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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 J+Immunol
2016 ; 197
(11
): 4351-4359
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gab.com Text
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IL-18 and Subcapsular Lymph Node Macrophages are Essential for Enhanced B Cell
Responses with TLR4 Agonist Adjuvants
#MMPMID27794001
Desbien AL
; Dubois Cauwelaert N
; Reed SJ
; Bailor HR
; Liang H
; Carter D
; Duthie MS
; Fox CB
; Reed SG
; Orr MT
J Immunol
2016[Dec]; 197
(11
): 4351-4359
PMID27794001
show ga
Designing modern vaccine adjuvants depends on understanding the cellular and
molecular events that connect innate and adaptive immune responses. The synthetic
TLR4 agonist glycopyranosyl lipid adjuvant (GLA) formulated in a
squalene-in-water emulsion (GLA-SE) augments both cellular and humoral immune
responses to vaccine Ags. This adjuvant is currently included in several vaccines
undergoing clinical evaluation including those for tuberculosis, leishmaniasis,
and influenza. Delineation of the mechanisms of adjuvant activity will enable
more informative evaluation of clinical trials. Early after injection, GLA-SE
induces substantially more Ag-specific B cells, higher serum Ab titers, and
greater numbers of T follicular helper (T(FH)) and Th1 cells than alum, the SE
alone, or GLA without SE. GLA-SE augments Ag-specific B cell differentiation into
germinal center and memory precursor B cells as well as preplasmablasts that
rapidly secrete Abs. CD169(+) SIGNR1(+) subcapsular medullary macrophages are the
primary cells to take up GLA-SE after immunization and are critical for the
innate immune responses, including rapid IL-18 production, induced by GLA-SE.
Depletion of subcapsular macrophages (SCM?) or abrogation of IL-18 signaling
dramatically impairs the Ag-specific B cell and Ab responses augmented by GLA-SE.
Depletion of SCM? also drastically reduces the Th1 but not the T(FH) response.
Thus the GLA-SE adjuvant operates through interaction with IL-18-producing SCM?
for the rapid induction of B cell expansion and differentiation, Ab secretion,
and Th1 responses, whereas augmentation of T(FH) numbers by GLA-SE is independent
of SCM?.
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