The immune system is the system of specialized cells and organs that protect an organism from outside biological influences.

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(Though in a broad sense, almost every organ has a protective function - for example, the tight seal of the skin or the acidic environment of the stomach.) When the immune system is functioning properly, it protects the body against bacteria and viral infections, destroying cancer cells and foreign substances.

If the immune system weakens, its ability to defend the body also weakens, allowing pathogens, including viruses that cause common colds and flu, to grow and flourish in the body.

The immune system also performs surveillance of tumor cells, and immune suppression has been reported to increase the risk of certain types of cancer..

For more information about the topic Immune system, read the full article at Wikipedia.org, or see the following related articles:

Natural killer cell — Natural killer cells (also known as NK cells, K cells, and killer cells) are a type of lymphocyte (a white blood cell) and a component of innate …  > read more

White blood cell — White blood cells (also called leukocytes or immune cells) are cells which form a component of the blood. They help to defend the body against …  > read more

T cell — T cells are a subset of lymphocytes that play a large role in the immune response. The abbreviation “T” stands for thymus, the organ in which their …  > read more

Antiviral drug — Antiviral drugs are a class of medication used specifically for treating viral infections. Like antibiotics, specific antivirals are used for …  > read more

Note: This page refers to an article that is licensed under the GNU Free Documentation License. It uses material from the article Immune system at Wikipedia.org. See the Wikipedia copyright page for more details.

ScienceDaily (July 11, 2008) — Medical science may be a significant step closer to climbing into the driver’s seat of an important class of immune cells, researchers at Washington University School of Medicine in St. Louis report in Nature Immunology.

The researchers showed that a single protein, HS1, enables key functions of natural killer (NK) cells, which kill early cancers and fight off viral infections. The protein allows the NK cells to pursue their targets, latch on to them and configure the cellular machinery it uses to kill them.

“Further study of how HS1 controls these processes may open up new possibilities for revving up the NK cells to fight infection and cancer,” says senior author John Cooper, M.D., Ph.D., professor of cell biology and physiology. “We also may be able to use this same protein to inhibit the activities of other immune cells and prevent them from contributing to autoimmune conditions such as diabetes.”

Cooper, who is a member of the Siteman Cancer Center at Washington University and Barnes-Jewish Hospital, studies how different types of cells use a primary component of their skeletal system known as an actin network. Earlier, his laboratory had probed the role of a protein called cortactin in specialized cells that break down bones. They showed that cortactin’s effects on the actin network made it possible for the cells to form a tightly sealed bond with bones.

“This bond is analogous to a plunger,” says first author Boyd Butler, Ph.D., a postdoctoral fellow in Cooper’s laboratory. “The cell sits down on the bone, seals tightly, and then starts secreting the acid and other compounds that break down the bone.”

NK cells have to form a similar plunger-like bond, known as a lytic synapse, with the targets they attack. They do not make cortactin but produce HS1, which is a very similar protein. Butler decided to see what would happen to NK cells in human blood samples if he turned down their ability to make HS1. The resulting cells were severely disabled: They couldn’t effectively pursue target cells, bind to them or prepare to kill them.

Prior research by other scientists had revealed that when NK cells are in motion or attacking a target, HS1 has chemical modifications attached to it at specific points. Giving the NK cells normal HS1 restored their lost functions, but when researchers gave the NK cells HS1 where these attachment points had been altered, the cells were selectively disabled. Changing one attachment point prevented them from pursuing target cells, while changing the other impaired their ability to bind to targets and kill them.

“Tight regulation is very important to prevent NK cells from harming the body’s own tissues,” Boyd says. “This ability to switch where the control signal goes makes HS1 a powerful regulator of NK cell activity–it allows the cells to provide just the right services at the right time.”

Cooper and Boyd plan follow-up studies that will start at the attachment points on HS1 and trace connections with and influences on other proteins.

“NK cells are very good at nipping early cancers in the bud,” says Cooper. “If we can better understand how they’re activated, this could lead us to ways to make them better killers of cancers and cells infected by viruses and other invaders.”

Funding from the National Institutes of Health, the National Institute of Allergy and Infectious Diseases and the Siteman Cancer Center supported this research.

Journal reference:

1. Butler B, Katendieck DH, Cooper JA. Differentially phosphorylated forms of HS1 mediate distinct functions in natural killer cells. Nature Immunology, Online June 29, 2008

Adapted from materials provided by Washington University in St. Louis, via EurekAlert!, a service of AAAS.

ScienceDaily (May 9, 2008) — Infection with human immunodeficiency virus (HIV), which leads to acquired immunodeficiency syndrome (AIDS), is an epidemic of global concern. According to the most recent estimates, released in November 2007, by the Joint United Nations Programme on HIV/AIDS (UNAIDS) and the World Health Organization (WHO), an estimated 33.2 million worldwide are living with HIV infection currently. Although the rates of infection appear to be decreasing, there are obviously immense implications for achieving improvements in HIV/AIDS treatment.

The functioning of natural killer (NK) cells, which are a major element of the innate immunity system and are involved in the body’s first line of defense against infections such as HIV, is decreased in both HIV and depression. A group of researchers who have previously found that stress and depression impair NK cell function and accelerate the course of HIV/AIDS are now publishing a new report in Biological Psychiatry.

In this study, they recruited both depressed and non-depressed HIV-infected women and studied the ex vivo effects of three drugs, a selective serotonin reuptake inhibitor (SSRI), a substance P antagonist, and a glucocorticoid antagonist, on their NK cell activity. These drugs were selected because, as the authors state, each “affect[s] underlying regulatory systems that have been extensively investigated in both stress and depression research as well as immune and viral research.”

The scientists found that the SSRI citalopram, and the substance P antagonist CP 96,345, but not the glucocorticoid receptor antagonist RU486, increased NK cell activity. According to Dr. Dwight Evans, corresponding author of the article: “The present findings provide evidence that natural killer cell function in HIV infection may be enhanced by selective serotonin reuptake inhibition and also by substance P antagonism in both depressed and non-depressed individuals.”

John H. Krystal, M.D., Editor of Biological Psychiatry and affiliated with both Yale University School of Medicine and the VA Connecticut Healthcare System, comments: “There has been growing evidence that the compromise of immune function associated with depression influences the outcomes of infectious diseases and cancer. Antidepressant treatments are beginning to be studied for their potential positive effects on immune function.”

He adds that “the paper by Evans et al. suggests that antidepressant treatment may have positive effects on natural killer cell activity in cells isolated from individuals infected with HIV with and without depression. This type of bridge between the brain and the rest of the body deserves further attention.” Dr. Evans agrees, noting that “these findings begin to pave the way towards initiating clinical studies addressing the potential role of serotonergic agents and substance P antagonists in improving natural killer cell innate immunity, possibly delaying HIV disease progression and extending survival with HIV infection.”

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Journal reference:

1. Selective Serotonin Reuptake Inhibitor and Substance P Antagonist Enhancement of Natural Killer Cell Innate Immunity in Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome. Dwight L. Evans, Kevin G. Lynch, Tami Benton, Benoit Dubé, David R. Gettes, Nancy B. Tustin, Jian Ping Lai, David Metzger and Steven D. Douglas. Drs. Evans, Lynch, Benton, Dubé, and Metzger and Mr. Gettes are affiliated with the Department of Psychiatry, with Dr. Evans also with the Departments of Medicine and Neuroscience, and Dr. Douglas is with the Department of Pediatrics, all at the University of Pennsylvania School of Medicine in Philadelphia, Pennsylvania. Ms. Tustin and Drs. Lai and Douglas are with the Division of Allergy and Immunology, Joseph J. Stokes Research Institute of The Children’s Hospital of Philadelphia, in Philadelphia, Pennsylvania. Biological Psychiatry, Volume 63, Issue 9 (May 1, 2008).

Adapted from materials provided by Elsevier, via EurekAlert!, a service of AAAS.

ScienceDaily (Nov. 17, 2007) — Natural HIV-1 infection does not always elicit a protective immune response, according to a new study.

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A team of researchers from Washington University, the Fred Hutchinson Cancer Research Center of Seattle, and the University of Nairobi show how HIV-1 vaccines may not be as reliable against superinfection as once thought.

Superinfection of HIV-1 occurs when an individual infected with one strain of HIV-1 acquires a second strain. Currently there are over 20 published cases of HIV-1 superinfection, most of which have been focused on individuals who have been carefully monitored during their infection. These cases prove that an HIV-1 vaccine may not always protect against infection by a different strain. But because there have been reports of selected individuals, it has been unclear how commonly HIV-1 re-infection occurs.

To address this question, Dr. Julie Overbaugh and her research team investigated the incidence of HIV-1 superinfection in 36 high-risk women followed roughly five years after their initial infection.

Seven cases of superinfection were found; five of them occurring over a year past initial infection. Additionally, three of the seven cases displayed a virus from the same HIV-1 genetic subtype.

This study suggests that immune responses found in natural HIV-1 infection, which fail to provide protection against re-infection, may not be the best path to an effective HIV-1 vaccine.

Journal article: Piantadosi A, Chohan B, Chohan V, McClelland RS, Overbaugh J (2007) Chronic HIV-1 infection frequently fails to protect against superinfection. PLoS Pathog 3(11):e177. doi:10.1371/journal.ppat.0030177

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Adapted from materials provided by Public Library of Science, via EurekAlert!, a service of AAAS.

Written by Dr. James Meschino, D.C., M.S.,
– Research and Clinical Director, RenaiSanté Institute of Integrative Medicine –

Recent And Historical Use Of Reishi Mushroom Extract
Reishi mushroom (Ganoderma lucidum) is called “the mushroom of immortality” in China and has been used in Oriental Medicine for over 2,000 years. ^(1,2) In recent years its active ingredients have been the subject of intensive research regarding their apparent ability to help prevent or treat certain types of cancer, aid in the treatment of liver disease, HIV infection, acute or recurrent herpetic infections, high blood pressure, chronic bronchitis, allergies and asthma, and favorably modulate immune function. ⁽³⁾ The reishi mushroom grows wild on decaying logs and tree stumps in the coastal provinces of China. The fruiting body of the mushroom is used medicinally. ⁽⁴⁾

Active Constituents: Reishi mushrooms contain a number of active agents that are known to modulate function of the immune system in humans. The primary agents include:

1. Specific Polysaccharides - which occur in the form of Beta-D-glucans bound to amino acids. These agents are known to possess immune-modulating and anti-cancer properties. (3)
2. Triterpene compounds - known as ganoderic acids, which have been shown to lower blood pressure, reduce platelet stickiness and may decrease LDL-cholesterol. (5)
3. Other major active constituents - including sterols, coumarin and mannitol. (5)

Clinical Application and Mechanism of Action

1. Anti-Cancer Agent: Cancer studies in animals have shown a 50% tumor regression rate with reishi mushroom extract treatment (e.g., connective tissue cancer model in mice). ⁽⁶⁾ Reishi mushroom extract is used by some cancer surgeons in Japan to treat cancer patients and significant anti-tumor and immunostimulation effects have been noted in many of these cases. ⁽⁷⁾ Polysaccharides from reishi mushrooms and from other types of folk-medicinal fungi are patented in Japan for use as immunomodulators in the treatment of cancer. They are combined with chemo- and radiotherapy and have demonstrated an ability to reduce side effects, increase the efficacy of treatments, and are used to accelerate recovery from disease. ^(8,9)
   Studies from China have shown that reishi mushroom extract potentiates the tumoricidal capacity of macrophages and T-cells. ^(10,11) Reishi mushroom extract is known to have other immune modulating effects and antioxidant properties as well. ^{(12,13,14,15,16)}
2. Immune System Enhancement: (Bronchitis, Asthma, Allergies, Herpetic Conditions and HIV Infection) As noted above, reishi mushroom extract modulates many components of the immune system, which in part, account for its apparent anti-tumor properties. Chronic bronchitis in the elderly has been shown to respond favorably to treatment using a concentrated reishi mushroom product in a trial involving 2,000 cases in China. This study demonstrated a better than 60% success rate. After several months of treatment there was a noted rise in the levels of immunoglobulin A in the sputum. ⁽¹⁰
   The combination of astragalus and reishi mushroom extract represents an effective means of daily immune support and a therapeutic intervention for a large number of immune compromised states (e.g.,chronic fatigue, chronic bronchitis, herpes I and II recurrent infections, post-herpetic neuralgia, recurrent apthous ulcers or canker sores, the common cold, HIV infection, etc.) and for patients undergoing chemo-or radiation therapy.
3. Cardiovascular Health: (High Blood Pressure and Reduced Platelet Aggregation) Two human controlled studies revealed that reishi mushroom extract can reduce high blood pressure to a significant degree (systolic and diastolic), even in patients who had previously failed to respond to established anti-hypertensive medications. ^(30,31) Animal studies reveal that reishi mushroom extract reduces blood pressure through a central inhibition of sympathetic nerve activity, although it does not slow heart rate or induce a sedative effect in general. ⁽³²
4. Liver Protective Effects: (Hepatoprotective Properties) Reishi is prescribed in China for the treatment of chronic and acute hepatitis. ⁽³⁶⁾ Various ganoderic acids in reishi mushrooms have strong antihepatotoxic properties, ⁽³⁷⁾ which under experimental conditions have been shown to protect liver cells from chemically-induced injury, including protection from the highly toxic and lethal substance, carbon tetrachloride. ^(38,39)

ScienceDaily (Aug. 15, 2005) — Monash University scientists have rejuvenated the immune systems of mice and humans using a common hormone.

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The scientists, led by Associate Professor Richard Boyd and Dr Jayne Sutherland from the Monash Immunology and Stem Cell Laboratories, have revitalised the thymus which produces the T cells required to fight infection but which shuts down from early adulthood.Their achievement, published in the August issue of the Journal of Immunology, has offered new hope for patients with cancer, AIDS and other immunodeficiencies and for transplant patients.

The Monash study showed inhibiting sex steroids through the Leuteinizing Hormone-Releasing Hormone could help regrow the thymus, increase output of new T cells, enhance T cell responses and improve recovery following bone marrow transplants. It also showed, for the first time, that prostate cancer patients who had their sex steroids temporarily blocked had increased levels of new T cells in their blood.

The researchers found inhibiting sex steroids improved the production of haemopoietic stem cells in bone marrow. These cells provide ‘fuel’ for the bone marrow and thymus to produce blood cells.

Associate Professor Boyd said the immune system deteriorated severely with age, and was further destroyed by severe viral infection and common cancer treatments such as chemotherapy and radiotherapy.

“The resulting immunodeficiency can allow cancer relapse and leave patients at greater risk of infections which are often fatal,” he said. “The ability to overcome these immune system deficiencies provides a completely new approach to treating cancer and may work in many other severe clinical conditions such as HIV/AIDS. It may also boost the effectiveness of vaccines to cancer and infections.”

Because the scientists have been able to manipulate the way the thymus grows back, they believe they should be able to rebuild the immune system of patients who are receiving transplants so donor material is not rejected.

The group has initiated pre-clinical trials using this technology to induce immune tolerance to organ transplants. The trials, led by clinical immunologist Dr David Sachs, are being undertaken at the Massachusetts General Hospital, the largest teaching affiliate of Harvard Medical School.

The technology, licensed to Norwood Immunology, is also about to be used in clinical trials in leading US cancer centres on patients receiving chemotherapy and haemopoietic stem cell transplants.

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Adapted from materials provided by Research Australia, via EurekAlert!, a service of AAAS.

Some types of chemotherapy make it harder for your bone marrow to produce new white blood cells. White blood cells help your body fight infection. Therefore, it is important to avoid infections, since chemotherapy decreases the number of your white blood cells.

There are many types of white blood cells. One type is called neutrophil. When your neutrophil count is low, it is called neutropenia. Your doctor or nurse may do blood tests to find out whether you have neutropenia.

It is important to watch for signs of infection when you have neutropenia. Check for fever at least once a day, or as often as your doctor or nurse tells you to. You may find it best to use a digital thermometer. Call your doctor or nurse if your temperature is 100.5°F or higher.

• Your doctor or nurse will check your white blood cell count throughout your treatment. If chemotherapy is likely to make your white blood cell count very low, you may get medicine to raise your white blood cell count and lower your risk of infection.
• Wash your hands often with soap and water. Be sure to wash your hands before cooking and eating, and after you use the bathroom, blow your nose, cough, sneeze, or touch animals. Carry hand sanitizer for times when you are not near soap and water.
• Use sanitizing wipes to clean surfaces and items that you touch. This includes public telephones, ATM machines, doorknobs, and other common items.
• Be gentle and thorough when you wipe yourself after a bowel movement. Instead of toilet paper, use a baby wipe or squirt of water from a spray bottle to clean yourself. Let your doctor or nurse know if your rectal area is sore or bleeds or if you have hemorrhoids.
• Stay away from people who are sick. This includes people with colds, flu, measles, or chicken pox. You also need to stay away from children who just had a “live virus” vaccine for chicken pox or polio. Call your doctor, nurse, or local health department if you have any questions.
• Stay away from crowds. Try not to be around a lot of people. For instance, plan to go shopping or to the movies when the stores and theaters are less crowded.

• Be careful not to cut or nick yourself. Do not cut or tear your nail cuticles. Use an electric shaver instead of a razor. And be extra careful when using scissors, needles, or knives.
• Watch for signs of infection around your catheter. Signs include drainage, redness, swelling, or soreness. Let your doctor or nurse know about any changes you notice near your catheter.
• Maintain good mouth care. Brush your teeth after meals and before you go to bed. Use a very soft toothbrush. You can make the bristles even softer by running hot water over them just before you brush. Use a mouth rinse that does not contain alcohol. Check with your doctor or nurse before going to the dentist. (For more about taking care of your mouth, see Mouth and Throat Changes.)
• Take good care of your skin. Do not squeeze or scratch pimples. Use lotion to soften and heal dry, cracked skin. Dry yourself after a bath or shower by gently patting (not rubbing) your skin. (For more information about taking care of your skin, see Skin and Nail Changes.)
• Clean cuts right away. Use warm water, soap, and an antiseptic to clean your cuts. Do this every day until your cut has a scab over it.
• Be careful around animals. Do not clean your cat’s litter box, pick up dog waste, or clean bird cages or fish tanks. Be sure to wash your hands after touching pets and other animals.
• Do not get a flu shot or other type of vaccine without first asking your doctor or nurse. Some vaccines contain a live virus, which you should not be exposed to.
• Keep hot foods hot and cold foods cold. Do not leave leftovers sitting out. Put them in the refrigerator as soon as you are done eating.

• Wash raw vegetables and fruits well before eating them.
• Do not eat raw or undercooked fish, seafood, meat, chicken, or eggs. These may have bacteria that can cause infection.

• Do not have food or drinks that are moldy, spoiled, or past the freshness date.
• Call your doctor right away (even on the weekend or in the middle of the night) if you think you have an infection. Be sure you know how to reach your doctor after office hours and on weekends. Call if you have a fever of 100.5°F or higher, or when you have chills or sweats. Do not take aspirin, acetaminophen (such as Tylenol®), ibuprofen products, or any other drugs that reduce fever without first talking with your doctor or nurse. Other signs of infection include:
  • Redness
  • Swelling
  • Rash
  • Chills
  • Cough
  • Earache
  • Headache
  • Stiff neck
  • Bloody or cloudy urine
  • Painful or frequent need to urinate
  • Sinus pain or pressure

ScienceDaily (Jul. 26, 2007) — Cancer patients who receive a drug that stimulates the growth of infection-fighting white blood cells may be significantly less likely to die from a chemotherapy-related complication characterized by fever and low white blood cell levels, according to a multi-institutional study led by researchers from the University of Rochester School of Medicine and Dentistry and the Duke Comprehensive Cancer Center.

“Chemotherapy drugs target cancer cells, but they can affect healthy cells as well, including infection-fighting white blood cells,” said Nicole M. Kuderer, M.D., a hematology-oncology fellow at Duke and lead author on the publication. “When patients’ white blood cell counts drop too low, they are at risk for dangerous infections that can cause death.”

Often, chemotherapy must be delayed, reduced in strength or halted when a patient’s white blood cell count is too low, potentially leading to poorer outcomes, she added.

“Patients taking a drug known as granulocyte colony-stimulating factor early in their chemotherapy were about half as likely to develop dangerously low white blood cell counts with fever, and half as likely to die from infection,” Kuderer said. “This study represents an important part of the effort to better treat this common complication in cancer patients receiving chemotherapy.”

The researchers published their findings in the July 20, 2007 issue of the Journal of Clinical Oncology. The work was part of research being conducted by the Awareness of Neutropenia in Chemotherapy (ANC) Study Group, a multi-institution, university-based network of investigators whose work is unrestrictedly funded by Amgen, the maker of a commonly utilized white blood cell booster that goes by the names Neupogen and Neulasta. Kuderer also receives funding from the National Institutes of Health.

This study compiled the results of 17 trials involving more than 3,000 patients receiving chemotherapy of varying intensity to treat several different types of cancers. The researchers found that nearly 40 percent of the patients who did not receive the white blood cell booster early in treatment developed the fever and low white blood cell levels called febrile neutropenia, compared to only 22 percent of the patients who took the drug in conjunction with their chemotherapy, Kuderer said.

While white blood cell boosters were known to help patients receiving very intense doses of chemotherapy, this study showed that the drugs are also a benefit to cancer patients receiving more common chemotherapy doses, Kuderer said.

Recently revised American Society of Clinical Oncology (ASCO) and National Comprehensive Cancer Center Network (NCCN) guidelines for the use of drugs such as Neulasta and Neupogen align with the conclusions reached by this study.

“The new guidelines recommend using these types of drugs when at-risk patients begin chemotherapy, rather than waiting for complications to develop,” said Jeffrey Crawford, M.D., chief of the division of medical oncology at Duke and one of the study’s investigators. “The new recommendations also suggest that we need better methods to identify patients who are at higher risk of developing febrile neutropenia, and future studies will be aimed at doing just that.”

White blood cell boosters can have side effects, including bone pain, which need to be reviewed and discussed with each patient, Crawford said.

Other investigators on the study include Gary Lyman of Duke and David Dale of the University of Washington.

Duke University Medical Center (2007, July 26). White Blood Cell Booster May Help Cancer Patients Avoid Deadly Complications. ScienceDaily. Retrieved December 4, 2007, from http://www.sciencedaily.com­ /releases/2007/07/070725110020.htm