The Long Arm of the Immune System

Dendritic cells are an important component of the immune system. They reside in our tissues and bloodstream in their immature form. When they are exposed to a pathogen, they use sucker like projections from their many “arms” to capture it and eat it. Once ingested, they break the pathogen down and isolate the antigens that are specific to this pathogen, after which they travel through the blood system or the spleen to one of the Lymph nodes. Here they attempt to find the B and T-cells that allow our bodies to fight off pathogens. Interestingly, the dendritic cells also appear to determine if killer T-cells or antibodies are produced as a response to the pathogen.
Some scientists are attempting to use this phenomenon to inoculate our bodies against cancer. With some cancer patients, scientists are taking monocytes, cells that become either macrophages or dendritic cells, and culturing them along with antigens of the specific cancer the patient has. Once the dendritic cells mature and are ready to present the antigen to B and T-cells, the scientists inject them back into the patient. Although this does not cure cancer, or allow the body to completely fight it off, it has been show to make patients immune responses stronger than they would have been. However, there are some problems with this technique. Because cancers are mutating by definition, it is possible that the cancer could stop presenting the antigen that the body was targeting, rendering the vaccine useless. Also, if the antigen the scientists have isolated is present elsewhere in the body, it could lead to the body destroying other things than the cancer.
Another thing scientists are attempting to learn about dendritic cells is how to shut them down. In autoimmune diseases, dendritic cells appear to be hyperactive. For example, when a patient has lupus, it appears that their dendritic cells mature in their blood stream, due to a protein that their cells release, and then ingest the patient’s DNA, which they then present to a B and T-cell, creating an immunity to the bodies own DNA. By learning more about the mechanisms that control dendritic cells, scientists hope to eventually be able to control our immune system responses.

-Dylan Karle

Source: Scientific American, November 2002 issue

New HIV model may help in finding T cells that can fight against the virus

Chinese researches have recently developed a new HIV model in hopes of incorporating HIV’s behavioral dynamics into the modeling system. This new model suggests that a particular type of T cell could be useful in fighting HIV in a vaccine. Scientists from Xiamen University have been able to incorporate the ways HIV responds to antibodies, and its random mutations, into their model. This new model is able to act like the actual HIV virus does in real life.

(The structure of HIV)

In the past, clinical trials have shown that in the acute first phase of human infection (about 2-6 after the virus enters the host body), HIV behaves normally. Our body sends T Cells to fight the virus, which is growing stronger. T cells work when they are activated by the presence of their specific pathogen in the body. They have markers on the outside of their cells that bind to an antigen that is only on the HIV virus. They then begin to reproduce and go to the part of the body that is infected, where they begin to attack the virus. This is different from how the innate immune system works in that T cells are not only limited to attacking the virus when it is in the blood stream, since they can also kill infected cells, killing the virus before it can produce more viruses in that infected cell.

(A T cell attacking a virus)

In most viruses, T cells are able to completely fight off the virus and use their memory to patrol the bloodstream in case the virus ever comes back, in which case they would be able to recognize the virus immediately and fight it off again. However, in HIV, the T Cells are not able to completely kill the virus, which stores itself away and spends years recuperating its strength. HIV has the ability to target CD4+ T cells, which are the master regulators of our immune system. They also have many mutating properties. Researchers believe that these two factors are what allow HIV to escape total annihilation. During the time HIV hides and regains strength, it is also slowly attacking our immune system.

However, the body has CD8+ T cells. Until this new HIV model, scientists had never seen a simulation which includes how the CD8+ T cells could fight in the battle against HIV. CD8+ T cells may be able to provoke a stronger response against HIV because they are not targeted by the virus like our CD4+ T cells are. They also appear to be more able to put the virus down during the first acute phase of the infection in the initial 2-6 weeks. By putting these particular T cells into an AIDS vaccine, we may have gotten one step closer in being able to fight off the HIV virus.

-Emma G.

Sources:
http://www.medicalnewstoday.com/articles/187222.php
http://www.sciencemuseum.org.uk/on-line/lifecycle/images/1-2-5-3-5-2-2-0-0-0-0.jpg
http://biology.kenyon.edu/slonc/gene-web/Lentiviral/hiv_image.jpg

Seeing Disease Symptoms May Make One's Immune System More Aggressive

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Seeing Disease Symptoms May Make One's Immune System More Aggressive

Study Relates Seeing Disease Symptoms to Increase in Immune System Aggressiveness


Seeing an ill person on the street, in a building, or even in a picture, may make one's immune system work harder. Though most people have a psychological response to seeing a sick person (they want to stay away), scientists have recently discovered that seeing an ill person may trigger an aggressive physical response by the immune system. In the University of British Columbia a study was done that showed different people pictures of sick people to see it there was a response from the immune system. "It seems like it's probably good for the immune system to be responding especially aggressively at times when it looks like you are likely to be coming into contact with something that might make you sick." says Mark Schaller. He also says that his may help fight off pathogens. Pathogens are barteria, viruses or basically anything that can cause a disease. The researchers found that seeing sick people make other people have a physiological response and want to stay away from the sick person.

The researchers also wanted to find out if a person's immune system acts differently when they see a sick person. So, they set up an experiment to test this. They showed 10 minute slides to people on 2 different days. There were 3 types of slide shows. First a neutral one that was not expected to trigger any reaction from the immune system which was of furniture. Then the subjects were shown either a slide show of ill people, or a slide show of guns. Before and after each showing a blood sample was taken from each individual. The scientists added a little bacteria to the sample to test for a specific component called interleukin-6 which protects the immune system cells. The results of the experiment showed that the people who watched the disease sideshow had a stronger response by their immune system than the people who watched the gun or furniture slide shows.
















Acknowledgments: None.


Questions to Consider:


Do you think that there could be other responses in the body like this one that could be useful to our health or well-being?


Do you think that this is a reasonable response to seeing a sick person? For example, when you see a sick person do you want to stay away from them or do you not notice this response?

Do you think the researchers could have done anything differently that would have made the experiment better? What would you have done if you had to come up with an experiment to test the researchers second question?


Works Cited:

ScienceDaily. Retrieved April 29, 2010, from http://www.sciencedaily.com­ /releases/2010/04/100427111248.htm

Herbert, Wray. "'I feel your disease.'" Association for Psychological Science.
N.p., Apr. 2010. Web. 29 Apr. 2010. .


Allergy details: Retrieved April 29, 2010, from http://www.allergy-details.com/health-t/wikipedia-features-immune-system/


Lily, Arielle and Arianne- Section 2 Magenta

Epigenetics

Epigenetics

The remote large areas of northern Sweden are an unlikely place to begin a story about genetic science. The kingdom's northern county, Norrbotten, has barely any human life. An average of six people live in each square mile and this tiny population can reveal a lot about how genes work in our everyday lives.

Norrbotten is very isolated. In the 19th century, if the harvest was bad, people starved. The years people starved were the hardest for their vulnerability. For example, 1800, 1812, 1821, 1836 and 1856 were years of total crop failure and extreme suffering. But in 1801, 1822, 1828, 1844 and 1863, the land spilled so much wealth that the same people who had gone hungry in previous winters were able to feed themselves for months.

In the 1980s, Dr. Lars Olov Bygren, a preventive-health specialist who is now at the prestigious Karolinska Institute in Stockholm, began to think what long-term effects the celebration and famine years might have had on children growing up in Norrbotten in the 19th century and not just on them but on their kids and grandkids as well. He picked a random group of 99 individuals born in the Overkalix parish of Norrbotten in 1905 and used historical records to trace their parents and grandparents back to birth. By analyzing accurate natural records, Bygren and two colleagues figured how much food was available to the parents and grandparents when they were young.

Around the time he started collecting the data, Bygren had become interested with research showing that conditions in the womb could affect your health not only when you were a fetus but well into adulthood. In 1986, the Lancet published the first of two groundbreaking papers showing that if a pregnant woman ate poorly, her child would be extremely higher than the average possibility for heart disease as an adult. Bygren thought whether that effect could start before pregnancy: Could parents' experiences early in their lives somehow change the traits they passed to their offspring?

It was a different idea. After all, we have had a lasting deal with biology: whatever choices we make during our lives might ruin our short-term memory or make us fat or hurry to death, but they won't change our genes — our actual DNA. Which meant that when we had our own kids, the genetic slate would be wiped clean.

Also, any such effects of nurture (environment) on a species' nature (genes) were not supposed to happen so quickly. Charles Darwin, whose On the Origin of Species celebrated its 150th anniversary in November, taught us that evolutionary changes take place over many generations and through millions of years of natural selection. But, now, Bygren and other scientists have collected historical evidence showing that powerful environmental conditions (near death from starvation, for instance) can somehow leave an imprint on the genetic material in eggs and sperm. These genetic imprints can short-circuit evolution and pass along new traits in a single generation.

For instance, Bygren's research showed that in Overkalix, boys who enjoyed those rare overabundant winters — kids who went from normal eating to gluttony in a single season — produced sons and grandsons who lived shorter lives. Far shorter: in the first paper Bygren wrote about Norrbotten, which was published in 2001 in the Dutch journal Acta Biotheoretica, he showed that the grandsons of Overkalix boys who had overeaten died an average of six years earlier than the grandsons of those who had endured a poor harvest. Once Bygren and his team controlled for certain socioeconomic variations, the difference in longevity jumped to an astonishing 32 years. Later papers using different Norrbotten cohorts also found significant drops in life span and discovered that they applied along the female line as well, meaning that the daughters and granddaughters of girls who had gone from normal to gluttonous diets also lived shorter lives. To put it simply, the data suggested that a single winter of overeating as a youngster could initiate a biological chain of events that would lead one's grandchildren to die decades earlier than their peers did. How could this be possible?

Bygren's data — along with those of many other scientists working separately over the past 20 years — have given birth to a new science called epigenetics. At its most basic, epigenetics is the study of changes in gene activity that do not involve alterations to the genetic code but still get passed down to at least one successive generation. These patterns of gene expression are governed by the cellular material — the epigenome — that sits on top of the genome, just outside it (hence the prefix epi-, which means above). It is these epigenetic "marks" that tell your genes to switch on or off, to speak loudly or whisper. It is through epigenetic marks that environmental factors like diet, stress and prenatal nutrition can make an imprint on genes that is passed from one generation to the next.

Epigenetics presentation

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PTSD is linked to genes

A neurological disorder is now being linked to DNA



Post Traumatic Stress Disorder (PTSD) is a psychiatric illness that affects the brain after it goes through a traumatic experience. It was first identified in Vietnam veterans who have experienced traumatic event. The types of traumatic events range from losing a loved one, experiences in prison, assault, domestic abuse, rape, war experiences. Symptoms of the disorder may be immediate or delayed up to 6 months after the event. It can affect individuals of any age, race, or gender. Everyone experiences some stress from traumatic events but not every one gets PTSD. Physicians and psychologists can interview patients with symptoms of PTSD, though there is no definite test to diagnose it. Diagnosis is based on the onset of symptoms, history of trauma, and history of traumatic event.
A recent study identified genes as potential biologic markers linked to PTSD. Scientists involved with the study screened surviving victims of the Rwandan genocide. The death toll of the genocide has been estimated at 1 out of 5 people or at least 500,000 people. Exact numbers are not available, but estimates have determined most Rwandans experienced significant trauma by witnessing traumatic events or losing loved one. The study evaluated blood samples and reviewed medical records from 424 Rwanda genocide survivors living in the Nakivale refugee camp in southwestern Uganda. All participants experienced trauma but one group was diagnosed with PTSD orwith and one group was PTSD-free. Scientist hypothesized that a "traumatic load" can be calculated to quantify the amount of trauma a person experiences. A traumatic load was defined as "the number of traumatic events he or she experiences." Basically they concluded the higher the traumatic load, the higher the chance of developing PTSD. The study found a "dose-response" relationship between traumatic load and the widespread appearance of lifetime PTSD. The hypothesis suggests a direct relationship where the higher amount of traumatic load, the more likely the chance of developing PTSD. Scientists also found genetic biomarkers directly linked to the "traumatic load" The COMT (catechol-O-methyltransferase) is an enzyme produced by all individuals with some variability. COMT "digests" the chemicals produced when stress occurs. Previously, COMT has been linked with the feeling of fear. With this in mind, The people with less COMT have a higher stress load leaving them more vulnerable to PTSD. This study may provide information putting us one step closer to finding a biologic intervention for prevention or treatment of mental disorders related to stress like PTSD .

Ptsd

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questions:
Is PTSD an issue
do you think that if scientist continue to study the COMT enzyme do you think they will cure PTSD?
Do you think this experiment makes sense?
Do you think some people can be less likely to have a mental disorder
Is it okay to study people who have already gone through such an ordeal like genocide
If you could run the experiment, what changes would you make to it

New Technique Strengthens Immune Cells to Fight Cancer

Konstantine Adamopoulos

New Stanford University Research has recently begun to show, enhance, and grow T-cells in living mice and in human cell cultures. These breakthroughs may be the key to pote

ntially surpassing the drawbacks of current immune cell therapy, which has not proven to be the most effective mechanism for the human body.

The way this new mechanism works is by means of a relatively new branch of biology, synthetic biology, "in which researchers can build new functions into cells by integrating pre-designed genetic components," or simply, in which researchers can alter cells with existing genetic makeups of other molecules.

Where the bar is raised between the old method of immune cell care and this new method, is to a height at which the adoptive immunotherapy targets the events that occur when the immune system cannot detect a pathogen or disease. This system works by harvesting T-cells from a patient, modifying the cells, then injecting them back into the place in the body where the disease is most prevalent.

In the past, this has been quite ineffective, due to the fact that the T-cells have not been able to destroy the pathogen on its own without help from other molecules. The new approach, is to further engineer the T-cells so that they can be self-dependent. In other words, 'fix' them and make them strong enough to battle pathogens and bacteria on their own.

Sources: Stanford University Medical Center. "New Technique Reinforces Immune Cells That Seek and Destroy Cancer." ScienceDaily 27 April 2010. 27 April 2010. http://www.sciencedaily.com/releases/2010/04/100426151623.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencedaily+%28

ScienceDaily%3A+Latest+Science+News%29&utm_content=Netvibes

http://www.thelatestnews.in/wp-content/uploads/2009/04/immune-cell.jpg

http://metafysica.nl/l_flower.jpg