Aging changes in immunity
Your immune system helps protect your body from foreign or harmful substances. Examples are bacteria, viruses, toxins, cancer cells, and blood or tissues from another person. The immune system makes cells and antibodies that destroy these harmful substances.
AGING CHANGES AND THEIR EFFECTS ON THE IMMUNE SYSTEM
As you grow older, your immune system does not work as well. The following immune system changes may occur:
The immune system becomes slower to respond. This increases your risk of getting sick. Flu shots or other vaccines may not work as well or protect you for as long as expected.
An autoimmune disorder may develop. This is a disease in which the immune system mistakenly attacks and damages or destroys healthy body tissues.
Your body may heal more slowly. There are fewer immune cells in the body to bring about healing.
The immune system's ability to detect and correct cell defects also declines. This can result in an increased risk of cancer.
https://medlineplus.gov/ency/article/004008.htm
Aging changes in immunity
Aging changes in immunity
Debbie
Causes, consequences, and reversal of immune system aging
Causes, consequences, and reversal of immune system aging
Abstract
The effects of aging on the immune system are manifest at multiple levels that include reduced production of B and T cells in bone marrow and thymus and diminished function of mature lymphocytes in secondary lymphoid tissues. As a result, elderly individuals do not respond to immune challenge as robustly as the young. An important goal of aging research is to define the cellular changes that occur in the immune system and the molecular events that underlie them. Considerable progress has been made in this regard, and this information has provided the rationale for clinical trials to rejuvenate the aging immune system.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3582124/
Abstract
The effects of aging on the immune system are manifest at multiple levels that include reduced production of B and T cells in bone marrow and thymus and diminished function of mature lymphocytes in secondary lymphoid tissues. As a result, elderly individuals do not respond to immune challenge as robustly as the young. An important goal of aging research is to define the cellular changes that occur in the immune system and the molecular events that underlie them. Considerable progress has been made in this regard, and this information has provided the rationale for clinical trials to rejuvenate the aging immune system.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3582124/
Debbie
Your Immune System Is Made, Not Born
Your Immune System Is Made, Not Born
ADVERTISEMENT
Some people seem better than others at fighting the flu, and you might suspect they were born that way. A new study of twins, however, suggests otherwise.
In one of the most comprehensive analyses of immune function performed to date, researchers analyzed blood samples from 105 sets of healthy twins. They measured immune cell populations and their chemical messengers—204 parameters in all—before and after participants received a flu shot. Differences in three fourths of these parameters depended less on genetics than on environmental factors, such as diet and prior infections. Genetics had almost no effect on how well individuals responded to the flu vaccine, judged by antibodies produced against the injected material. And among identical twin siblings, who have the same genome, immune system features differed more strikingly within older twin pairs than in younger sets. The findings, published January 15 in Cell, argue that life habits and experiences shape our body’s defenses more than the DNA passed down from our parents.
Although prior twin studies had hinted that nonheritable factors contribute to some autoimmune disorders, such as multiple sclerosis, the recent analysis was one of the first to quantify genetic and environmental effects on the general immune system. “We were surprised by the degree of environmental influence on so many components,” says Mark Davis of Stanford University School of Medicine, senior author on the new study.
One finding was particularly striking. A single environmental factor—a past infection with common cytomegalovirus—affected 58 percent of the tested parameters. Whereas the results don’t show whether these changes produce an overall stronger or weaker immune response, they do indicate “cytomegalovirus has a really profound effect,” Davis says. The Epstein–Barr virus, another microbe that frequently infects people, had no such effect.
Cytomegalovirus’s profound influence on the immune system is, perhaps, not so shocking. In order to survive, viruses must hijack a person’s host cells to churn out more viral particles. “They have to get past physical and innate barriers—it is tough to succeed,” says Peter Barry, a biologist who studies cytomegalovirus at the University of California, Davis. “The fact that a virus is still around means it is really good at what it does.”
Indeed, cytomegalovirus has learned to set up shop almost anywhere in the human body. Yet although more than three of five adults have been infected with the microbe, most would not know it. That is because roughly one tenth of a person’s circulating T cells are specific for cytomegalovirus. “It takes a ridiculously large chunk of our immune repertoire to keep this virus in check,” Barry says. Scientists are uncertain as to why the Epstein-Barr virus, which also infects most people and lingers in the body, doesn’t trigger a big ongoing immune response like cytomegalovirus does. It could be that the Epstein-Barr virus primarily infects B cells whereas cytomegalovirus can hide in a variety of cell types. Davis says his team is taking a closer look at Epstein-Barr virus’ effects on the twins’ immune parameters and plans to report the findings soon.
Some researchers think the cytomegalovirus findings could explain why the elderly tend to respond poorly to the flu vaccine. T cells develop in the thymus, but this gland shrinks with age, slowing production of new T cells and leaving us stuck with the ones in circulation. As we get older, a growing proportion of that T-cell pool is used up on cytomegalovirus, with fewer cells available to fight seasonal infections. In the Stanford study, the heightened divergence of immune parameters in older twin pairs lends credence to this theory, Barry says.
But there is also evidence to suggest cytomegalovirus could have benefits. Research in mice shows that cytomegalovirus-infected animals do better at fighting off bacterial pathogens. And in a study of monkeys, researchers discovered that a cytomegalovirus-based vaccine protected 50 percent of animals from infection by simian immunodeficiency virus.
Based on the new study, it is hard to say if being infected with cytomegalovirus is good or bad for the immune system. Ultimately, it is going to depend on the individual, notes Chris Benedict, an immunologist at the La Jolla Institute for Allergy and Immunology in California. Infectious diseases and autoimmune disorders are two of our biggest killers. “It’s always a balancing act,” Benedict adds. “The immune system has to respond well to infections but not so robustly that it causes autoimmunity.” For someone with an underactive immune system, cytomegalovirus might rev things up just enough to fend off a harmful pathogen. But if a person’s immune cells hover on the verge of hyperactivity, cytomegalovirus could push the system into danger.
Seeing this microbe singlehandedly shift such a wide range of immune parameters calls for caution in interpreting personal DNA tests that claim to predict one’s risk of a host of diseases from Alzheimer’s to cancer. “Clearly some types of mutations are bad news but sequencing your genome is not going to tell you everything about your health,” Davis says. “There’s a whole dialogue that goes on between your genome and the environment.”
He considers the new findings a key step toward his eventual goal of capturing that cross talk with a benchmark assay that measures the health of a person’s immune defenses at the systems level. “We’ve been working on pieces of the immune system for a long time. But we don’t understand too much about how the whole system fits together,” Davis says. “We now have the tools to begin doing
https://www.scientificamerican.com/arti ... -not-born/
ADVERTISEMENT
Some people seem better than others at fighting the flu, and you might suspect they were born that way. A new study of twins, however, suggests otherwise.
In one of the most comprehensive analyses of immune function performed to date, researchers analyzed blood samples from 105 sets of healthy twins. They measured immune cell populations and their chemical messengers—204 parameters in all—before and after participants received a flu shot. Differences in three fourths of these parameters depended less on genetics than on environmental factors, such as diet and prior infections. Genetics had almost no effect on how well individuals responded to the flu vaccine, judged by antibodies produced against the injected material. And among identical twin siblings, who have the same genome, immune system features differed more strikingly within older twin pairs than in younger sets. The findings, published January 15 in Cell, argue that life habits and experiences shape our body’s defenses more than the DNA passed down from our parents.
Although prior twin studies had hinted that nonheritable factors contribute to some autoimmune disorders, such as multiple sclerosis, the recent analysis was one of the first to quantify genetic and environmental effects on the general immune system. “We were surprised by the degree of environmental influence on so many components,” says Mark Davis of Stanford University School of Medicine, senior author on the new study.
One finding was particularly striking. A single environmental factor—a past infection with common cytomegalovirus—affected 58 percent of the tested parameters. Whereas the results don’t show whether these changes produce an overall stronger or weaker immune response, they do indicate “cytomegalovirus has a really profound effect,” Davis says. The Epstein–Barr virus, another microbe that frequently infects people, had no such effect.
Cytomegalovirus’s profound influence on the immune system is, perhaps, not so shocking. In order to survive, viruses must hijack a person’s host cells to churn out more viral particles. “They have to get past physical and innate barriers—it is tough to succeed,” says Peter Barry, a biologist who studies cytomegalovirus at the University of California, Davis. “The fact that a virus is still around means it is really good at what it does.”
Indeed, cytomegalovirus has learned to set up shop almost anywhere in the human body. Yet although more than three of five adults have been infected with the microbe, most would not know it. That is because roughly one tenth of a person’s circulating T cells are specific for cytomegalovirus. “It takes a ridiculously large chunk of our immune repertoire to keep this virus in check,” Barry says. Scientists are uncertain as to why the Epstein-Barr virus, which also infects most people and lingers in the body, doesn’t trigger a big ongoing immune response like cytomegalovirus does. It could be that the Epstein-Barr virus primarily infects B cells whereas cytomegalovirus can hide in a variety of cell types. Davis says his team is taking a closer look at Epstein-Barr virus’ effects on the twins’ immune parameters and plans to report the findings soon.
Some researchers think the cytomegalovirus findings could explain why the elderly tend to respond poorly to the flu vaccine. T cells develop in the thymus, but this gland shrinks with age, slowing production of new T cells and leaving us stuck with the ones in circulation. As we get older, a growing proportion of that T-cell pool is used up on cytomegalovirus, with fewer cells available to fight seasonal infections. In the Stanford study, the heightened divergence of immune parameters in older twin pairs lends credence to this theory, Barry says.
But there is also evidence to suggest cytomegalovirus could have benefits. Research in mice shows that cytomegalovirus-infected animals do better at fighting off bacterial pathogens. And in a study of monkeys, researchers discovered that a cytomegalovirus-based vaccine protected 50 percent of animals from infection by simian immunodeficiency virus.
Based on the new study, it is hard to say if being infected with cytomegalovirus is good or bad for the immune system. Ultimately, it is going to depend on the individual, notes Chris Benedict, an immunologist at the La Jolla Institute for Allergy and Immunology in California. Infectious diseases and autoimmune disorders are two of our biggest killers. “It’s always a balancing act,” Benedict adds. “The immune system has to respond well to infections but not so robustly that it causes autoimmunity.” For someone with an underactive immune system, cytomegalovirus might rev things up just enough to fend off a harmful pathogen. But if a person’s immune cells hover on the verge of hyperactivity, cytomegalovirus could push the system into danger.
Seeing this microbe singlehandedly shift such a wide range of immune parameters calls for caution in interpreting personal DNA tests that claim to predict one’s risk of a host of diseases from Alzheimer’s to cancer. “Clearly some types of mutations are bad news but sequencing your genome is not going to tell you everything about your health,” Davis says. “There’s a whole dialogue that goes on between your genome and the environment.”
He considers the new findings a key step toward his eventual goal of capturing that cross talk with a benchmark assay that measures the health of a person’s immune defenses at the systems level. “We’ve been working on pieces of the immune system for a long time. But we don’t understand too much about how the whole system fits together,” Davis says. “We now have the tools to begin doing
https://www.scientificamerican.com/arti ... -not-born/
Last edited by D.ap on Sun Oct 10, 2021 6:33 am, edited 2 times in total.
Debbie
Re: Aging changes in immunity
Perhaps Covid triggered or related studies will advance the immune system knowledge greatly, as there are still so many basic commonly found facts that have no solid explanation.
Olga
Re: Aging changes in immunity
Agreed Olga !
Once you reach puberty, the thymus starts to slowly shrink and become replaced by fat. By age 75, the thymus is little more than fatty tissue. Fortunately, the thymus produces all of your T cells by the time you reach puberty.Jun 10, 2014
Debbie
Re: Aging changes in immunity
Aging, Immunity, and COVID-19: How Age Influences the Host Immune Response to Coronavirus Infections?
https://www.frontiersin.org/articles/10 ... 71416/full
Hello Olga ,
Came accross the above article when I was researching HSC and how it deteriorates over a life time , in reference to immune responses.
As you pointed out , with the data on COVID , being extensively studied and immune responses, there will be a-lot of info to be paralleled and be discovered in relationship to immune check point inhibitors usage and the link to success of introducing ICIs.The aging process brings a change in the system of hematopoietic stem cells (HSCs) and immunity against the age related disease like cancer. ... In HSCs, p53 continuously suppresses self-renewal and differentiation associated with aging; as a result, the proliferation and functionality of HSCs are decreased.
My question would be is age one of the many determining factors to how well ICI works?
Obviously health and environment aid in the success.😊
Debbie
Re: Aging changes in immunity
Aging, Immunity, and COVID-19: How Age Influences the Host Immune Response to Coronavirus Infections?
Introduction
The novel coronavirus severe acute respiratory syndrome coronavirus 2 causing the Coronavirus disease (COVID-19) pandemic has ravaged the world with over 72 million total cases and over 1.6 million deaths worldwide as of early December 2020. An overwhelming preponderance of cases and deaths is observed within the elderly population, and especially in those with pre-existing conditions and comorbidities. Aging causes numerous biological changes in the immune system, which are linked to age-related illnesses and susceptibility to infectious diseases. Age-related changes influence the host immune response and therefore not only weaken the ability to fight respiratory infections but also to mount effective responses to vaccines. Immunosenescence and inflamm-aging are considered key features of the aging immune system wherein accumulation of senescent immune cells contribute to its decline and simultaneously increased inflammatory phenotypes cause immune dysfunction. Age-related quantitative and qualitative changes in the immune system affect cells and soluble mediators of both the innate and adaptive immune responses within lymphoid and non-lymphoid peripheral tissues. These changes determine not only the susceptibility to infections, but also disease progression and clinical outcomes thereafter. Furthermore, the response to therapeutics and the immune response to vaccines are influenced by age-related changes within the immune system. Therefore, better understanding of the pathophysiology of aging and the immune response will not only help understand age-related diseases but also guide targeted management strategies for deadly infectious diseases like COVID-19.“
Pathophysiology of ageing - PubMed
https://pubmed.ncbi.nlm.nih.gov/12120891/
Introduction
The novel coronavirus severe acute respiratory syndrome coronavirus 2 causing the Coronavirus disease (COVID-19) pandemic has ravaged the world with over 72 million total cases and over 1.6 million deaths worldwide as of early December 2020. An overwhelming preponderance of cases and deaths is observed within the elderly population, and especially in those with pre-existing conditions and comorbidities. Aging causes numerous biological changes in the immune system, which are linked to age-related illnesses and susceptibility to infectious diseases. Age-related changes influence the host immune response and therefore not only weaken the ability to fight respiratory infections but also to mount effective responses to vaccines. Immunosenescence and inflamm-aging are considered key features of the aging immune system wherein accumulation of senescent immune cells contribute to its decline and simultaneously increased inflammatory phenotypes cause immune dysfunction. Age-related quantitative and qualitative changes in the immune system affect cells and soluble mediators of both the innate and adaptive immune responses within lymphoid and non-lymphoid peripheral tissues. These changes determine not only the susceptibility to infections, but also disease progression and clinical outcomes thereafter. Furthermore, the response to therapeutics and the immune response to vaccines are influenced by age-related changes within the immune system. Therefore, better understanding of the pathophysiology of aging and the immune response will not only help understand age-related diseases but also guide targeted management strategies for deadly infectious diseases like COVID-19.“
.Ageing is characterized by a gradual decline in organ functional reserves which reduces the ability to maintain homeostasis under conditions of stress. Introduction of cell culture and molecular biology techniques has provided new experimental tools for the analysis of ageing at the molecular level
Pathophysiology of ageing - PubMed
https://pubmed.ncbi.nlm.nih.gov/12120891/
Debbie
Re: Aging changes in immunity
Pathophysiology of ageing - PubMed
https://pubmed.ncbi.nlm.nih.gov/12120891/
K e y w o r d s : mechanisms of ageing, functional parameters, cellular ageing
“The past few years have seen an unparalleled increase in biomedical research aiming at defining molecular basis of ageing. This worldwide interest was dic- tated to a large extent by alarming demographic data showing that both the num- ber and the percentage of elderly people in societies had been growing steadily. It is difficult to answer a question of how old one must be to be treated as an eld- erly man. For practical reasons this criterion has been set for 65 years of age. However, it is necessary to emphasize early in this review that the calendar age itself is an imperfect indicator of ageing. From the clinical point of view, the two people of the same calendar age are likely to differ far more when elderly than when at any other stage of life. This is because their physical condition is relat- ed not only to ageing, but also psychological and social status, and important- ly the presence of chronic diseases.“
https://pubmed.ncbi.nlm.nih.gov/12120891/
K e y w o r d s : mechanisms of ageing, functional parameters, cellular ageing
“The past few years have seen an unparalleled increase in biomedical research aiming at defining molecular basis of ageing. This worldwide interest was dic- tated to a large extent by alarming demographic data showing that both the num- ber and the percentage of elderly people in societies had been growing steadily. It is difficult to answer a question of how old one must be to be treated as an eld- erly man. For practical reasons this criterion has been set for 65 years of age. However, it is necessary to emphasize early in this review that the calendar age itself is an imperfect indicator of ageing. From the clinical point of view, the two people of the same calendar age are likely to differ far more when elderly than when at any other stage of life. This is because their physical condition is relat- ed not only to ageing, but also psychological and social status, and important- ly the presence of chronic diseases.“
Debbie
Re: Aging changes in immunity
Senescence and Aging: Does It Impact Cancer Immunotherapies?
Abstract
Cancer incidence increases drastically with age. Of the many possible reasons for this, there is the accumulation of senescent cells in tissues and the loss of function and proliferation potential of immune cells, often referred to as immuno-senescence. Immune checkpoint inhibitors (ICI), by invigorating immune cells, have the potential to be a game-changers in the treatment of cancer. Yet, the variability in the efficacy of ICI across patients and cancer types suggests that several factors influence the success of such inhibitors. There is currently a lack of clinical studies measuring the impact of aging and senescence on ICI-based therapies. Here, we review how cellular senescence and aging, either by directly altering the immune system fitness or indirectly through the modification of the tumor environment, may influence the cancer-immune response.
Keywords: immune checkpoint inhibitors; aging; senescence; cancer; tumor
https://www.mdpi.com/2073-4409/10/7/1568/htm
Abstract
Cancer incidence increases drastically with age. Of the many possible reasons for this, there is the accumulation of senescent cells in tissues and the loss of function and proliferation potential of immune cells, often referred to as immuno-senescence. Immune checkpoint inhibitors (ICI), by invigorating immune cells, have the potential to be a game-changers in the treatment of cancer. Yet, the variability in the efficacy of ICI across patients and cancer types suggests that several factors influence the success of such inhibitors. There is currently a lack of clinical studies measuring the impact of aging and senescence on ICI-based therapies. Here, we review how cellular senescence and aging, either by directly altering the immune system fitness or indirectly through the modification of the tumor environment, may influence the cancer-immune response.
Keywords: immune checkpoint inhibitors; aging; senescence; cancer; tumor
https://www.mdpi.com/2073-4409/10/7/1568/htm
Debbie
Re: Aging changes in immunity
Immunosenescence is a process of immune dysfunction that occurs with age and includes remodeling of lymphoid organs, leading to changes in the immune function of the elderly, which is closely related to the development of infections, autoimmune diseases, and malignant tumors.
Debbie