Diamond Ling
National Institutes of Health
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Featured researches published by Diamond Ling.
Cell Reports | 2012
Lai Wei; Baoying Liu; Jingsheng Tuo; Defen Shen; Ping Chen; Zhiyu Li; X. Liu; Jia Ni; Pradeep K. Dagur; H. Nida Sen; Shayma Jawad; Diamond Ling; Stanley Park; Sagarika Chakrabarty; Catherine B. Meyerle; Elvira Agrón; Frederick L. Ferris; Emily Y. Chew; J. Philip McCoy; Emily D. Blum; Peter J. Francis; Michael L. Klein; Robyn H. Guymer; Paul N. Baird; Chi-Chao Chan; Robert B. Nussenblatt
Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly population worldwide. Although recent studies have demonstrated strong genetic associations between AMD and SNPs in a number of genes, other modes of regulation are also likely to play a role in the etiology of this disease. We identified a significantly decreased level of methylation on the IL17RC promoter in AMD patients. Furthermore, we showed that hypomethylation of the IL17RC promoter in AMD patients led to an elevated expression of its protein and messenger RNA in peripheral blood as well as in the affected retina and choroid, suggesting that the DNA methylation pattern and expression of IL17RC may potentially serve as a biomarker for the diagnosis of AMD and likely plays a role in disease pathogenesis.
Journal of Immunology | 2015
Baoying Liu; Ashwin Dhanda; Sima Hirani; Emily L. Williams; H. Nida Sen; Fernando Martinez Estrada; Diamond Ling; Ian Thompson; Megan Casady; Zhiyu Li; Han Si; William Tucker; Lai Wei; Shayma Jawad; Amol Sura; Jennifer Dailey; Susan Hannes; Ping Chen; Jason L. Chien; Siamon Gordon; Richard W J Lee; Robert B. Nussenblatt
Human peripheral monocytes have been categorized into three subsets based on differential expression levels of CD14 and CD16. However, the factors that influence the distribution of monocyte subsets and the roles that each subset plays in autoimmunity are not well studied. In this study, we show that circulating monocytes from patients with autoimmune uveitis exhibit a skewed phenotype toward intermediate CD14++CD16+ cells, and that this is associated with glucocorticoid therapy. We further demonstrate that CD14++CD16+ monocytes from patients and healthy control donors share a similar cell-surface marker and gene expression profile. Comparison of the effects of intermediate CD14++CD16+ monocytes with classical CD14++CD16− and nonclassical CD14+CD16++ monocytes revealed that the intermediate CD14++CD16+ subset had an attenuated capacity to promote both naive CD4+ T cell proliferation and polarization into a Th1 phenotype, and memory CD4+ T cell proliferation and IL-17 expression. Furthermore, CD14++CD16+ cells inhibit CD4+ T cell proliferation induced by other monocyte subsets and enhance CD4+ T regulatory cell IL-10 expression. These data demonstrate the impact of glucocorticoids on monocyte phenotype in the context of autoimmune disease and the differential effects of monocyte subsets on effector T cell responses.
Investigative Ophthalmology & Visual Science | 2013
Shayma Jawad; Baoying Liu; Zhiyu Li; Robert Katamay; M.M. Campos; Lai Wei; H. Nida Sen; Diamond Ling; Fernando Martinez Estrada; Chi-Chao Chan; Robert N. Fariss; Siamon Gordon; Robert B. Nussenblatt
PURPOSE Laser-induced choroidal neovascularization (CNV) is a widely used model to mimic many features of CNV resulting from wet AMD. Macrophages have been implicated in the pathogenesis of AMD. Class A scavenger receptors, scavenger receptor-A (SR-A) and macrophage receptor with collagenous domain (MARCO), are expressed on macrophages and are associated with macrophage function. The goal of this study is to examine the role of macrophage scavenger receptors in immune cell recruitment and the formation of CNV. METHODS Laser photocoagulation was performed in wild-type and knockout mice with deletion of SR-A (SR-A(-/-)), MARCO (MARCO(-/-)), or both SR-A and MARCO double knockout (DKO). Immune cell recruitment at different time points and CNV lesions at 14 days after laser treatment were evaluated through immunostaining and confocal microscopy. Microarray analysis was performed in eyes 1 day after laser injury. RESULTS Wild-type eyes showed higher chemokine/receptor expression compared with knockout eyes after laser injury. Scavenger receptor deficiency markedly impaired the recruitment of neutrophils and macrophages to CNV lesions at 1- and 3-days post laser injury, respectively. Significantly reduced CNV volumes were found in the eyes from scavenger receptor knockout mice compared with wild-type mice. CONCLUSIONS The deficiency of scavenger receptors impairs the formation of CNV and immune cell recruitment. Our findings suggest a potential role for scavenger receptors in contributing to CNV formation and inflammation in AMD.
British Journal of Ophthalmology | 2013
Diamond Ling; Baoying Liu; Shayma Jawad; Ian A. Thompson; Chandrasekharam N. Nagineni; Jennifer Dailey; Jason L. Chien; Benjamin Sredni; Robert B. Nussenblatt
Purpose AS101 is a non-toxic organotellurium-IV compound with demonstrated immunomodulating activity in vitro and in vivo. Inflammatory responses are attributed to the pathophysiology of numerous ocular diseases. In this study, we wished to elucidate whether AS101 could mitigate pro-inflammatory activity in human retinal pigment epithelial (RPE) cells, which are heavily involved in ocular immune responses, induced by pro-inflammatory IL-β activity. Methods Primary and transformed RPE cells treated with varying concentrations of AS101 were used in this study. Real-time PCR and ELISA assays were used to detect cytokine/chemokine mRNA expression and protein production. Western blot was used to detect changes in the NFκB pathway. Cell viability and proliferation were detected using a Vi-Cell XR cell counter. To measure the cytoprotective capacity of AS101, cell numbers were compared between cells treated with IL-1β or lipopolysaccharide (LPS) and cells treated with IL-1β or LPS in the presence of AS101. Results AS101 inhibited IL-1β-induced mRNA expression and protein production of IL-6 and IL-8 in RPE cells. The viability of RPE cells treated with IL-1β and LPS was unaffected. AS101 slightly inhibited RPE cell growth in the presence of higher levels of IL-1β. Also, AS101 downregulated the IL-1β activity by inhibiting the phosphorylation of p65, an NFκB subunit. Conclusions The results demonstrate that AS101 reduces IL-1β-induced inflammatory responses in the RPE. In previous studies, AS101 exhibited therapeutic effects in various disease models and was a safe profile in clinical trials. These results suggest that AS101 may have potent anti-inflammatory potential in the eye and confer the downregulation of RPE inflammatory responses in a pathological environment.
British Journal of Ophthalmology | 2011
Mengjun Hu; Baoying Liu; Shayma Jawad; Diamond Ling; Megan Casady; Lai Wei; Robert B. Nussenblatt
Investigative Ophthalmology & Visual Science | 2015
Susan Hannes; Baoying Liu; Zhiyu Li; Diamond Ling; H. Nida Sen; Robert B. Nussenblatt
Investigative Ophthalmology & Visual Science | 2012
Diamond Ling; Baoying Liu; Hatice Nida Sen; Megan Casady; Zhiyu Li; Lai Wei; Shayma Jawad; Robert B. Nussenblatt
Investigative Ophthalmology & Visual Science | 2012
Baoying Liu; H. Nida Sen; Diamond Ling; Megan Casady; Shayma Jawad; Zhiyu Li; Lai Wei; Robert B. Nussenblatt
Investigative Ophthalmology & Visual Science | 2011
Zhiyu Li; Baoying Liu; Robert Katamay; Stephan R. Thurau; Gerhild Wildner; Diamond Ling; Lai Wei; Chi-Chao Chan; Robert B. Nussenblatt
Investigative Ophthalmology & Visual Science | 2011
Baoying Liu; Diamond Ling; H. Nida Sen; Silu Lucy Tan; Zhiyu Li; Lai Wei; Robert B. Nussenblatt