Human Evolution

[Darwinsbulldog]

Melis, A. P., F. Warneken, et al. (2011). "Chimpanzees help conspecifics obtain food and non-food items." Proceedings of the Royal Society B: Biological Sciences 278(1710): 1405-1413.

Chimpanzees (Pan troglodytes) sometimes help both humans and conspecifics in experimental situations in which immediate selfish benefits can be ruled out. However, in several experiments, chimpanzees have not provided food to a conspecific even when it would cost them nothing, leading to the hypothesis that prosociality in the food-provisioning context is a derived trait in humans. Here, we show that chimpanzees help conspecifics obtain both food and non-food items—given that the donor cannot get the food herself. Furthermore, we show that the key factor eliciting chimpanzees' targeted helping is the recipients' attempts to either get the food or get the attention of the potential donor. The current findings add to the accumulating body of evidence that humans and chimpanzees share the motivation and skills necessary to help others in situations in which they cannot selfishly benefit. Humans, however, show prosocial motives more readily and in a wider range of contexts.

http://rspb.royalsocietypublishing.o.../1405.abstract
http://rspb.royalsocietypublishing.o.../1405.full.pdf

[Darwinsbulldog]

Pregnancy: Why Mother's Immune System Does Not Reject Developing Fetus as Foreign Tissue

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Researchers at NYU School of Medicine have made an important discovery that partially answers the long-standing question of why a mother's immune system does not reject a developing fetus as foreign tissue. (Credit: © PeterPunk / Fotolia)

ScienceDaily (June 7, 2012) — Researchers at NYU School of Medicine have made an important discovery that partially answers the long-standing question of why a mother's immune system does not reject a developing fetus as foreign tissue.
"Our manuscript addresses a fundamental question in the fields of transplantation immunology and reproductive biology, namely, how do the fetus and placenta, which express antigens that are disparate from the mother, avoid being rejected by the maternal immune system during pregnancy?" explained lead investigator Adrian Erlebacher, MD, PhD, associate professor of pathology and a member of the NYU Cancer Institute at NYU Langone Medical Center. "What we found was completely unexpected at every level."
The researchers discovered that embryo implantation sets off a process that ultimately turns off a key pathway required for the immune system to attack foreign bodies. As a result, immune cells are never recruited to the site of implantation and therefore cannot harm the developing fetus.
The study, funded by grants from the National Institutes of Health and the American Cancer Society, appears in the June 8 issue of Science.
A central feature of the body's natural immune defense against transplanted foreign tissues and pathogens is the production of chemokines as a result of the local inflammatory response. The chemokines recruit various kinds of immune cells, including activated T cells, which accumulate and attack the tissue or pathogen. The chemokine-mediated recruitment of activated T cells to sites of inflammation is an integral part of the immune response.
During pregnancy however, the foreign antigens of the developing fetus and the placenta come into direct contact with cells of the maternal immune system, but fail to evoke the typical tissue rejection response seen with organ transplants.
Several years ago, Erlebacher and his research team found that T cells, poised to attack the fetus as a foreign body, were somehow unable to perform their intended role. The finding prompted the researchers to wonder if perhaps there was some sort of barrier preventing the T cells from reaching the fetus. They turned their attention to studying the properties of the decidua, the specialized structure that encases the fetus and placenta, and there, in a mouse model, they found new answers.
The research team has discovered that the onset of pregnancy causes the genes that are responsible for recruiting immune cells to sites of inflammation to be turned off within the decidua. As a result of these changes, T cells are not able to accumulate inside the decidua and therefore do not attack the fetus and placenta.
Specifically, they revealed that the implantation of an embryo changes the packaging of certain chemokine genes in the nuclei of the developing decidua's stromal cells. The change in the DNA packaging permanently deactivates, or "silences," the chemokine genes. Consequently, the chemokines are not expressed and T cells are not recruited to the site of embryo implantation.
Also of note, the observed change in the DNA packaging was a so-called 'epigenetic' modification, meaning a modification that changes gene expression without the presence of a hereditable gene mutation.
"These findings give insight into mechanisms of fetal-maternal immune tolerance, as well as reveal the epigenetic modification of chemokine genes within tissue stromal cells as a modality for limiting the trafficking of activated T cells," Dr. Erlebacher said. "It turns out that the cells that typically secrete the chemoattractants to bring the T cells to sites of inflammation are inhibited from doing so in the context of the pregnant uterus. The decidua appears instead as a zone of relative immunological inactivity."
Inappropriate regulation of this process, Dr. Erlebacher explained, could cause inflammation and the accumulation of immune cells at the maternal-fetal interface, which could lead to complications of human pregnancy, including preterm labor, spontaneous abortion and preeclampsia.
Erlebacher and his team will next look to see if these epigenetic modifications are also present within the human decidua, and whether the failure to generate them appropriately is associated with complications of human pregnancy. He explained that the study's findings also raise the possibility that the same kind of mechanism could enhance a tumor's ability to survive inside its host. The findings could have implications for autoimmune diseases, organ transplantation and cancer, as well as pregnancy.
"This is a very exciting finding for us because it gives a satisfying explanation for why the fetus isn't rejected during pregnancy, which is a fundamental question for the medical community with clear implications for human pregnancy," Dr. Erlebacher said. "It also reveals a new modality for controlling T cell trafficking in peripheral tissues that could provide insight into a myriad of other conditions and diseases."

http://www.sciencedaily.com/releases...0607142244.htm

Source:-

Nancy, P., E. Tagliani, et al. (2012). "Chemokine Gene Silencing in Decidual Stromal Cells Limits T Cell Access to the Maternal-Fetal Interface." Science 336(6086): 1317-1321.

The chemokine-mediated recruitment of effector T cells to sites of inflammation is a central feature of the immune response. The extent to which chemokine expression levels are limited by the intrinsic developmental characteristics of a tissue has remained unexplored. We show in mice that effector T cells cannot accumulate within the decidua, the specialized stromal tissue encapsulating the fetus and placenta. Impaired accumulation was in part attributable to the epigenetic silencing of key T cell–attracting inflammatory chemokine genes in decidual stromal cells, as evidenced by promoter accrual of repressive histone marks. These findings give insight into mechanisms of fetomaternal immune tolerance, as well as reveal the epigenetic modification of tissue stromal cells as a modality for limiting effector T cell trafficking.

http://www.sciencemag.org/content/336/6086/1317

[riddlemethis]

That's some mind boggling evolution right there! Talk about convoluted.

Would've just been better to design it so the embryo didn't act immunologically as a parasite? :wink:

Take that creationists.

[wolty]

That is so interesting.


Sent telepathically.

[Darwinsbulldog]

I read somewhere that endogenous retrovirus[a "tamed" retrovirus that often has a function in the host] might have been involved in the evolution of the placental mammals. I will try to find it. Retros copy their genes into our DNA. Mostly, it is harmful. Perhaps in the case of humans, it is-far better to lay an egg than a women to have a "John Hurt Moment" [1] every time we want to reproduce!

1. Referring of course to the "birth" of one of Lt. Ripley's Bad Guys from Cane's chest in the Alien movie. Of course the kind retrovirus responsible, could not have known that a species that would became human would be so stupid as to decide to walk upright with a big head, thus throwing god's plan for us into utter chaos.

[riddlemethis]

Originally Posted by Darwinsbulldog

I read somewhere that endogenous retrovirus[a "tamed" retrovirus that often has a function in the host] might have been involved in the evolution of the placental mammals. I will try to find it. Retros copy their genes into our DNA. Mostly, it is harmful. Perhaps in the case of humans, it is-far better to lay an egg than a women to have a "John Hurt Moment" [1] every time we want to reproduce!

1. Referring of course to the "birth" of one of Lt. Ripley's Bad Guys from Cane's chest in the Alien movie. Of course the kind retrovirus responsible, could not have known that a species that would became human would be so stupid as to decide to walk upright with a big head, thus throwing god's plan for us into utter chaos.

my emphasis: not to mention having young who are self sufficient in a matter of months rather than decades!

[Darwinsbulldog]

Indeed!

Ah, here we go...!

Sugimoto, J. and D. J. Schust (2009). "Review: Human Endogenous Retroviruses and the Placenta." Reproductive Sciences 16(11): 1023-1033.

Up to 8% of the human genome is of retroviral origin. These stably integrated retroviral sequences that characterize the human endogenous retrovirus (HERV) arose from retroviral infections that occurred more than 25 million years ago. The host and the retrovirus have subsequently coevolved as retrovirally derived genetic material is propagated in a Mendelian fashion. Although most HERV sequences are silenced, several have been described that are functional. The effects of some HERV-derived products are linked to human disease; others appear essential to human organ function. The human placenta, unique in its active expression of retroviral sequences that are not expressed in other tissues, may hold the key to an improved understanding of the functional significance of HERVs. In this review, we discuss the contribution of retroelements, particularly HERVs, to placental function and dysfunction. We describe fusogenic and immunosuppressive HERV activities and emphasize epigenetic regulation of retroelement expression.

http://rsx.sagepub.com/content/16/11/1023.abstract

Just type ERV + placenta into google scholar and heaps of references turn up!

[I am on my laptop at the moment with an older Version of Endnotes and an out of date database].

[Darwinsbulldog]

Archie, E. A., J. Altmann, et al. (2012). "Social status predicts wound healing in wild baboons." Proceedings of the National Academy of Sciences 109(23): 9017-9022.

Social status can have striking effects on health in humans and other animals, but the causes often are unknown. In male vertebrates, status-related differences in health may be influenced by correlates of male social status that suppress immune responses. Immunosuppressive correlates of low social status may include chronic social stress, poor physical condition, and old age; the immunosuppressive correlates of high status may include high testosterone and energetic costs of reproduction. Here we test whether these correlates could create status-related differences in immune function by measuring the incidence of illness and injury and then examining healing rates in a 27-y data set of natural injuries and illnesses in wild baboon males. We found no evidence that the high testosterone and intense reproductive effort associated with high rank suppress immune responses. Instead, high-ranking males were less likely to become ill, and they recovered more quickly than low-ranking males, even controlling for differences in age. Notably, alpha males, who experience high glucocorticoids, as well as the highest testosterone and reproductive effort, healed significantly faster than other males, even other high-ranking males. We discuss why alpha males seem to escape from the immunosuppressive costs of glucocorticoids but low-ranking males do not, including the idea that glucocorticoids' effects depend on an individual's physiological and social context.

FULL PAPER AVAILABLE:-

http://www.pnas.org/content/109/23/9017.abstract

[Darwinsbulldog]

Prufer, K., K. Munch, et al. (2012). "The bonobo genome compared with the chimpanzee and human genomes." Nature advance online publication.

Two African apes are the closest living relatives of humans: the chimpanzee (Pan troglodytes) and the bonobo (Pan paniscus). Although they are similar in many respects, bonobos and chimpanzees differ strikingly in key social and sexual behaviours1, 2, 3, 4, and for some of these traits they show more similarity with humans than with each other. Here we report the sequencing and assembly of the bonobo genome to study its evolutionary relationship with the chimpanzee and human genomes. We find that more than three per cent of the human genome is more closely related to either the bonobo or the chimpanzee genome than these are to each other. These regions allow various aspects of the ancestry of the two ape species to be reconstructed. In addition, many of the regions that overlap genes may eventually help us understand the genetic basis of phenotypes that humans share with one of the two apes to the exclusion of the other.

http://www.nature.com/nature/journal...ture11128.html

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[the_gelf]

How interesting, we are more closely related to a bonobo than a chimp is Perhaps that explains our rampant homosexuality