Jeak Ling Ding

National University of Singapore

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Bow Ho

National University of Singapore

Bow Ho

National University of Singapore

Nguan Soon Tan

Nanyang Technological University

Naxin Jiang

National University of Singapore

Zhiwei Ang

Children's Hospital of Philadelphia

Shu‐Chun Chang

Taipei Medical University

Thorsten Wohland

National University of Singapore

Jun Zhi Er

National University of Singapore

Patricia Miang Lon Ng

Singapore Immunology Network

Vladimı́r Frecer

International Centre for Applied Research and Sustainable Technology

Cooperative Institutions

National University of Singapore

173

Agency for Science, Technology and Research

Nanyang Technological University

Singapore Immunology Network

National University Health System

Institute of Molecular and Cell Biology

National University Hospital

Massachusetts Institute of Technology

Chinese Academy of Sciences

Taipei Medical University

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Macrophages protect mycoplasma‐infected chronic myeloid leukemia cells from natural killer cell killing

Immunology and Cell Biology (2019)

Qing Wei Winnie Choo Ricky Abdi Gunawan Koean Shu‐Chun Chang Wee Joo Chng Ming Chun Chan

Macrophages (Mϕ) have been reported to downmodulate the cytotoxicity of natural killer (NK) cell against solid tumor cells. However, the collaborative role between NK cells and Mϕ remains underappreciated, especially in hematological cancers, such as chronic myeloid leukemia (CML). We observed a higher ratio of innate immune cells (Mϕ and NK) to adaptive immune cells (T and B cells) in CML bone marrow aspirates, prompting us to investigate the roles of NK and Mϕ in CML. Using coculture models simulating the tumor inflammatory environment, we observed that Mϕ protects CML from NK attack only when CML was itself mycoplasma-infected and under chronic infection-inflammation condition. We found that the Mϕ-protective effect on CML was associated with the maintenance of CD16 level on the NK cell membrane. Although the NK membrane CD16 (mCD16) was actively shed in Mϕ + NK + CML trioculture, the NK mCD16 level was maintained, and this was independent of the modulation of sheddase by tissue inhibitor of metalloproteinase 1 or inhibitory cytokine transforming growth factor beta. Instead, we found that this process of NK mCD16 maintenance was conferred by Mϕ in a contact-dependent manner. We propose a new perspective on anti-CML strategy through abrogating Mϕ-mediated retention of NK surface CD16.

10.1111/imcb.12309

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Citations (7)

Biotechnology Letters (1997)

Roopashree S. Dwarakanath Bow Ho Jeak Ling Ding

10.1023/a:1018307118879

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Citations (14)

SARM modulates MyD88-mediated TLR activation through BB-loop dependent TIR-TIR interactions

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (2015)

Emil Carlsson Jeak Ling Ding Bernadette Byrne

TRIF

HEK 293 cells

10.1016/j.bbamcr.2015.11.021

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Citations (53)

TLR Cross-talk Confers Specificity to Innate Immunity

International Reviews of Immunology (2014)

Rebecca Suet Ting Tan Bow Ho Bernard P. Leung Jeak Ling Ding

Cross-talk within the innate immune pathways is highly complex and contains many unknowns. Here, we discuss the different combinations of PAMPs, together with the sequence, order, and dosage of consecutive PAMP challenges, which determine the nature of the immune response by macrophages. The engagement of different Toll-like receptor (TLR) ligands leads to quantitatively and qualitatively unique cytokine production, showing that TLR pathway crosstalk enables the innate immune system to orchestrate immediate local and global responses. It is likely that multiple pathways are involved in the regulation of cytokine synergy, including many that have yet to be discovered.

Crosstalk

Innate lymphoid cell

10.3109/08830185.2014.921164

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Structure and Magnetic Properties of Melt-Spun Nd33(FexAl)67 Alloys

Journal of Metastable and Nanocrystalline Materials (2001)

Lina Si Jeak Ling Ding Yuan Yuan Li X.Z. Wang

10.4028/www.scientific.net/jmnm.10.553

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Lipid-free apolipoprotein A-I exerts an antioxidative role against cell-free hemoglobin.

PubMed (2012)

Ruijuan Du Imelda Winarsih Bow Ho Jeak Ling Ding

Cell-free hemoglobin (Hb) resulting from hemolysis is redox-active. It disrupts the oxidoreducing microenvironment, shifting the balance unfavorably towards tissue cytotoxicity. Thus, immediate suppression of the Hb-redox activity and removal of the cell-free plasma Hb is vital for maintaining homeostasis and survival. Among several known Hb-binding plasma proteins, haptoglobin (Hp) is the primary antioxidant of Hb. However, Hb-mediated oxidative stress persists in the covalently bound Hb-Hp aggregates or when Hp is depleted during a severe hemolysis. We therefore inquired whether there is an alternative anti-oxidative defense tactic in the blood. Here, we identified an Hb-interactome in the plasma, constituting Hb, Hp and lipid-free apolipoprotein A-I (apoAI). We found that apoAI acts rapidly as a secondary antioxidant to interact with Hb and quench the Hb-redox activity. We showed that apoAI either acts independently or collaborates with Hp to downregulate Hb-redox activity. Following the association between apoAI and Hb, the apoAI facilitates the uptake of Hb by interacting with a scavenger receptor class B type 1 (SR-BI) displayed on macrophages and hepatocytes. Our findings suggest that apoAI mediates an efficient pathway for the elimination of cytotoxic Hb redox activity.

Scavenger Receptor

Haptoglobin

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An antimicrobial factor from the plasma of the horseshoe crab, Carcinoscorpius rotundicauda

Elements (2021)

Jeak Ling Ding Derek Sa Yeo Bow Ho

Horseshoe crab

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Citations (1)