Transient modification within a pool of CD4 T cells in the maternal spleen

Bonney, Elizabeth A.; Shepard, Michelle; Bizargity, Peyman

doi:10.1111/j.1365-2567.2011.03486.x

Cited by 11 publications

(13 citation statements)

References 43 publications

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“…Within the T cell pool, we also found that both splenic CD4 (Bonney et al, 2011) and CD8 T cells (Norton et al, 2010) undergo a period of enhanced proliferation during normal gestation. Because PD-1 signaling is thought to play an important role in T cell homeostasis by limiting the expansion of activated cells, we hypothesized that pregnancy should alter the expression of Pd-1 in the spleen.…”

Section: Resultsmentioning

confidence: 55%

“…This is likely related to increased expression of receptors to cytokines, such as interleukin 7 and interleukin 15, that are known to support homeostatic proliferation. This turnover is also likely driven by increased expression of both pro and anti apoptotic genes (Norton et al, 2010) and related to exposure and recognition of male-specific antigens (Bonney et al, 2011; Lissauer et al, 2012). Homeostatic proliferation in response to chronic antigen stimulation can to lead to “exhaustion”, marked by expression of a discreet set of genes and decreased immune function (Wherry et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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PD-1 Regulates T Cell Proliferation in a Tissue and Subset-Specific Manner During Normal Mouse Pregnancy

Shepard

Bonney

2013

Immunological Investigations

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The regulation of T cell homeostasis during pregnancy has important implications for maternal tolerance and immunity. Evidence suggests that Programmed Death-1 (PD-1) participates in regulation of T cell homeostasis and peripheral tolerance. To examine the contribution of PD-1 signaling on T cell homeostasis during normal mouse pregnancy, we examined T cell number or proportion, PD-1 expression, proliferation, and apoptosis by flow cytometry, BrdU incorporation, and TUNEL assay in pregnant mice given anti-PD-1 blocking antibody or control on days 10, 12, and 14 of gestation. We observed tissue, treatment, and T cell-specific differences in PD-1 expression. Both pregnancy and PD-1 blockade increased T cell proliferation in the spleen while this effect was limited to CD4 T cells in the uterine- draining nodes. In the uterus, PD-1 blockade markedly altered the composition of the T cell pool. These studies support the idea that pregnancy is a state of dynamic T cell homeostasis and suggest that this state is partially supported by PD-1 signaling.

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Section: Resultsmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 99%

PD-1 Regulates T Cell Proliferation in a Tissue and Subset-Specific Manner During Normal Mouse Pregnancy

Shepard

Bonney

2013

Immunological Investigations

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“…[21][22][23][24] We have studied T-cell homeostasis in mice and observed changes in the maternal immune system that persist PP. [21][22][23][25][26][27] There may be accumulation of TREGs in PP that may protect subsequent pregnancies.…”

Section: Introductionmentioning

confidence: 99%

Impact of Immune Deficiency on Remodeling of Maternal Resistance Vasculature 4 Weeks Postpartum in Mice

et al. 2017

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Pregnancy manifests changes in the vascular and immune systems that persist postpartum (PP), have important implications for future pregnancies, and may modify responses to cardiovascular stress in late life. The association between immune and vascular function and the generation or progression of cardiovascular disease beg the question of whether altered immunity modifies pregnancy-induced changes in the vasculature. Our objective was to compare changes in the function and remodeling of systemic resistance vessels 4 weeks PP in normal C57BL/6 (B6), and immunodeficient mice recombinase 1-deficient/B6 (Rag1). Immune deficiency did not change the responsiveness to acetylcholine (ACh) and phenylephrine at baseline but decreased arterial distensibility and increased stiffness PP. Adoptive transfer of CD8 T cells into Rag1 À/À mice decreased the response to ACh while increasing distensibility and wall thickness. When compared to PP Rag1 À/À , vessels from PP CD4-deficient mice, which have B cells and CD8 T cells, but no CD4 cells, show increased distensibility and decreased responsiveness to ACh in a pattern similar to that seen in Rag1 À/À given CD8 T cells prior to mating. These studies suggest a key role for T cell, particularly CD8 T cell, associated factors in the PP remodeling of maternal resistance vessels.

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“…Since then several investigators have produced evidence in these systems that the maternal T cells are “aware” that the host is pregnant (Bonney, et al 2011), undergo proliferation and death (Norton, et al 2010) and are able to respond to fetal antigens (Erlebacher, et al 2007, Norton, et al 2010). For most mice, neither the increased presence of T cells specific for fetal antigen nor manipulations to increase fetal antigen specific T cell proliferation or function has resulted in specific pregnancy loss (see review by Moldenhauer, et al 2010).…”

Section: Introductionmentioning

confidence: 99%