The August 1, 2008 edition of the Journal of Immunology contains a fascinating article by the AAI’s new president, Olivera Finn. Dr. Finn has been a cancer researcher for more that 20 years, working on the mechanisms whereby the human immune system recognizes (or fails to recognize) tumors. She is the discoverer of MUC-1, a glycoprotein that is found in an altered form in many different kinds of cancers. Dr. Finn’s contributions to the science of immunology are impressive, but her article reveals a woman who thinks even more deeply about the roots of disease and wellness as they relate to immune system function throughout life.
For the last few years there have been suggestions in the literature that exposure to infectious agents early in life is essential for the prevention of allergies later in life. The hygiene hypothesis implies that rearing children in an environment that is too clean might cause them to have more allergic illnesses in adulthood. In he paper, Dr. Finn extends the hygiene hypothesis to include cancer as well. In her work, both in vitro and in vivo, patients who had certain infections at a young age developed protective immunity against both the infectious agent and to a group of antigens called tumor-associated antigens. As adults these individuals had lower incidence of cancer.
Have you ever been confronted by someone who says: “How can you believe in a God when the world is full of disease and suffering?” What if it turns out that there are reasons for infection and disease that are part of an even larger plan we know nothing about? While I am not suggesting that I know the whole reason, research like this makes me wonder if we are just seeing the tip of some infinite rationale?
Even more intriguing is Dr. Finn’s penultimate paragraph where she suggests that there might be a very small subset of proteins that could comprise a “universal vaccine” capable of preventing all forms of infectious disease, cancer, and autoimmune disease. Her theory is intriguing, though scientifically mind-bending. It makes me wonder, is this a form of divine providence, heretofore unknown? Time will tell.
Friday, August 22, 2008
Saturday, August 16, 2008
Update from APA
For the first time since my wife completed her PhD I am a guest at a professional conference. It is really a terrific feeling seeing Kay in her element and respected for her work. But that is not the subject of this entry.
I attended an interesting talk yesterday afternoon on Rhesus monkeys. The researcher, Dr. Steven Sumi, has worked with a large colony of these animals for over 20 years. They are genetically similar to humans, as are most primates, but are not our closest genetic relative.
If you carefully observe these animals you will notice that there are several sub-populations within the larger family groups. The subject of this study was a population (5-10% in the wild) that is overly aggressive and prone to taking serious risks, including alcoholism and binge drinking. These little monkeys are mostly male, and - if their behavior cannot be corrected - are kicked out of the family and not allowed to return. Aggressive behavior is not welcome in these matriarchal family groups.
Tie to genetics - In humans several genes have been associated with risk taking behaviors, alcoholism, aggression, etc, including (but not limited to) an uptake transporter for the neurotransmitter serotonin (5-HIAA). According to Dr. Sumi there is a single nuceotide polymorphism (SNP) that causes the amount of the transporter to be dysregulated (lower than normal). (At this point I need to pause and point out that I am at a psychology meeting and not a neuroscience meeting. While the behavioral aspects of Dr. Sumi's talk were excellent, his presentation of the genetic and molecular data was rather weak. I suspect that he collaborates with a group of geneticists who do that aspect of the work.)
Back to the presentation - interestingly, the mutation in 5-HIAA that we see in humans also shows up in the Rhesus monkey... and only in the group that is overly aggressive! There seems to be a strong, positive correlation between the presence of the mutated 5-HIAA and aggressive, risky behaviors.
Left alone the correlative relationship of gene to behavior would be interesting, but watch this: if a baby monkey with the bad version of 5-HIAA is reared by an experienced mother with good mothering skills the effect of the bad gene can be completely reversed!!! This represents an excellent example of nurture overwhelming nature.
What's missing? Quite a bit actually. First, Dr. Sumi never intimated whether these animals were homozygous or heterozygous for the mutated 5-HIAA, so we have no way of knowing how much of a contribution was made by the mutated gene. As far as I can tell, no knock-in, knock-out, or RNAi experiments have been done on these animals to determine the full measure of gene involvement. I would suggest that this research needs to be expanded by the molecular biology community.
One last observation made by Dr. Sumi bears mention. The mutated form of 5-HIAA is only seen in the most widely dispersed and biologically successful primates: Rhesus monkeys and humans. He suggested that the reason this gene stays around in the gene pool is that it is necessary for our survival as a species.
I attended an interesting talk yesterday afternoon on Rhesus monkeys. The researcher, Dr. Steven Sumi, has worked with a large colony of these animals for over 20 years. They are genetically similar to humans, as are most primates, but are not our closest genetic relative.
If you carefully observe these animals you will notice that there are several sub-populations within the larger family groups. The subject of this study was a population (5-10% in the wild) that is overly aggressive and prone to taking serious risks, including alcoholism and binge drinking. These little monkeys are mostly male, and - if their behavior cannot be corrected - are kicked out of the family and not allowed to return. Aggressive behavior is not welcome in these matriarchal family groups.
Tie to genetics - In humans several genes have been associated with risk taking behaviors, alcoholism, aggression, etc, including (but not limited to) an uptake transporter for the neurotransmitter serotonin (5-HIAA). According to Dr. Sumi there is a single nuceotide polymorphism (SNP) that causes the amount of the transporter to be dysregulated (lower than normal). (At this point I need to pause and point out that I am at a psychology meeting and not a neuroscience meeting. While the behavioral aspects of Dr. Sumi's talk were excellent, his presentation of the genetic and molecular data was rather weak. I suspect that he collaborates with a group of geneticists who do that aspect of the work.)
Back to the presentation - interestingly, the mutation in 5-HIAA that we see in humans also shows up in the Rhesus monkey... and only in the group that is overly aggressive! There seems to be a strong, positive correlation between the presence of the mutated 5-HIAA and aggressive, risky behaviors.
Left alone the correlative relationship of gene to behavior would be interesting, but watch this: if a baby monkey with the bad version of 5-HIAA is reared by an experienced mother with good mothering skills the effect of the bad gene can be completely reversed!!! This represents an excellent example of nurture overwhelming nature.
What's missing? Quite a bit actually. First, Dr. Sumi never intimated whether these animals were homozygous or heterozygous for the mutated 5-HIAA, so we have no way of knowing how much of a contribution was made by the mutated gene. As far as I can tell, no knock-in, knock-out, or RNAi experiments have been done on these animals to determine the full measure of gene involvement. I would suggest that this research needs to be expanded by the molecular biology community.
One last observation made by Dr. Sumi bears mention. The mutated form of 5-HIAA is only seen in the most widely dispersed and biologically successful primates: Rhesus monkeys and humans. He suggested that the reason this gene stays around in the gene pool is that it is necessary for our survival as a species.
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