When an organism gets into your body and causes an infection, your body gathers its defences and fights against them. This is the basic principle of how vaccines work.

Certain cells in your blood make what are called ‘antibodies’, molecules which are designed to attack specific germs and viruses. These attach to the invaders in your bloodstream and prevent them from invading other cells. Each virus or bacterium has an individual shape, and the antibodies are designed to fit exactly to that shape.

This is how vaccines work to convince your body that the vaccination is a ‘full-blooded’ attack by the offending viruses or bacteria, and stimulate them into action to develop the ‘memory’ or ‘blueprint’ for the antibody in the event of future invasion.

This is all done by your white blood cells. You have two types called B cells and T cells. The B cells manufacture the antibodies while the T cells have two functions. The ‘helper’ T cells help the B cells to make the antibodies while the ‘killer’ T cells kill any cells which have been invaded by the viruses or bacteria, and prevent them from reproducing. . How vaccines work to stimulate this action is to mislead the white cells into believing that your body has been infected.

Your body reacts to kill the invaders in two ways: directly through the antibodies, and indirectly through the T cells destroying any infected cells and preventing reproduction.

Viruses cannot reproduce by themselves: they have to use the host’s cells for this. If the T cells continually kill off any invaded cells, the invaders themselves must eventually be killed off by the antibodies If the virus or bacterium is strong and reproduce too quickly, the host can be overcome before it can produce enough antibodies to kill them off. The pus which occurs during an infection is the mix of dead white blood cells and bacteria/virus cells destroyed by them.

If your body survives the attack, your B cells retain a memory of the structure of the invaders and should the same viruses or bacteria ever return, antibodies can rapidly be produced and the infection killed off before it starts. The stimulation of this memory is exactly how vaccines work.

Vaccines produce the same memory effect without the patient having to suffer the disease. The organisms that cause the disease are either killed or weakened, then introduced into your body. The strength is calculated to be just enough to enable your white cells to manufacture the antibodies. This is how vaccines work to give you protection against future infection without actually making you ill. The strength of the vaccine is designed to allow this. The dead vaccine can also work, but less efficiently, and the effect is not generally as long lasting.

The ‘live’ vaccines produce life-long immunity after only one or two doses, but the ‘dead’, or ‘inactivated’, ones need multiple doses to get the correct effect. Some dead vaccines even need booster doses throughout your life. Examples of these are tetanus and diphtheria vaccines, normally given together every 10 years as the Td vaccine. The measles vaccine is an example of a ‘live’ vaccine’.

Vaccinations do not affect your ability to fight off other infections you have not been immunized against

Exposure to 1918 influenza virus activates memory B-cells
by Scientist Live

Exposure to 1918 influenza virus activates memory B-cells

Date: 16/09/2008

Recent research has revealed that infection and natural exposure to the 1918 influenza virus made survivors immune to the disease for the remaining of their lives. Antibodies produced by cells isolated from these survivors served as an effective therapy to protect mice from the highly lethal 1918 infection. The study entitled “Neutralizing antibodies derived from the B cells of 1918 influenza pandemic survivors,” was published in the journal Nature. Dr. Chris Basler and his colleagues at Mount Sinai School of Medicine’s Department of Microbiology contributed to the research findings. Scientist LiveScientist Live spoke with Dr. Basler about his findings.Can you briefly discuss the effects of the 1918 influenza pandemic and why it was so devastating?

The big question is: why did it kill so many people worldwide? The simple answer is we do not really know. The fact is that now that we have been able to reconstruct the virus in the lab and test it in several animal models. In each case the virus has displayed an unusual degree of virulence. We are beginning to understand why this may be the case. There is some evidence that the virus over-activates the immune response and the hyper-activation of this response may account for the severity of disease. At this point, however, I would say that this is more a hypothesis hypothesis than a definitive answer.

Another thing that we have begun to do is to define the gene segments of the virus need for high virulence in mice. the virus has eight different sequences encoding eleven different proteins, and we can implicate three or four of these proteins as being important for high virulence phenotype. But we don’t at this point really know the exact mechanism that makes the 1918 virus so deadly.Can you provide an overview of the study you participated in and what you discovered?

The genesis of the study goes back to the public response we received to a paper that described the reconstruction of the 1918 virus. One thing that happened was we started receiving calls and emails from people saying that they had the flu in 1918 as young children or that they knew members of their family had been infected or died of the flu. Many actually offered to contribute to future studies of the virus. It was in interesting idea. What could you do if you had blood from people who had been exposed to the 1918 flu virus? Independently our clinical collaborator Dr. Eric Altschuler had come up with the same idea and it was: Could you obtain blood from these individuals, could you isolate cells from the blood that would make antibodies for 1918 virus and could you use those to characterize the memory immune response? The other side of that question was: can you use antibodies produced in these people as potential therapeutic against the virus? To put this all together, we needed someone who had real expertise in human immunology so we turned to Dr. James Crowe at Vanderbilt University. Then the experimental plan is very straight forward. Dr. Altschuler obtained blood from people born 1915 or earlier. We at Mt. Sinai demonstrated the presence of antibodies. Then the cells were transported to Vanderbilt University where Dr. Crowe was able to isolate memory B-cells which would make antibodies. These then used to isolate the rare B-cells that make antibodies against the 1918 flu. Then we were able to show that the antibodies specifically bind to the 1918 virus and to haemagglutinin protein in particular.

Did your findings fulfill expectations? Surprises?We knew already, based on previous studies, that people who had been alive in 1918 and who were still alive today would have antibodies against the virus. What was surprising and technically challenging was that we could isolate memory B-cells that appear to be very specific to the 1918 virus which suggests that they were derived from initial exposure to the virus and that B-cells. It’s remarkable that these cells were still present in the blood and could be isolated.

The other striking thing about the antibodies we isolated is that they are very potent. They bind to the hemagglutinin proteins with high affinity.

Can the B-Cells be used in vaccine development?For the most part, the antibodies we isolated are very specific to the 1918 virus. So they would neutralize that and another old influenza virus called Swine 30 virus. Other later human influenza viruses of the H1N1 type weren’t recognized by 4 out of 5 antibodies we characterized in detail. One of the antibodies we do have reacts with the 1918 and selectively with some other later viruses. This ability to cross-neutralize different fu viruses is interesting and we are trying to understand how that happens, what this antibody is actually recognizing. Understanding this and other cross-reactive antibodies might suggest ways to make flu vaccines more bradly protective.

Complete Information on Demyelinating disease with Treatment and Prevention

A demyelinating disease is any circumstance that results in harm to the overprotective coating that surrounds nerves in your mind and spinal cord. This impairs the conduction of signals in the affected nerves, causing disability in superstar, campaign, cognition, or new functions depending on which nerves are involved. Multiple sclerosis is the most common demyelinating disease. In this disorder, your immune system mistakenly attacks the myelin sheath or the cells that produce and maintain the myelin sheath. A number of other types of demyelinating disorders have been associated with optic neuritis. They are: acute transverse myelitis, Guillain barre syndrome, Devic’s neuromyelitis optica, Charcot marie tooth syndrome, multifocal demyelinating neuropathy, and acute disseminated encephalomyelitis. Demyelinating diseases causes inflammation and wound to the sheath and finally to the nerves that it surrounds. The outcome may be dual areas of scarring, which can finally decelerate or halt heart signals that curb muscle coordination, power, superstar and imagination. The majority of plaques congregate along periventricular draining veins, but plaques also commonly occur within the spinal cord, optic nerves, brain stem, and white matter of the cerebral hemispheres and cerebellum. Plaques can also occur in the connecting pathways of subcortical white matter. Demyelination in gray matter may account for a large fraction of the lesion burden. Longer standing lesions are characterized by a total loss of myelin and oligodendrocytes, an intense astrogliosis, variable degrees of axonal loss, and a scant residual infiltrate of mononuclear cells, some of which are immunoglobulin-secreting B cells. The diagnosis is made on the ground of the clinical signs and symptoms. The diagnosis of Multiple sclerosis requires evidence of the spreading of lesions in the system over moment and the cautious expulsion of new causes. Treatment of multiple sclerosis can be discussed in terms of the management of acute relapses, the prevention of relapses as modification of the disease process, and the management of symptoms and fixed neurologic deficits. A short, tapering course of oral corticosteroids may be given afterward. Equivalent doses of oral corticosteroids may have a similar effect, but treatment with lower doses is controversial. Treatment depends on the type of demyelinating disease but may include corticosteroid medications. Although corticosteroids have a short-term beneficial effect when used for acute exacerbations, their long-term effect on the course of multiple sclerosis is less clear.

Exposure to 1918 influenza virus activates memory B-cells
by Scientist Live

Exposure to 1918 influenza virus activates memory B-cells

Date: 16/09/2008

Recent research has revealed that infection and natural exposure to the 1918 influenza virus made survivors immune to the disease for the remaining of their lives. Antibodies produced by cells isolated from these survivors served as an effective therapy to protect mice from the highly lethal 1918 infection. The study entitled “Neutralizing antibodies derived from the B cells of 1918 influenza pandemic survivors,” was published in the journal Nature. Dr. Chris Basler and his colleagues at Mount Sinai School of Medicine’s Department of Microbiology contributed to the research findings. Scientist LiveScientist Live spoke with Dr. Basler about his findings.Can you briefly discuss the effects of the 1918 influenza pandemic and why it was so devastating?

The big question is: why did it kill so many people worldwide? The simple answer is we do not really know. The fact is that now that we have been able to reconstruct the virus in the lab and test it in several animal models. In each case the virus has displayed an unusual degree of virulence. We are beginning to understand why this may be the case. There is some evidence that the virus over-activates the immune response and the hyper-activation of this response may account for the severity of disease. At this point, however, I would say that this is more a hypothesis hypothesis than a definitive answer.

Another thing that we have begun to do is to define the gene segments of the virus need for high virulence in mice. the virus has eight different sequences encoding eleven different proteins, and we can implicate three or four of these proteins as being important for high virulence phenotype. But we don’t at this point really know the exact mechanism that makes the 1918 virus so deadly.Can you provide an overview of the study you participated in and what you discovered?

The genesis of the study goes back to the public response we received to a paper that described the reconstruction of the 1918 virus. One thing that happened was we started receiving calls and emails from people saying that they had the flu in 1918 as young children or that they knew members of their family had been infected or died of the flu. Many actually offered to contribute to future studies of the virus. It was in interesting idea. What could you do if you had blood from people who had been exposed to the 1918 flu virus? Independently our clinical collaborator Dr. Eric Altschuler had come up with the same idea and it was: Could you obtain blood from these individuals, could you isolate cells from the blood that would make antibodies for 1918 virus and could you use those to characterize the memory immune response? The other side of that question was: can you use antibodies produced in these people as potential therapeutic against the virus? To put this all together, we needed someone who had real expertise in human immunology so we turned to Dr. James Crowe at Vanderbilt University. Then the experimental plan is very straight forward. Dr. Altschuler obtained blood from people born 1915 or earlier. We at Mt. Sinai demonstrated the presence of antibodies. Then the cells were transported to Vanderbilt University where Dr. Crowe was able to isolate memory B-cells which would make antibodies. These then used to isolate the rare B-cells that make antibodies against the 1918 flu. Then we were able to show that the antibodies specifically bind to the 1918 virus and to haemagglutinin protein in particular.

Did your findings fulfill expectations? Surprises?We knew already, based on previous studies, that people who had been alive in 1918 and who were still alive today would have antibodies against the virus. What was surprising and technically challenging was that we could isolate memory B-cells that appear to be very specific to the 1918 virus which suggests that they were derived from initial exposure to the virus and that B-cells. It’s remarkable that these cells were still present in the blood and could be isolated.

The other striking thing about the antibodies we isolated is that they are very potent. They bind to the hemagglutinin proteins with high affinity.

Can the B-Cells be used in vaccine development?For the most part, the antibodies we isolated are very specific to the 1918 virus. So they would neutralize that and another old influenza virus called Swine 30 virus. Other later human influenza viruses of the H1N1 type weren’t recognized by 4 out of 5 antibodies we characterized in detail. One of the antibodies we do have reacts with the 1918 and selectively with some other later viruses. This ability to cross-neutralize different fu viruses is interesting and we are trying to understand how that happens, what this antibody is actually recognizing. Understanding this and other cross-reactive antibodies might suggest ways to make flu vaccines more bradly protective.

What are Antibodies?

Antibodies, also called immunoglobulins are large y-shaped proteins which function to identify and help remove foreign antigens such as viruses and bacteria.

Antibodies are created by plasma cells which are derived from the B-cells in the immune system.

Every different antibody recognizes a specific foreign antigen. This is because the two tips of its “Y” are different to each antibody are allow different antibodies to bind to different foreign antigens. When the antibody binds to a bacteria, it tags the microbe or virus for attack by the immune system such as killer T-cells. Sometimes, antibodies can directly neutralize the foreign body. The production of antibodies by B-cells is the main function of the humoral immune system.

Due to the amazing specificity of antibodies, they have some important practical applications in both medicine for the detection of HIV and other viruses in blood, and in research to purify and detect proteins in the study of molecular biology.

For all your Antibody needs and for more antibody information, please visit Antibody Station.

http://www.antibodystation.com

You may ONLY use this article, if you maintain the author’s information and website address.

Hairy cell leukemia

Hairy cell leukemia (HCL) is a rare cancer of the blood. It affects B cells, a type of white blood cell (lymphocyte). HCL is due to increase of a clonal malignant B cell that infiltrates the reticuloendothelial cells, mainly the bone marrow, resulting in bone marrow failure. Somewhere between 600 and 800 people are effected with hairy cell leukemia every year in the United States. Hairy cell leukemia affects more men than women, and it occurs most commonly in middle-aged or older adults. Children and teenagers don’t get hairy cell leukemia. This disease is observed more commonly in whites. Occasionally, hairy cell leukemia has occurred in members of the same family. However, this is uncommon and no hereditary pattern has been established. Hairy cell leukemia (HCL) is associated with gram-positive and gram-negative bacterial infections as well as atypical mycobacterial and invasive fungal infections. HCL is related with other general immunologic disorders with scleroderma, polymyositis, polyarteritis nodosa, erythematous maculopapules, and pyoderma gangrenosum. Other rare conditions may be linked with HCL, such as acquired issue VIII antibodies, paraproteinemia, and systemic mast cell disease. The symptoms and signs of hairy cell leukemia are nonspecific and resemble those of other illnesses. The most common symptoms and presenting complaints are weakness and tiredness due to anemia. Some symptoms and signs are pain or fullness in the upper left side of the abdomen, as a effect of an enlarged spleen, on explained weight loss, a loss of a sense of well-being and an infection accompanied by fever and chills. Hairy cells accumulate in the bone marrow and prevent the marrow from producing enough normal blood cells. People with this disease may not need treatment in the early stages. Several treatments are available, and successful manage of the disease is common. Chemotherapy is cancer treatments that utilize drugs to prevent the growth of cancer cells, either by killing the cells or by stopping them from dividing. Biological therapy (immunotherapy) attempts to make cancer cells more recognizable to your immune system. Surgery to remove your spleen (splenectomy) was the first treatment used in hairy cell leukemia, though it’s used only rarely today.

Complete Information on Demyelinating disease with Treatment and Prevention

A demyelinating disease is any circumstance that results in harm to the overprotective coating that surrounds nerves in your mind and spinal cord. This impairs the conduction of signals in the affected nerves, causing disability in superstar, campaign, cognition, or new functions depending on which nerves are involved. Multiple sclerosis is the most common demyelinating disease. In this disorder, your immune system mistakenly attacks the myelin sheath or the cells that produce and maintain the myelin sheath. A number of other types of demyelinating disorders have been associated with optic neuritis. They are: acute transverse myelitis, Guillain barre syndrome, Devic’s neuromyelitis optica, Charcot marie tooth syndrome, multifocal demyelinating neuropathy, and acute disseminated encephalomyelitis. Demyelinating diseases causes inflammation and wound to the sheath and finally to the nerves that it surrounds. The outcome may be dual areas of scarring, which can finally decelerate or halt heart signals that curb muscle coordination, power, superstar and imagination. The majority of plaques congregate along periventricular draining veins, but plaques also commonly occur within the spinal cord, optic nerves, brain stem, and white matter of the cerebral hemispheres and cerebellum. Plaques can also occur in the connecting pathways of subcortical white matter. Demyelination in gray matter may account for a large fraction of the lesion burden. Longer standing lesions are characterized by a total loss of myelin and oligodendrocytes, an intense astrogliosis, variable degrees of axonal loss, and a scant residual infiltrate of mononuclear cells, some of which are immunoglobulin-secreting B cells. The diagnosis is made on the ground of the clinical signs and symptoms. The diagnosis of Multiple sclerosis requires evidence of the spreading of lesions in the system over moment and the cautious expulsion of new causes. Treatment of multiple sclerosis can be discussed in terms of the management of acute relapses, the prevention of relapses as modification of the disease process, and the management of symptoms and fixed neurologic deficits. A short, tapering course of oral corticosteroids may be given afterward. Equivalent doses of oral corticosteroids may have a similar effect, but treatment with lower doses is controversial. Treatment depends on the type of demyelinating disease but may include corticosteroid medications. Although corticosteroids have a short-term beneficial effect when used for acute exacerbations, their long-term effect on the course of multiple sclerosis is less clear.

Complete Information on Castleman’s disease

Castleman’s disease is an uncommon lymphoproliferative disorder. It is characterized by non-cancerous (benign) growths (tumors) that may develop in the lymph node tissue throughout the body. It involves hyperproliferation of certain B cells that often produce cytokines. There are several variants of Castleman’s disease. Unicentric Castleman’s disease involves tissue growths at only a single site; Multicentric Castleman’s disease (MCD) involves growths at multiple sites. Castleman disease affects both males and females, and may occur at any age, but typically it does not affect children. The disease of Castleman can be classified as a unicentric against multicentric. The disease of Unicentric Castleman is usually a solitary mass of slow growth typically located in mediastinium or the mesenteries. There are no constitutional symptom and no altitude of the acute reagents of phase (Interleukin 6, esr and CRP). Symptoms if the present are due for a purpose of mass of cumbersome lymphadenopathy. The Disease De Multicentric Castleman. The symptoms of “B” including/understanding serious tiredness, harms known, weight-loss, anorexia are in general present. These symptoms typically are driven by interleukin 6 overproduction. Interleukin 6 overproduction too cause an intense stage to respond with ESR, CRP, the fibrinogen, thrombocytosis which rises, with hypergammaglobinemia. The Multicentric Castleman disease runs the kind which even more competes, possibly advances to the non-Hodgkin lymphoma. The Multicentric Castleman disease frequently requests the system therapy. The treatment is the tumor surgery removes for the tumor after the Castleman disease transparent blood vessel character. The kind of cortical hormone or the chemotherapeutics medicine is perhaps used.The Anti-IL6 therapy includes suramin, anti-IL6- or the anti-IL6 feeling organ immune body. Suramin is the polysulfonated urea compound early by the use is a sleeping sickness. Suramin too adjusts the cytokine secretion. The Anti-IL6 immune body is the specially high efficiency is controlling the IL6 correlation the symptom. The Anti-IL6 feeling organ immune body is used started in MIRT by the equivalent if not the best response compares is observed and the IL6 immune body. Other therapies scatter the advantage including the anti-angiogenesis element to step much with the anti-IL6 therapy.

Complete Information on Castleman’s disease

Castleman’s disease is an uncommon lymphoproliferative disorder. It is characterized by non-cancerous (benign) growths (tumors) that may develop in the lymph node tissue throughout the body. It involves hyperproliferation of certain B cells that often produce cytokines. There are several variants of Castleman’s disease. Unicentric Castleman’s disease involves tissue growths at only a single site; Multicentric Castleman’s disease (MCD) involves growths at multiple sites. Castleman disease affects both males and females, and may occur at any age, but typically it does not affect children. The disease of Castleman can be classified as a unicentric against multicentric. The disease of Unicentric Castleman is usually a solitary mass of slow growth typically located in mediastinium or the mesenteries. There are no constitutional symptom and no altitude of the acute reagents of phase (Interleukin 6, esr and CRP). Symptoms if the present are due for a purpose of mass of cumbersome lymphadenopathy. The Disease De Multicentric Castleman. The symptoms of “B” including/understanding serious tiredness, harms known, weight-loss, anorexia are in general present. These symptoms typically are driven by interleukin 6 overproduction. Interleukin 6 overproduction too cause an intense stage to respond with ESR, CRP, the fibrinogen, thrombocytosis which rises, with hypergammaglobinemia. The Multicentric Castleman disease runs the kind which even more competes, possibly advances to the non-Hodgkin lymphoma. The Multicentric Castleman disease frequently requests the system therapy. The treatment is the tumor surgery removes for the tumor after the Castleman disease transparent blood vessel character. The kind of cortical hormone or the chemotherapeutics medicine is perhaps used.The Anti-IL6 therapy includes suramin, anti-IL6- or the anti-IL6 feeling organ immune body. Suramin is the polysulfonated urea compound early by the use is a sleeping sickness. Suramin too adjusts the cytokine secretion. The Anti-IL6 immune body is the specially high efficiency is controlling the IL6 correlation the symptom. The Anti-IL6 feeling organ immune body is used started in MIRT by the equivalent if not the best response compares is observed and the IL6 immune body. Other therapies scatter the advantage including the anti-angiogenesis element to step much with the anti-IL6 therapy.

What are Antibodies?

Antibodies, also called immunoglobulins are large y-shaped proteins which function to identify and help remove foreign antigens such as viruses and bacteria.

Antibodies are created by plasma cells which are derived from the B-cells in the immune system.

Every different antibody recognizes a specific foreign antigen. This is because the two tips of its “Y” are different to each antibody are allow different antibodies to bind to different foreign antigens. When the antibody binds to a bacteria, it tags the microbe or virus for attack by the immune system such as killer T-cells. Sometimes, antibodies can directly neutralize the foreign body. The production of antibodies by B-cells is the main function of the humoral immune system.

Due to the amazing specificity of antibodies, they have some important practical applications in both medicine for the detection of HIV and other viruses in blood, and in research to purify and detect proteins in the study of molecular biology.

For all your Antibody needs and for more antibody information, please visit Antibody Station.

http://www.antibodystation.com

You may ONLY use this article, if you maintain the author’s information and website address.