Adipose Tissue: A Tertiary Lymphoid Organ: Does It Change with Age?

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Abstract

In this manuscript, we summarize published results showing that obesity and aging are inflammatory conditions associated with serious health problems, increased risk for disease and death. We show that fat mass increases with age and represents a major contributor to insulin resistance and the metabolic syndrome. We summarize the effects of age on the adipose tissue (AT), related to the abundance, distribution, cellular composition, endocrine signaling and function of the tissue. The AT is an immunological tissue, with several hallmarks of innate and adaptive immune responses. We show that in both mice and humans, the AT is heavily infiltrated by immune cells that have receptors for pro-inflammatory cytokines and chemokines secreted by the adipocytes and also by the immune cells that have infiltrated the AT. We also show that the AT provides an environment for the secretion of IgG antibodies with anti-self (autoimmune) reactivity. As we have previously shown, this is due to the release of self antigens following cell death due to hypoxia, as well as to the expression of activation-induced cytidine deaminase, the enzyme of class switch recombination, and the transcription factor T-bet by the resident B cells, which also express the membrane marker CD11c, both involved in the production of autoimmune IgG antibodies. We show data in support of the AT as a tertiary lymphoid organ (TLO), showing the examples of TLOs that develop within the AT, such as fat-associated lymphoid clusters and milky spots, as well as artery TLOs that develop in the adventitia areas of the aorta.

Original languageEnglish (US)
JournalGerontology
DOIs
StateAccepted/In press - Jan 1 2019

Fingerprint

Adipose Tissue
Immunoglobulin G
Fats
Adventitia
Autoantigens
Adaptive Immunity
Chemokines
Adipocytes
Innate Immunity
Genetic Recombination
Aorta
Insulin Resistance
Anti-Idiotypic Antibodies
B-Lymphocytes
Cell Death
Arteries
Obesity
Cytokines
Membranes
Antibodies

Keywords

  • Adipose tissue
  • Aging
  • Immunosenescence
  • Inflammaging

ASJC Scopus subject areas

  • Aging
  • Geriatrics and Gerontology

Cite this

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title = "Adipose Tissue: A Tertiary Lymphoid Organ: Does It Change with Age?",
abstract = "In this manuscript, we summarize published results showing that obesity and aging are inflammatory conditions associated with serious health problems, increased risk for disease and death. We show that fat mass increases with age and represents a major contributor to insulin resistance and the metabolic syndrome. We summarize the effects of age on the adipose tissue (AT), related to the abundance, distribution, cellular composition, endocrine signaling and function of the tissue. The AT is an immunological tissue, with several hallmarks of innate and adaptive immune responses. We show that in both mice and humans, the AT is heavily infiltrated by immune cells that have receptors for pro-inflammatory cytokines and chemokines secreted by the adipocytes and also by the immune cells that have infiltrated the AT. We also show that the AT provides an environment for the secretion of IgG antibodies with anti-self (autoimmune) reactivity. As we have previously shown, this is due to the release of self antigens following cell death due to hypoxia, as well as to the expression of activation-induced cytidine deaminase, the enzyme of class switch recombination, and the transcription factor T-bet by the resident B cells, which also express the membrane marker CD11c, both involved in the production of autoimmune IgG antibodies. We show data in support of the AT as a tertiary lymphoid organ (TLO), showing the examples of TLOs that develop within the AT, such as fat-associated lymphoid clusters and milky spots, as well as artery TLOs that develop in the adventitia areas of the aorta.",
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AU - Blomberg, Bonnie B.

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N2 - In this manuscript, we summarize published results showing that obesity and aging are inflammatory conditions associated with serious health problems, increased risk for disease and death. We show that fat mass increases with age and represents a major contributor to insulin resistance and the metabolic syndrome. We summarize the effects of age on the adipose tissue (AT), related to the abundance, distribution, cellular composition, endocrine signaling and function of the tissue. The AT is an immunological tissue, with several hallmarks of innate and adaptive immune responses. We show that in both mice and humans, the AT is heavily infiltrated by immune cells that have receptors for pro-inflammatory cytokines and chemokines secreted by the adipocytes and also by the immune cells that have infiltrated the AT. We also show that the AT provides an environment for the secretion of IgG antibodies with anti-self (autoimmune) reactivity. As we have previously shown, this is due to the release of self antigens following cell death due to hypoxia, as well as to the expression of activation-induced cytidine deaminase, the enzyme of class switch recombination, and the transcription factor T-bet by the resident B cells, which also express the membrane marker CD11c, both involved in the production of autoimmune IgG antibodies. We show data in support of the AT as a tertiary lymphoid organ (TLO), showing the examples of TLOs that develop within the AT, such as fat-associated lymphoid clusters and milky spots, as well as artery TLOs that develop in the adventitia areas of the aorta.

AB - In this manuscript, we summarize published results showing that obesity and aging are inflammatory conditions associated with serious health problems, increased risk for disease and death. We show that fat mass increases with age and represents a major contributor to insulin resistance and the metabolic syndrome. We summarize the effects of age on the adipose tissue (AT), related to the abundance, distribution, cellular composition, endocrine signaling and function of the tissue. The AT is an immunological tissue, with several hallmarks of innate and adaptive immune responses. We show that in both mice and humans, the AT is heavily infiltrated by immune cells that have receptors for pro-inflammatory cytokines and chemokines secreted by the adipocytes and also by the immune cells that have infiltrated the AT. We also show that the AT provides an environment for the secretion of IgG antibodies with anti-self (autoimmune) reactivity. As we have previously shown, this is due to the release of self antigens following cell death due to hypoxia, as well as to the expression of activation-induced cytidine deaminase, the enzyme of class switch recombination, and the transcription factor T-bet by the resident B cells, which also express the membrane marker CD11c, both involved in the production of autoimmune IgG antibodies. We show data in support of the AT as a tertiary lymphoid organ (TLO), showing the examples of TLOs that develop within the AT, such as fat-associated lymphoid clusters and milky spots, as well as artery TLOs that develop in the adventitia areas of the aorta.

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