Disguised as an informal history of immunology, Daniel Davis’ multi-tasking book brings us up to speed on immune system research. This includes a new understanding of immune function in the brain as well as in pregnancy. Formerly, the immune system was thought to remain outside the blood-brain barrier, to avoid damaging neurons. Now it’s increasingly clear that the immune system not only plays a role in learning and mental illness, its cells function very much like neurons.
Like neurons, they form synapses. These are juncture points where proteins are emitted and received by other cells. Molecular immunologist Davis’ own contribution to the research has been to show that these synapses occur in more than one kind of immune cell, and that the synapse is where the immune cell gets switched on and off either to destroy a cell or withdraw. Not only do immune cells act like neurons, Davis points out that “…stroke and many other neurological problems can be triggered or exacerbated by immune responses.” Narcolepsy may even be an auto-immune disease.
The newer research also shows that immune function determines the success of pregnancy, by affecting how well the placenta embeds in the uterine wall. Too much immune response from the mother and the placenta will be rejected or weakened.
In a rare presentation for a lay audience, Davis lays out the fundamental way the system works. Certain “compatibility” genes, which let our body recognize the difference between self and other, exist in nearly all our cells. Their role is to make proteins that hold up to the cell’s surface components of various proteins inside the cell. This way, an immune system cell an tell whether it has encountered a healthy “self” cell or one possessed by a virus.
We each have six of these compatibility genes in our cells, three from the mother and three from the father. Sounds straightforward, but because of the subtypes (A,B, and C) of each, and a thousand or so different versions of each subtypes, the actual range of combinations is astronomical. Depending on which combination you have, you might be protected from certain diseases but not others. Davis reasons that, for the human race as a whole, these genes could cover the spectrum of disease, thus ensuring that some subgroup or tribe can defend against almost any pathogen. But there is no one optimal combination. And there are trade-offs. The same gene that gives some protection against HIV also causes ankylosing spondylitis, an arthritic autoimmune disease of the spine.
Davis even speculates, based on the notorious (and inconclusive) sweaty t-shirt experiments, that compatibility genes might determine sexual preference in humans as they do in mice. It’s not hard to see how compatibility for successful pregnancy and warding off of disease would be a winning combination in natural selection.
The book is by no means all science and no play. Davis uses brief sketches of the major players’ lives to show us how science really works—through collaboration and a very human exchange of ideas. He starts with Peter Medawar, who showed, back in the 50s, that transplant rejection is the result of an immune cell reaction. He goes on to introduce us to the discoverers of the thymus-mediatedT-cells that discriminate between self and other, the antibody- secreting B-cells and the tumor-hunting Natural Killer cells.
Immunology has since moved on to a whole new era, one in which proteins and genes can be manipulated within the cell itself. Several women have played key roles in this more recent research. Pamela Bjorkman gave us the actual structure of the compatibility gene through X-ray crystallography. Form follows function in that the top of this protein is a clamp for seizing and presenting protein bits on the surface of the cell. The illustration of this on p. 77 (location 1473) is alone worth the price of the book.
Whither immune cell research? Davis notes that “. . . our variation in these genes has been linked to many neurological disorders such as schizophrenia or bipolar disorder.22 This is consistent with an intimate connection between compatibility genes and our nervous system. But researchers studying schizophrenia, and other neurological diseases, differ in their view of how important these genes are. Although many tens of studies link compatibility genes to schizophrenia, dispute remains because each comes to a different conclusion about which versions of these genes are risk factors for illness.23”
Indeed, because it’s very rare for any single gene (as in Huntington’s disease) to cause a disease, immunologist Eric Schacht’s approach has been a multivariate one, to find out which sets of genes function together to influence a specific disease. This requires some higher-order number-crunching.
As for me, an allergy sufferer, who had an adolescent tendency towards depression, I’m happy to find confirmation of my long-held intuition that the immune system plays a role in mental illness. But I wonder whether victims of autism, bipolar disorder and schizophrenia have ever been systematically screened for the presence of Immunoglobulin E, the immune factor responsible for allergy and autoimmune disease. Wouldn’t this be a simpler way of establishing whether this system underlies much mental illness? If all such sufferers do belong to the 20% of the world’s population that has this immune activity (originally a system for fighting parasites), wouldn’t this be useful to know in developing therapies? Wouldn’t then the treatments, at least from some of these diseases, tend to be similar to that of allergy or certain autoimmune conditions?
The science in Davis’ book requires concentration and attention, but it isn’t beyond anyone who’s had a good high-school biology course. I used the Kindle Notes function to highlight and review. Kudos to Davis for enlightening us non-scientists with an engaging, illuminating and very well-written work.
Patricia Lawson, author of HARD ASPECTS, a satire on offshore academia.
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