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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Circulation
2014 ; 129
(16
): 1677-87
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Innate response activator B cells aggravate atherosclerosis by stimulating T
helper-1 adaptive immunity
#MMPMID24488984
Hilgendorf I
; Theurl I
; Gerhardt LM
; Robbins CS
; Weber GF
; Gonen A
; Iwamoto Y
; Degousee N
; Holderried TA
; Winter C
; Zirlik A
; Lin HY
; Sukhova GK
; Butany J
; Rubin BB
; Witztum JL
; Libby P
; Nahrendorf M
; Weissleder R
; Swirski FK
Circulation
2014[Apr]; 129
(16
): 1677-87
PMID24488984
show ga
BACKGROUND: Atherosclerotic lesions grow via the accumulation of leukocytes and
oxidized lipoproteins in the vessel wall. Leukocytes can attenuate or augment
atherosclerosis through the release of cytokines, chemokines, and other
mediators. Deciphering how leukocytes develop, oppose, and complement each
other's function and shape the course of disease can illuminate our understanding
of atherosclerosis. Innate response activator (IRA) B cells are a recently
described population of granulocyte macrophage colony-stimulating
factor-secreting cells of hitherto unknown function in atherosclerosis. METHODS
AND RESULTS: Here, we show that IRA B cells arise during atherosclerosis in mice
and humans. In response to a high-cholesterol diet, IRA B cell numbers increase
preferentially in secondary lymphoid organs via Myd88-dependent signaling. Mixed
chimeric mice lacking B cell-derived granulocyte macrophage colony-stimulating
factor develop smaller lesions with fewer macrophages and effector T cells.
Mechanistically, IRA B cells promote the expansion of classic dendritic cells,
which then generate interferon ?-producing T helper-1 cells. This IRA B
cell-dependent T helper-1 skewing manifests in an IgG1-to-IgG2c isotype switch in
the immunoglobulin response against oxidized lipoproteins. CONCLUSIONS:
Granulocyte macrophage colony-stimulating factor-producing IRA B cells alter
adaptive immune processes and shift the leukocyte response toward a T
helper-1-associated milieu that aggravates atherosclerosis.
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