Cryopreservation Decreases Receptor PD-1 and Ligand PD-L1 Coinhibitory Expression on Peripheral Blood Mononuclear Cell-Derived T Cells and Monocytes

Campbell, Donald E.; Tustin, Nancy B.; Riedel, Eric; Tustin, R. Don; Taylor, Joan; Murray, Jennifer B.; Douglas, Steven D.

doi:10.1128/cvi.00259-09

Cited by 38 publications

(34 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These findings are generally consistent with our earlier observations (3). In an earlier study, we did not see an increase in IL-10 production in cultures treated with anti-PD-1 antibodies.…”

Section: Discussionsupporting

confidence: 93%

Programmed Death 1 Receptor ChangesEx Vivoin HIV-Infected Adults following Initiation of Highly Active Antiretroviral Therapy

Spitsin

Tustin

Riedel

et al. 2012

Clin. Vaccine Immunol.

View full text Add to dashboard Cite

ABSTRACTThis study investigates the short-term effects of highly active antiretroviral therapy (HAART) on programmed death 1 receptor (PD-1) expression and lymphocyte function. We compared lymphocytes from human immunodeficiency virus (HIV)-infected adults prior to the initiation of HAART with lymphocytes from the same subjects following 2 months of treatment. Short-term HAART resulted in a moderate increase in the expression of PD-1 on both CD4+and CD8+T cells; yet, there was still a significant reduction in viral load and recovery of CD4+T cells. After 2 months of HAART, lymphocytes from the subjects had a reduction in lymphoproliferative responses to phytohemagglutinin (PHA) and an increased response to theCandidarecall antigen and the HIV antigen p24 compared to pretreatment lymphocytes. PHA-stimulated peripheral blood mononuclear cells (PBMCs) from samples obtained 2 months after HAART produced higher levels of Th-1 cytokines (gamma interferon [IFN-γ] and tumor necrosis factor alpha[TNF-α]) than the levels observed for samples taken before treatment was initiated. There were no significant changes in the proinflammatory cytokine interleukin-2 (IL-2) or Th-2 cytokines (IL-4, IL-5, and IL-10) in the corresponding samples.Ex vivoPD-1 blockade significantly augmented PHA-induced lymphoproliferation as well as the levels of Th-1 cytokines and to a lesser extent the levels of Th-2 cytokines in PBMC cultures. The ability to downregulate PD-1 expression may be important in enhancing immune recovery in HIV infection.

show abstract

Section: Discussionsupporting

confidence: 93%

Programmed Death 1 Receptor ChangesEx Vivoin HIV-Infected Adults following Initiation of Highly Active Antiretroviral Therapy

Spitsin

Tustin

Riedel

et al. 2012

Clin. Vaccine Immunol.

View full text Add to dashboard Cite

show abstract

“…For both adult and neonatal specimens we observed small fractions of PD1+ Vδ2 T cells ex vivo The values for adults were lower than previously reported (34), probably due to our use of frozen specimens (35), different combination of fluorochromes and differences in instrumentation. For both groups PD1 expression peaked around 4–5 days after ZOL stimulation, reaching comparable proportions of positive cells, and declined between days 5 and 10 after activation (Figure 1C,D).…”

Section: Resultscontrasting

confidence: 74%

Prolonged PD1 Expression on Neonatal Vδ2 Lymphocytes Dampens Proinflammatory Responses: Role of Epigenetic Regulation

Hsu

Boudova

Mvula

et al. 2016

The Journal of Immunology

View full text Add to dashboard Cite

A successful pregnancy depends on the maintenance of tolerance at the fetal–maternal interface; strong inflammation in the placental bed is generally associated with adverse fetal outcomes. Among the mechanisms that foster tolerance and limit inflammation, the fetal immune system favors Th2 or regulatory responses over Th1 responses. The unintended consequence of this functional program is high susceptibility to infections. Human Vδ2 T cells mount innate-like responses to a broad range of microorganisms and are poised for Th1 responses before birth. In infants they likely play a key role in protection against pathogens by exerting early Th1 effector functions, improving function of other innate cells, and promoting Th1 polarization of adaptive responses. However, their propensity to release Th1 mediators may require careful regulation during fetal life to avoid exaggerated proinflammatory responses. We investigated molecules with the potential to act as a rheostat for fetal Vδ2 cells. Programmed death 1 (PD1) is a negative regulator of T cell responses and a determinant of tolerance, particularly at the fetal–maternal interface. Neonatal Vδ2 cells upregulate PD1 shortly after activation and, unlike their adult counterparts, express this molecule for at least 28 d. Engagement of PD1 by one of its ligands, PDL1, effectively dampens TCR-mediated responses (TNF-α production and degranulation) by neonatal Vδ2 cells and may thus help maintain their activity within safe limits. PD1 expression by neonatal Vδ2 cells is inversely associated with promoter DNA methylation. Prolonged PD1 expression may be part of a functional program to control Vδ2 cell inflammatory responses during fetal life.

show abstract

“…48 The authors showed that cryopreservation actually decreased the expression of both PD-1 and PD-L1 in peripheral blood cells. Using a similar approach with different antibodies, a study showed a higher expression of PD-1/PD-L1 in CD4/CD8 T lymphocytes from chronic lymphocytic leukemia patients when compared with age-matched controls.…”

Section: Strategies To Measure Pd-l1/pd-1 Expression Immunohistochemimentioning

confidence: 99%

Programmed Death Ligand-1 (PD-L1) Expression in the Programmed Death Receptor-1 (PD-1)/PD-L1 Blockade: A Key Player Against Various Cancers

Guan¹,

Lim

Mekhail³

et al. 2017

Archives of Pathology &Amp; Laboratory Medicine

View full text Add to dashboard Cite

Context.— Immune checkpoint pathways, including programmed death receptor-1/programmed death ligand-1 (PD-1/PD-L1) signaling pathway, which are important in mediating self-tolerance and controlling self-damage, can sometimes be manipulated by cancer cells to evade immune surveillance. Recent clinical trials further demonstrate the efficacy of PD-1/PD-L1–targeted therapy in various cancers and reveal a new era of cancer immunotherapy. Objective.— To review the mechanism of the PD-1/PD-L1 signaling pathway, the regulation of this pathway, PD-1/PD-L1 as a predictive and/or prognostic marker in various cancers, and strategies of measuring PD-L1 expression. Data Sources.— Representative medical literature regarding PD-L1 expression in various cancers, including the preliminary results of the Blue Proposal, which compares different immunohistochemical stains for PD-L1 reported in the recent American Association of Cancer Research (AACR) Annual Meeting (April 16–20, 2016). Conclusion.— Either PD-1/PD-L1–targeted therapy alone or in combination with other treatment modalities provides benefit for patients with advanced cancers. Because of the complexity of cancer immunity, we still do not have a reliable biomarker to predict the response of PD-1/PD-L1–targeted therapy. Future studies, including methods beyond immunohistochemical stains, are needed to develop reliable biomarker/biomarkers for pathology laboratories to aid in selecting patients who will benefit most from PD-1/PD-L1–targeted therapy.

show abstract

Cryopreservation Decreases Receptor PD-1 and Ligand PD-L1 Coinhibitory Expression on Peripheral Blood Mononuclear Cell-Derived T Cells and Monocytes

Cited by 38 publications

References 19 publications

Programmed Death 1 Receptor ChangesEx Vivoin HIV-Infected Adults following Initiation of Highly Active Antiretroviral Therapy

Programmed Death 1 Receptor ChangesEx Vivoin HIV-Infected Adults following Initiation of Highly Active Antiretroviral Therapy

Prolonged PD1 Expression on Neonatal Vδ2 Lymphocytes Dampens Proinflammatory Responses: Role of Epigenetic Regulation

Programmed Death Ligand-1 (PD-L1) Expression in the Programmed Death Receptor-1 (PD-1)/PD-L1 Blockade: A Key Player Against Various Cancers

Contact Info

Product

Resources

About