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Review
. 2017 Aug 28:8:1003.
doi: 10.3389/fimmu.2017.01003. eCollection 2017.

Adipose Tissue Inflammation Induces B Cell Inflammation and Decreases B Cell Function in Aging

Daniela Frasca  1 , Bonnie B Blomberg  1
Affiliations
Review

Adipose Tissue Inflammation Induces B Cell Inflammation and Decreases B Cell Function in Aging

Daniela Frasca et al. Front Immunol. .

Abstract

Aging is the greatest risk factor for developing chronic diseases. Inflamm-aging, the age-related increase in low-grade chronic inflammation, may be a common link in age-related diseases. This review summarizes recent published data on potential cellular and molecular mechanisms of the age-related increase in inflammation, and how these contribute to decreased humoral immune responses in aged mice and humans. Briefly, we cover how aging and related inflammation decrease antibody responses in mice and humans, and how obesity contributes to the mechanisms for aging through increased inflammation. We also report data in the literature showing adipose tissue infiltration with immune cells and how these cells are recruited and contribute to local and systemic inflammation. We show that several types of immune cells infiltrate the adipose tissue and these include macrophages, neutrophils, NK cells, innate lymphoid cells, eosinophils, T cells, B1, and B2 cells. Our main focus is how the adipose tissue affects immune responses, in particular B cell responses and antibody production. The role of leptin in generating inflammation and decreased B cell responses is also discussed. We report data published by us and by other groups showing that the adipose tissue generates pro-inflammatory B cell subsets which induce pro-inflammatory T cells, promote insulin resistance, and secrete pathogenic autoimmune antibodies.

Keywords: aging; antibody responses; immunity; inflammation; obesity.

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Figures

Figure 1
Figure 1
Mechanisms by which the visceral adipose tissue (VAT) impairs antibody responses. The adipocytes in the VAT secrete more pro-inflammatory chemokines which attract B cells via chemokine receptors, as well as pro-inflammatory cytokines. Age-associated B cells (ABCs) are preferentially induced and we hypothesize that these cells make pro-inflammatory cytokines and pathogenic antibodies. Marginal zone B cells are not affected. Immune cells traffic to the spleen and periphery where there are more ABC in aged and obese mice. Before antigen stimulation the cells secrete increased amounts of inflammatory cytokines (TNF-α/IL-6), making them refractory to further stimulation. Fewer antibody-secreting cells producing less Ig are made after antigen stimulation of “refractory” B cells.
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