Immunosenescence refers to the dysregulation of the function in the immune system and leads to less effectiveness in responding to pathogens and cancer cells. It is associated with not only the aging process but also the low-grade, chronic inflammation. Sepsis is now considered to be an abnormal host protective immune syndrome, in which the patients are in a state of persistent inflammation-immunosuppression. In older patients with sepsis, the impaired cellular regulatory immunity and humoral immunity caused by the state of immunosenescence may lead to severer disease progression and higher mortality. In addition, the profound immunosuppressive stage after the proinflammatory stage of sepsis is thought to have many similarities with the phenomenon of immunosenescence. Sepsis-induced immune characteristics of lymphopenia, thymic degeneration, telomere shortening, and increased immunosuppressive cells closely resemble the features of immunosenescence. Meanwhile, the expansion of myeloid-derived suppressor cells (MDSCs) plays a vital immunosuppressive role. In sepsis, MDSC is increased by emergency myelopoiesis to regulate the function of other immune cells and prevent excessive inflammation. It may create an immunosuppressive microenvironment that generates immunosenescence after the immune system’s remodeling. Therefore, while immunosenescence aggravates sepsis, sepsis-induced immunosuppression may also promote immunosenescence.
The goal of this Research Topic is to provide a forum to explore the interaction between sepsis-induced immunosuppression and immunosenescence including but not limited to the influence of MDSC on immunosenescence. A better understanding of this intricate process may develop tailored interventions and targeted novel therapeutic strategies for sepsis. Manuscripts from the following subtopics are welcome:
1) Cellular and molecular aspects of Immunosenescence
2) Immunosenescence and sepsis
3) Infection/vaccination and Immunosenescence
4) Immunosenescence, sepsis, and check point therapies
5) immunosenescence and MDSC-driven immunosuppression
6) Immunosenescence and sepsis-induced immunosuppression
7) Immunosenescence and altered control of homeostasis
8) Immunosenescence and the susceptibility to COVID-19 infection
9) Immune response after acute poisoning
Immunosenescence refers to the dysregulation of the function in the immune system and leads to less effectiveness in responding to pathogens and cancer cells. It is associated with not only the aging process but also the low-grade, chronic inflammation. Sepsis is now considered to be an abnormal host protective immune syndrome, in which the patients are in a state of persistent inflammation-immunosuppression. In older patients with sepsis, the impaired cellular regulatory immunity and humoral immunity caused by the state of immunosenescence may lead to severer disease progression and higher mortality. In addition, the profound immunosuppressive stage after the proinflammatory stage of sepsis is thought to have many similarities with the phenomenon of immunosenescence. Sepsis-induced immune characteristics of lymphopenia, thymic degeneration, telomere shortening, and increased immunosuppressive cells closely resemble the features of immunosenescence. Meanwhile, the expansion of myeloid-derived suppressor cells (MDSCs) plays a vital immunosuppressive role. In sepsis, MDSC is increased by emergency myelopoiesis to regulate the function of other immune cells and prevent excessive inflammation. It may create an immunosuppressive microenvironment that generates immunosenescence after the immune system’s remodeling. Therefore, while immunosenescence aggravates sepsis, sepsis-induced immunosuppression may also promote immunosenescence.
The goal of this Research Topic is to provide a forum to explore the interaction between sepsis-induced immunosuppression and immunosenescence including but not limited to the influence of MDSC on immunosenescence. A better understanding of this intricate process may develop tailored interventions and targeted novel therapeutic strategies for sepsis. Manuscripts from the following subtopics are welcome:
1) Cellular and molecular aspects of Immunosenescence
2) Immunosenescence and sepsis
3) Infection/vaccination and Immunosenescence
4) Immunosenescence, sepsis, and check point therapies
5) immunosenescence and MDSC-driven immunosuppression
6) Immunosenescence and sepsis-induced immunosuppression
7) Immunosenescence and altered control of homeostasis
8) Immunosenescence and the susceptibility to COVID-19 infection
9) Immune response after acute poisoning
