From the first to the last breath, our immune system is continuously adapting to the different challenges posed by a plethora of pathogens. It needs to distinguish self from foreign and friend from foe. It must continuously seek and destroy invading pathogens and tolerate the commensal bacteria that reside in our perimeter, especially in the intestinal mucosa. To achieve this grade of specificity, a new tool has evolved since early vertebrates, the adaptive immune system. This adaptation, based on the specialization of individual cells and tissues, resulted in complex mechanisms that enable the immune system to recognize and memorize previous pathogen encounters. However, this continuous adaptation comes at a price. The recurrent exposure to foreign antigens leads to a state of low-grade chronic inflammation that is characteristic of elder individuals and was adequately coined inflammaging by Claudio Franceschi and colleagues in 2000.
As the output of new adaptive immune cells declines with age, due to thymic involution and bone marrow myeloid bias, the host’s response to infection gradually relies more and more on innate and terminally differentiated immune cells. These cells are major sources of inflammatory cytokines that exacerbate inflammation. Moreover, altered host proteins that are a consequence of damaged, senescent, or dead cells also accumulate with age and further stimulate the immune system. The obesity and diabetes pandemics further exacerbate this phenomenon because nutrient excess or overnutrition also drives metabolic inflammation. Adipose tissue disfunction, insulin resistance, and chronic inflammation are inter-related and trigger various age-related pathologies, from atherosclerosis to Alzheimer's disease.
In this special issue, we aim at understanding the process and the consequences of immune aging. We also aim at exploring new immunomodulatory strategies that may one day enable us to cope with these consequences.
To reach this goal we will narrow the scope of this issue to:
1) Cellular and molecular changes in the aging immune system.
2) Age-related alterations in immune cell population dynamics and receptor repertoire.
3) Host-pathogen interactions and how they reshape the immune response.
4) Commensal bacteria dynamics with age.
5) Tolerance mechanisms in the aged immune system.
6) Causes and consequences of age-related hematopoietic myeloid bias and thymic involution.
7) How vaccines reshape the immune system.
8) Pathophysiology of low-grade chronic inflammation and its contribution to the development of age-related pathologies.
9) Immunomodulatory strategies to reduce chronic inflammation and its consequences.
From the first to the last breath, our immune system is continuously adapting to the different challenges posed by a plethora of pathogens. It needs to distinguish self from foreign and friend from foe. It must continuously seek and destroy invading pathogens and tolerate the commensal bacteria that reside in our perimeter, especially in the intestinal mucosa. To achieve this grade of specificity, a new tool has evolved since early vertebrates, the adaptive immune system. This adaptation, based on the specialization of individual cells and tissues, resulted in complex mechanisms that enable the immune system to recognize and memorize previous pathogen encounters. However, this continuous adaptation comes at a price. The recurrent exposure to foreign antigens leads to a state of low-grade chronic inflammation that is characteristic of elder individuals and was adequately coined inflammaging by Claudio Franceschi and colleagues in 2000.
As the output of new adaptive immune cells declines with age, due to thymic involution and bone marrow myeloid bias, the host’s response to infection gradually relies more and more on innate and terminally differentiated immune cells. These cells are major sources of inflammatory cytokines that exacerbate inflammation. Moreover, altered host proteins that are a consequence of damaged, senescent, or dead cells also accumulate with age and further stimulate the immune system. The obesity and diabetes pandemics further exacerbate this phenomenon because nutrient excess or overnutrition also drives metabolic inflammation. Adipose tissue disfunction, insulin resistance, and chronic inflammation are inter-related and trigger various age-related pathologies, from atherosclerosis to Alzheimer's disease.
In this special issue, we aim at understanding the process and the consequences of immune aging. We also aim at exploring new immunomodulatory strategies that may one day enable us to cope with these consequences.
To reach this goal we will narrow the scope of this issue to:
1) Cellular and molecular changes in the aging immune system.
2) Age-related alterations in immune cell population dynamics and receptor repertoire.
3) Host-pathogen interactions and how they reshape the immune response.
4) Commensal bacteria dynamics with age.
5) Tolerance mechanisms in the aged immune system.
6) Causes and consequences of age-related hematopoietic myeloid bias and thymic involution.
7) How vaccines reshape the immune system.
8) Pathophysiology of low-grade chronic inflammation and its contribution to the development of age-related pathologies.
9) Immunomodulatory strategies to reduce chronic inflammation and its consequences.