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B cells treated with CTB-p210 acquire a regulatory phenotype in vitro and reduce atherosclerosis in apolipoprotein E deficient mice.

Abstract：

OBJECTIVE:Intranasal immunization with a fusion protein of the ApoB100-derived peptide p210 and the cholera toxin B subunit (CTB-p210) has previously been shown to induce mucosal tolerance and reduce atherosclerosis development, but the exact mode of action remains to be elucidated. Recent studies have indicated an important role for B cells in mucosal tolerance, in particular by induction of regulatory B (Bregs) and T cells (Tregs). In this study, we aimed to investigate if transfer of B cells pulsed with CTB-p210 can protect against atherosclerosis. METHOD AND RESULTS:First, we studied if CTB-p210 can induce Bregs and Tregs in vitro. After pulsing B cells from Apobtm2Sgyldlr-/- or Apoe-/- mice with CTB-p210 for 1 h and co-culturing them with naïve T cells for 48 h, we observed increased expression of membrane bound TGFβ/latency-associated peptide (mTGFβ/LAP) on B cells and an increased proportion of CD25hiFoxP3+ Tregs. Adoptive transfer of B cells pulsed with CTB-p210 into high-fat diet-fed Apoe-/- mice at 8, 10 and 12 weeks of age, reduced the plaque area in the aorta at 20 weeks of age as compared with control-treated (CTB-pOVA treated B cells or PBS) mice. Moreover, mice receiving p210-CTB treated B cells had increased levels of anti-p210 IgG antibodies. CONCLUSION:Our observations suggest that CTB-p210 pulsed B cells acquire a regulatory phenotype and induce Tregs in vitro. Adoptive transfer of CTB-p210, but not control-treated, B cells into Apoe-/- mice decreased atherosclerosis development.

journal_name

Vascul Pharmacol

journal_title

Vascular pharmacology

authors

Rattik S,Mantani PT,Yao Mattisson I,Ljungcrantz I,Sundius L,Björkbacka H,Terrinoni M,Lebens M,Holmgren J,Nilsson J,Wigren M,Nordin Fredrikson G

doi

10.1016/j.vph.2018.09.002

subject

Has Abstract

pub_date

2018-12-01 00:00:00

pages

54-61

eissn

1537-1891

issn

1879-3649

pii

S1537-1891(18)30221-0

journal_volume

111

pub_type

杂志文章

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