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    Monday, 17 March 2014 12:41

    Gene mutation in the fight against HIV

    mouseResearch conducted at the laboratory of the University of Pennsylvania, provides data to the first change in the targeted gene, which leads to the creation of genetically modified immune cells impermeable to the HIV virus.

    The study focuses on the use of a technique known as targeted gene editing.

    The aim is to change conformation of the CC chemokine receptor type 5 (CCR5) delta32, which represents a protein on the surface of T - cells that HIV uses to connect to and infect healthy cells.

    If the protein is changed even slightly, the virus is unable to continue its development. Although the modification of the protein is not able to kill the virus, its ability to proliferate is suppressed, generally used in drugs used for treatment of patients diagnosed with HIV.

    Only a small portion of the world population carries an allele that cause this conformational change in CCR5 - delta32.

    Basically everyone should copy inherited from both parents, which therefore does not allow inoculation with the virus. The fact is, however, that allele is owned by only 14% of the European population and carriage in African and Asian populations is even more rare.

    It is this mutation serves as inspiration for the study.

    There are involved only 20 subjects diagnosed as HIV positive by 2 persons they fell, due to the very low levels of T cells.

    In the remaining 18 patients, the T cells are subjected to the modification, and then monitor their response to the match, and the virus.

    In 6 th patient has seen a sharp rise in resistance to the virus, which even led to the discontinuation of drug therapy.

    Although immune cell lives on average about six weeks, the modified cells can be detected several months later.

    These changes have not eradicated the virus from the body, and although best results patients are not cured.

    Yet to be made additional tests and studies, the researchers, however, have an optimistic attitude and better predict outcome.

    Published in News
    Friday, 14 March 2014 13:18

    What cells of the immune system exist?

    B-targeting-rosa26-feeder-cells-human-primary-cells-mefCells of the immune system are responsible for the maintenance of the immune reactivity of the organism against penetrating viral and bacterial pathogens in the human body, which sometimes can cause dangerous health infections. Initially, the circuit is driven by the production of pluripotent stem cells that differentiate and give rise to clones of B-and T-cell lymphocytes, neutrophils, eosinophils, basophils, monocytes, dendritic cells, mast cells and red blood cells.

    Neutrophils are a special type of immune system cells, which are differentiated from myeloid stem cells. They migrate into the bloodstream at himiotaksichen signal from the body. By way of specific Fc-receptor fixed opsonized by the complement system and pathogen invasion within particles. They have the ability to destroy pathogens directly emptied by the strong bactericide them.

    Eosinophils are another type of special cells of the immune system. These granules have a strong cytotoxicity to the endothelium, epidermis, neuronal cells and proteins. Their main function is to synthesize mediators and cytokines.

    Basophil cells and mast cells contain receptors for immunoglobulin E. Their main function is to synthesize prostaglandins Class 2. They also provide protection against parasites come against immunoglobulin E-mediated allergic reactions. In this way, the body remains secure during falling of animal parasites in the food, which is particularly common in the consumption of food or poorly cleaned poorly processed meat products.

    Monocytes have a cytoplasm filled with specific granules. They originate from myeloid stem cells and differentiate into macrophages. Their main function is to phagocytose emptied environmental pathogenic microorganisms. These processes are carried out after activation by interferon or TNF, macrophages subsequently acquire strong cytotoxic activity and have a strong bactericidal effect against pathogens become trapped in the body.

    Dendritic cells are antigen presenting cells. They can migrate into the blood and lymph. They are activated by irritation of those who fell in the human pathogenic microorganisms. The next stage of their operation is not present on its surface MHC molecules of the system that is the major histocompatibility complex on. Also involved in the activation of clusters of differentiation in the body - CD-cells.

    T lymphocytes very well may be defined as "the heads of special operations to eliminate the invasion and destruction of pathogenic microorganisms." They are produced in the bone marrow pluripotent stem cells and then migrate to the thymus and mature there. Subsequently differentiate and acquire the specific T-cell reactivity - TCR.

    Accordingly, this type of cells are involved in the differentiation to a CD- cells , which are clusters of differentiation. CD4 + T - cell specific agents have adjuvant - inducing function . They give rise to a whole new spot in the production of protective cells against emptied into a person's body pathogenic microorganisms. CD8 + T-cell lymphocytes are the next most important clusters that need to be addressed. They have strong cytotoxic and suppressor role. Cast directly to the differentiation of killer cells and suppressor cells when the body is facing the threat of invasive blood-borne viruses and bacteria.

    The role of the immune system is to protect the body against foreign antigens, and do not react to cause outbreaks of disease events in the human body. They also prevent the occurrence of cross-reactions between antigens and the invasion of the body's own antigens. That function of the immune system is performed by the T-cells that acquire the ability to execute it in the thymus after three-step reactions.

    - The first step is differentiation of a double negative T cell lymphocytes. These are CD4-and CD8-cells.
    - The second stage is the occurrence of double positive cells - to develop CD4 + and CD8 + cells.
    - The third stage is the mixed cells, where they meet a single positive and single negative T-lymphocytes. There are two possible combinations. The first one is the manifestation of CD4-and CD8 + cells, and the second expression of CD4 + and CD8-cells.

    B-cell lymphocytes are another important cellular arm of the immune reactivity of the organism against environmental emptied the invasion of microorganisms. They are involved in humoral immunity by synthesis of antibodies. Each mature B lymphocyte produces only one type specific antibody that is expressed on the surface, such as a B cell receptor. Antibodies react against the onset of the invasion antigens.

    NK-cells are a specific cell type. They can be defined as "a SWAT team to fight pathogens." Their name comes from the abbreviation natural killers, which means that they kill directly taken into the body microorganisms without subjecting them to any attempts to phagocytic or neutralization. NK-cells are most pronounced cytotoxicity compared with all other members of the immune response. Thus limiting the spread of virus-infected cells in the human body.

    Published in Tech Tips
    Wednesday, 22 January 2014 15:34

    Body's own antibodies can cause leukemia

    rabbit-anti-elisa-targattAcute lymphoblastic leukemia is the most common form of blood cancer. Patients with leukemia in the body produced abnormal red blood cells. A research group from the UK to establish why some children do not respond to treatment of blood cancer .

    The immune system produces millions of different antibodies, but only has a limited amount of DNA that contain "instructions" for this. To generate huge variety of antibodies to protect the body, the DNA is mixed and the excess particles are removed . Particle removal genome likely is the cause resistance to treatment.

    Tools used to strengthen the body's resistance to infection, are also one of the reasons for the most common form of childhood leukemia, scientists say. Equipment for the production of millions of antibodies in the immune system can misfire, making the cells more susceptible to becoming cancerous. The findings are published in the journal Nature Genetics. Scientists at the Sanger Institute in Cambridgeshire and the Institute of Cancer Research in London mechanism used DNA shuffling to make antibodies capable of reducing the risk of developing cancer.

    In a study conducted on 57 children in E, the scientists compared the DNA of the healthy tissue of each child and the DNA of cancer of white blood cells. These data indicate that there are two phases of the disease. The first change occurred before birth, but the kids did not get ill from leukemia at once, and at the age of four to ten years there were further genetic changes caused by the same principle that immune cells use to produce antibodies. This knowledge leads to the fundamental understanding of the disease, but is unlikely to lead to new therapies.

    Experts say that the current therapies debilitating, many patients suffer relapses of cancer. The latest discovery really allow progress in understanding the actual biology, leading to blood cancer and its various forms. The resulting knowledge will develop in the future a more precise treatment, and increase the predictability of the results of the disease. Now nine out of ten sick children have good prospects of long-term survival, said Matt Kaiser, head of research at the children's charity the treatment of leukemia and lymphoma.

    Published in News

    hiv treatment gentaur antibodiesUntreated HIV infection destroys a person's immune system by killing infection-fighting cells, but precisely when and how HIV wreaks this destruction has been a mystery until now. New research by scientists at the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, reveals how HIV triggers a signal telling an infected immune cell to die. This finding has implications for preserving the immune systems of HIV-infected individuals.

    HIV replicates inside infection-fighting human immune cells called CD4+ T cells through complex processes that include inserting its genes into cellular DNA. The scientists discovered that during this integration step, a cellular enzyme called DNA-dependent protein kinase (DNA-PK) becomes activated. DNA-PK normally coordinates the repair of simultaneous breaks in both strands of molecules that comprise DNA. As HIV integrates its genes into cellular DNA, single-stranded breaks occur where viral and cellular DNA meet. Nevertheless, the scientists discovered, the DNA breaks during HIV integration surprisingly activate DNA-PK, which then performs an unusually destructive role: eliciting a signal that causes the CD4+ T cell to die. The cells that succumb to this death signal are the very ones mobilized to fight the infection.

    According to the scientists, these new findings suggest that treating HIV-infected individuals with drugs that block early steps of viral replication -- up to and including activation of DNA-PK and integration -- not only can prevent viral replication, but also may improve CD4+ T cell survival and immune function. The findings also may shed light on how reservoirs of resting HIV-infected cells develop and may aid efforts to eliminate these sites of persistent infection.

    Published in News

    immune cell gentaur antibodiesMelbourne researchers have discovered that the death of immune system cells is an important safeguard against the development of diseases such as type 1 diabetes, rheumatoid arthritis and lupus, which occur when the immune system attacks the body's own tissues.

    The finding suggests that these so-called autoimmune diseases could be treated with existing medications that force long-lived immune system cells to die.

    In the development of the immune system, some cells are produced that have the potential to attack the body's own tissues, causing autoimmune disease. The death of these 'self-reactive' immune cells through a process called apoptosis is an important safeguard against autoimmune disease.

    But Dr Kylie Mason, Dr Lorraine O'Reilly, Dr Daniel Gray, Professor Andreas Strasser and Professor David Huang from the Walter and Eliza Hall Institute, and Professor Paul Waring from the University of Melbourne have discovered that when immune cells lack two related proteins, called Bax and Bak, the cells can attack many healthy tissues, causing severe autoimmune disease. The research is published online January 22 in the journal Proceedings of the National Academy of Sciences.

    Bax and Bak are members of the 'Bcl-2 protein family', a large group of proteins that control cell death. Dr O'Reilly said it was thought that Bax and Bak acted like an irreversible switch in cells, determining when cells die by apoptosis. In healthy cells, Bax and Bak are in an 'inactive' form, but when cells are under stress or receive external signals instructing them to die, Bax and Bak switch into an 'active' form that starts the destruction of the cell by apoptosis. Without Bax and Bak, cells are highly protected against apoptosis.

    Dr O'Reilly said that some immune cells that lacked the proteins Bax and Bak were able to attack healthy tissues in many organs of the body. "Normally, these 'self-reactive' immune cells are deleted during development," she said. "In the absence of Bax and Bak, enough self-reactive cells survive development to persist in the body and cause autoimmune disease in organs such as the kidneys (glomerulonephritis), similar to what is seen in the most severe form of lupus.

    "Our findings confirm that defective apoptosis of immune cells can cause autoimmune disease, and that Bax and Bak are important determinants of immune cell death. We were also interested to see that, in our model, loss of Bak on its own was sufficient to cause autoimmune disease, albeit to a lesser extent than losing both Bak and Bax. This supports a recent discovery that humans with mutations in the BAK gene are predisposed to certain autoimmune diseases."

    The research provides hope for people with autoimmune diseases as Bax and Bak activity can be triggered by a new class of potential anti-cancer agents, called BH3-mimetics, which are currently in clinical trials for certain types of leukemia in Melbourne, Dr O'Reilly said. "Our findings suggest that BH3-mimetics might be an exciting new option for treatment for autoimmune conditions, by activating Bax and Bak and making the self-reactive immune cells which are causing the autoimmune disease to die," she said.

    Published in News
    Sunday, 10 February 2013 17:44

    Two Antibodies Are Better Than One

    A new approach mimicking the body’s natural defenses could help treat a therapy-resistant breast cancer

    Cancer drugs of the new, molecular generation destroy malignant breast tumors in a targeted manner:  They block characteristic molecules on tumor cells – receptors for the hormones estrogen or progesterone, or a co-receptor, called HER2, that binds to many growth factors. But about one in every six breast tumors has none of these receptors. Such cancers, called triple-negative, are particularly aggressive and notoriously difficult to treat.

    Some of these therapy-resistant cancers have a potential molecular target for cancer drugs, a growth-factor receptor called EGFR, but an EGFR-blocking drug has proved ineffective in treating them. In a study published recently in the Proceedings of the National Academy of Sciences, Weizmann Institute researchers propose a potential solution: to simultaneously treat triple-negative breast cancer with two EGFR-blocking antibodies instead of one. In a study in mice, the scientists showed that a certain combination of two antibodies indeed prevented the growth and spread of triple-negative tumors. The research team, led by Prof. Yosef Yarden of the Biological Regulation Department and Prof. Michael Sela of the Immunology Department, included Drs. Daniela Ferraro, Nadège Gaborit, Ruth Maron,  Hadas Cohen-Dvashi,  Ziv Porat and Fresia Pareja, and Sara Lavi, Dr. Moshit Lindzen and Nir Ben-Chetrit.

    Of the different combinations they tried, the scientists found that the approach worked when the two antibodies bound to different parts of the EGFR molecule. The combined action of the antibodies was stronger than would have been expected by simply adding up the separate effects of each.  Apparently, the use of the two antibodies created an entirely new anti-cancer mechanism: In addition to blocking the EGFR and recruiting the help of immune cells, the antibodies probably overwhelmed the EGFR by their sheer weight, causing it to collapse inward from the membrane into the tumor cell.
     
    Deprived of EGFR on its surface, the cells were no longer receiving the growth signals, preventing the growth of the tumor. This approach resembles the natural functioning of the immune system, which tends to block essential antigens at several sites by targeting them with multiple antibodies.

    If supported by further studies, the two-antibody approach, in combination with chemotherapy, might in the future be developed into an effective treatment for triple-negative breast cancer.
    Prof. Michael Sela is the incumbent of the W. Garfield Weston Professorial Chair of Immunology.
    Prof. Yosef Yarden’s research is supported by the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation; the M.D. Moross Institute for Cancer Research; the Steven and Beverly Rubenstein Charitable Foundation , Inc.; Julie Charbonneau, Canada; the European Research Council; and the Marvin Tanner Laboratory for Research on Cancer. Prof. Yarden is the incumbent of the Harold and Zelda Goldenberg Professorial Chair in Molecular Cell Biology.
     
     
    Published in News