darwinian mechanism. Previous parts of Ewert’s response can be found at the following links: Part One, Part Two, Part Three.]

Pathogen-directed activation of the immune response

The initiation of an immune response is designed so that the cellular and molecular components that are best equipped to deal with a pathogen are engaged. There are basically three response pathways. Non-protein antigens that have repeating carbohydrate units on their surface, such as are found on bacteria, can directly activate B cells. These B cell do not go through affinity maturation or class switch since multiple binding sites on the antigen make a strong bond with the B cell and the IgM class of antibody that is produced which has five receptors per molecule.

Responses to protein antigens fall into two classes, depending on whether the pathogen is intracellular or extracellular. Since intracellular antigens such as viruses are not accessible to circulating antibody, they activate cytotoxic T lymphocytes that are best equipped to kill them. This activation is directed by the Class I MHC antigen that is attached to the antigens as they are processed in cells. Extracellular proteins, which are best dealt with by circulating antibody, activate B cells to begin the process of affinity maturation and class switch that leads to the production of a monomeric IgG class of antibody. This latter pathway requires the assistance of a class of T lymphocytes called T helper cells (T_H) and the interaction of Class II MHC proteins.

As I was driving in to work, the local NPR station had on an interview with a guy who’s involved with gathering billions of seeds of various plant varieties into a “doomsday vault.” It is on a remote Norwegian island and intended as a precaution against the presumed devastations of global warming. There were few surprises in the conversation — the grim mood was well suited to the NPR target audience, which eats this stuff up — apart from one rather interesting question from a listener. The guest, Cary Fowler of the Global Crop Diversity Trust, was asked why his group bothers with seeds. In the future, won’t we be able to reconstitute life from the digital code of DNA?

Not necessarily, explained Fowler. He offered a few cryptic but telling comments about the complexities of gene expression, and how simply knowing the DNA sequence of a plant (or animal) may never be sufficient to generate life. Why? Part of the answer, implying a strong challenge to materialist explanations of life’s evolution, is suggested in a recent and illuminating essay, “Getting Over the Code Delusion,” in the Ethics and Public Policy Center journal, The New Atlantis.

Rare is the technical if otherwise quite accessible article that gives chills like this one does. Steve Talbott, a senior researcher at the Nature Institute, takes aim at the still-widespread illusion that DNA maps the construction of a living creature. In a 1992 essay, Nobel Prize-winning geneticist Walter Gilbert crowed that the time will come when a person will be able to say, of a human DNA sequence inscribed on a computer disk, “Here is a human being; it’s me!” How utterly naíve that has since been revealed to be.

Richard Dawkins calls DNA “a remarkable feat of digital information technology,” on the model of a computer albeit one that programs itself. Yet the burden of Talbott’s article is to show why the whole computer metaphor is inadequate. If you want a better one, the really apt metaphor would be drawn from the art of dance — or I’d say, music — with all that implies by way of purpose, agency, and expression.

I’ve received quite a bit of positive feedback about the responses to the Nature 15 Evolutionary Gems packet that we’ve been responding to since last summer. As a recap of this series, below are links to the 9 parts responding to what I’ve affectionately called “Nature‘s Evolution-Evangelism Packet.” Also, we’ve compiled the responses into a single PDF that can be used for educational purposes: Be sure to download the full PDF here. 

This month’s edition of Touchstone Magazine has a great column by the godfather of intelligent design, Phillip Johnson, offering his review of Stephen Meyer’s Signature in the Cell and his take on why the book has been met with such an uproar in the blogosphere: In another way, however, it is peculiar that there is such a furious and often ill-informed objection to a learned volume that isn’t even about the theory of biological evolution. The book advances well-reasoned arguments based on solid evidence about a prior problem — the origin of the cell’s information content — concerning which most scientists would concede that they know very little. The one thing that many of these scientists think they do know Read More ›

Scientific American recently reported on what has transpired since the completion of the Human Genome Project ten years ago. When the HGP was first announced in 2000, many scientists said that it would be the key to understanding disease and for developing cures. Ten years later, however, this has not been the case. The human genome project has aided in developing better research and technology, particularly in our abilities to sequence genes. It has also shown us that much of what we once considered junk DNA isn’t really junk at all. (See here, here, here, and here for past ENV discussions on junk DNA). However, scientists are coming to a sobering conclusion that perhaps their models and assumptions on the nature of disease may be mistaken.

Francis Collins is one of the world’s most prominent theistic evolutionists, and now a prominent piece of President Obama’s government. In this clip, God and Evolution contributors and other scholars respond to Francis Collins’ defense of theistic evolution in his book The Language of God. Display content from www.discovery.org Click here to display content from www.discovery.org. Always display content from www.discovery.org Open content directly In his book The Language of God: A Scientist Presents Evidence for Belief (2006) and other writings and interviews, Collins has described the paths that led him from atheism to religious belief and from an impatience with “messy” biology and a preference for the pristine realms of physics and chemistry to a fascination with DNA, RNA, Read More ›

[Editor’s Note: This is part three of a six-part response from microbiologist Don Ewert to Kathryn Applegate’s arguments that the vertebrate adaptive immune system is an example of Darwinian evolution in action. Part one can be found here, and part two is here.]

The second stage of B cell receptor development is initiated when a foreign protein enters our body and is detected by a circulating B cell using its cell surface antigen receptor (BCR). The BCRs that recognize these antigens improve their affinity (binding capacity) for the antigen by entering into a fine-tuning process called affinity maturation. This process ensures that highly effective antibody receptors are produced and released as cell-free antibodies into the circulation as the B cell completes its development. This increase in the strength of binding between a single antigenic determinant and an individual antibody combining site does not affect the specificity of the antibody, i.e. its ability to distinguish between small regions (epitopes) on the same antigen. Rather it allows for antibodies to remain bound to the foreign antigen for longer periods of time, thus giving the body a greater chance to clear the antigen-antibody complexes. The changes in the affinity of the receptor for an antigen results from the accumulation of nucleotide replacements that change the attractive and repulsive forces, mainly electrostatic forces, of the antigen combining site. The molecular mechanism for improving the affinity of the BCR is called somatic cell hypermutation (SHM), since the changes that are introduced in the DNA of the B cell (a somatic cell) cannot be passed on to the offspring of the animal.

[Editor’s Note: This is part two of a response from microbiologist Don Ewert to arguments from BioLogos’s Kathryn Applegate that our immune system shows the creative power Darwinian evolution. Part one can be found here.]

The intricate mechanism for generating antibody diversity from very few germline (existing) genes was discovered over thirty years ago. It involves shuffling gene segments and then fusing them to produce new combining sites for the antibody receptor displayed on individual B cells. How much of this process is pre-programmed and how much is random? Is this an example of the use of a “‘blind’ system to sustain and preserve life,” as Kathryn Applegate suggests? The evidence from decades of research reveals a complex network of highly regulated processes of gene expression that leave very little to chance, but permit the generation of receptor diversity without damaging the function of the immunoglobulin protein or doing damage to other sites in the genome.

The most remarkable aspect of antibody production is the mechanisms that generate the binding site of the antigen receptor. The antigen receptor of B cells are proteins called immunoglobulins. They have an antigen combining site at one end that binds to foreign proteins (variable or V region) and a tail, or constant region (C region), at the other end that controls the interaction with other components of the immune system that are responsible for eliminating the foreign invader. The variable end of the BCR heavy chain is generated by the shuffling and joining of gene segments from separate pools of V (45), D (23), and J (6) segments per cell and the random deletion and insertion of nucleotides at the joining sites. This process is duplicated on the second (light) chain of the immunoglobulin gene. The combined diversity generated by recombination which is limited by the number of gene segments and by nucleotide exchanges, which are unlimited, produces a potential repertoire of about 10¹¹ different receptor specificities. This process occurs during transcription of the DNA and involves a set of coordinated enzymatic reactions. The total number of available receptor specificities is limited by the number of B and T lymphocytes.

In my prior post, I explained that Kirk Fitzhugh, a scientist at the Natural History Museum of Los Angeles County (NHMLAC), wrongly claims that intelligent design (ID) is not testable. Fitzhugh’s error that ID is “immune to testing” is important. While he should have the academic freedom to believe and contend that ID is “immune to testing” and not scientific, he uses his claim that ID is not testable to justify suppressing ID. He anticipates this deficiency in his position, and thus writes: First, there’s the claim that science precludes expression of thought. In the context of ID, such a claim of overt suppression is inaccurate. Science is a process of acquiring ever-increasing causal understanding, and such a process has Read More ›

[Editor’s Note: Earlier this year, in a series of posts on the BioLogos website (“Adaptive Immunity: How Randomness Comes to the Rescue” and “Evolution and Immunity: Same Story“), Kathryn Applegate argued that the “random” processes of the vertebrate adaptive immune system serve as an example of how Darwinian mechanisms can generate biological complexity. Today, Discovery Institute presents part one of a response to Dr. Applegate from Donald L. Ewert, a research immunologist/virologist who spent much of his career studying the molecular and cell biology of the immune system, as well as theories about its evolution. Dr. Ewert received his Ph.D. from the University of Georgia in 1976. As a microbiologist, he operated a research laboratory at the Wistar Institute in Philadelphia for almost twenty years. The Wistar Institute is one of the world’s leading centers for biomedical research. His research, supported by National Institute of Health, National Science Foundation, and Department of Agriculture grants, has involved the immune system, viruses, and cellular biology.]

Introduction

In her articles on the BioLogos website, Kathryn Applegate attempts to show how the mechanisms used by the adaptive immune system to generate a diversity of antigen receptors are an example of Darwinian evolution. She focuses on aspects of these mechanisms that she characterizes as “blind” and “random,” stating, “Antibody production and evolution both involve mutation and selection.” She further claims that “the adaptive immune system harnesses the power of randomness to protect the body from assaults it has never seen before” and antibody “production requires randomness at multiple levels.” Applegate, however, frames her argument in theological terms, arguing that if “God uses natural processes — indeed, even a ‘blind’ system for generating massive amounts of diversity,” why could he not use the same mechanisms to “create life over long periods of time”?