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2014 ; 111
(43
): E4638-47
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Spleen supports a pool of innate-like B cells in white adipose tissue that
protects against obesity-associated insulin resistance
#MMPMID25313053
Wu L
; Parekh VV
; Hsiao J
; Kitamura D
; Van Kaer L
Proc Natl Acad Sci U S A
2014[Oct]; 111
(43
): E4638-47
PMID25313053
show ga
Lipid accumulation in obesity triggers a low-grade inflammation that results from
an imbalance between pro- and anti-inflammatory components of the immune system
and acts as the major underlying mechanism for the development of
obesity-associated diseases, notably insulin resistance and type 2 diabetes.
Innate-like B cells are a subgroup of B cells that respond to innate signals and
modulate inflammatory responses through production of immunomodulatory mediators
such as the anti-inflammatory cytokine IL-10. In this study, we examined
innate-like B cells in visceral white adipose tissue (VAT) and the relationship
of these cells with their counterparts in the peritoneal cavity and spleen during
diet-induced obesity (DIO) in mice. We show that a considerable number of
innate-like B cells bearing a surface phenotype distinct from the recently
identified "adipose natural regulatory B cells" populate VAT of lean animals, and
that spleen represents a source for the recruitment of these cells in VAT during
DIO. However, demand for these cells in the expanding VAT outpaces their
recruitment during DIO, and the obese environment in VAT further impairs their
function. We further show that removal of splenic precursors of innate-like B
cells through splenectomy exacerbates, whereas supplementation of these cells via
adoptive transfer ameliorates, DIO-associated insulin resistance. Additional
adoptive transfer experiments pointed toward a dominant role of IL-10 in
mediating the protective effects of innate-like B cells against DIO-induced
insulin resistance. These findings identify spleen-supplied innate-like B cells
in VAT as previously unrecognized players and therapeutic targets for
obesity-associated diseases.
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