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201. Development of the Asia Pacific Lupus Collaboration cohort

Author

Kandane‐Rathnayake, Rangi, primary, Golder, Vera, additional, Louthrenoo, Worawit, additional, Luo, Shue‐Fen, additional, Jan Wu, Yeong‐Jian, additional, Li, Zhanguo, additional, An, Yuan, additional, Lateef, Aisha, additional, Sockalingam, Sargunan, additional, Navarra, Sandra V., additional, Zamora, Leonid, additional, Hamijoyo, Laniyati, additional, Katsumata, Yasuhiro, additional, Harigai, Masayoshi, additional, Chan, Madelynn, additional, O’Neill, Sean, additional, Goldblatt, Fiona, additional, Hao, Yanjie, additional, Zhang, Zhuoli, additional, Al‐Saleh, Jamal, additional, Khamashta, Munther, additional, Takeuchi, Tsutomu, additional, Tanaka, Yoshiya, additional, Bae, Sang‐Cheol, additional, Lau, Chak Sing, additional, Hoi, Alberta, additional, Nikpour, Mandana, additional, and Morand, Eric F., additional

Published
2018
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204. Formyl peptide receptor activation inhibits the expansion of effector T cells and synovial fibroblasts and attenuates joint injury in models of rheumatoid arthritis

Author

Odobasic, Dragana, primary, Jia, Yuan, additional, Kao, Wenping, additional, Fan, Huapeng, additional, Wei, Xuemin, additional, Gu, Ran, additional, Ngo, Devi, additional, Kitching, A. Richard, additional, Holdsworth, Stephen R., additional, Morand, Eric F., additional, and Yang, Yuan H., additional

Published
2018
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205. Macrophage migration inhibitory factor is required for NLRP3 inflammasome activation

Author

Lang, Tali, primary, Lee, Jacinta P. W., additional, Elgass, Kirstin, additional, Pinar, Anita A., additional, Tate, Michelle D., additional, Aitken, Elizabeth H., additional, Fan, Huapeng, additional, Creed, Sarah J., additional, Deen, Nadia S., additional, Traore, Daouda A. K., additional, Mueller, Ivo, additional, Stanisic, Danielle, additional, Baiwog, Francesca S., additional, Skene, Colin, additional, Wilce, Matthew C. J., additional, Mansell, Ashley, additional, Morand, Eric F., additional, and Harris, James, additional

Published
2018
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207. Author Correction: Endogenous Annexin-A1 Regulates Haematopoietic Stem Cell Mobilisation and Inflammatory Response Post Myocardial Infarction in Mice In Vivo

Author

Qin, Cheng Xue, primary, Finlayson, Siobhan B., additional, Al-Sharea, Annas, additional, Tate, Mitchel, additional, De Blasio, Miles J., additional, Deo, Minh, additional, Rosli, Sarah, additional, Prakoso, Darnel, additional, Thomas, Colleen J., additional, Kiriazis, Helen, additional, Gould, Eleanor, additional, Yang, Yuan H., additional, Morand, Eric F., additional, Perretti, Mauro, additional, Murphy, Andrew J., additional, Du, Xiao-Jun, additional, Gao, Xiao-Ming, additional, and Ritchie, Rebecca H., additional

Published
2018
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210. Medical student psychological distress and academic performance

Author

Dendle, Claire, primary, Baulch, Julie, additional, Pellicano, Rebecca, additional, Hay, Margaret, additional, Lichtwark, Irene, additional, Ayoub, Sally, additional, Clarke, David M., additional, Morand, Eric F., additional, Kumar, Arunaz, additional, Leech, Michelle, additional, and Horne, Kylie, additional

Published
2018
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211. Gilz-Activin A as a Novel Signaling Axis Orchestrating Mesenchymal Stem Cell and Th17 Cell Interplay

Author

Luz-Crawford, Patricia, primary, Espinosa-Carrasco, Gabriel, additional, Ipseiz, Natacha, additional, Contreras, Rafael, additional, Tejedor, Gautier, additional, Medina, Daniel A., additional, Vega-Letter, Ana-Maria, additional, Ngo, Devi, additional, Morand, Eric F., additional, Pène, Jérôme, additional, Hernandez, Javier, additional, Jorgensen, Christian, additional, and Djouad, Farida, additional

Published
2018
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214. Endogenous Annexin-A1 Regulates Haematopoietic Stem Cell Mobilisation and Inflammatory Response Post Myocardial Infarction in Mice In Vivo

Author

Qin, Cheng Xue, primary, Finlayson, Siobhan B., additional, Al-Sharea, Annas, additional, Tate, Mitchel, additional, De Blasio, Miles J., additional, Deo, Minh, additional, Rosli, Sarah, additional, Prakoso, Darnel, additional, Thomas, Colleen J., additional, Kiriazis, Helen, additional, Gould, Eleanor, additional, Yang, Yuan H., additional, Morand, Eric F., additional, Perretti, Mauro, additional, Murphy, Andrew J., additional, Du, Xiao-Jun, additional, Gao, Xiao-Ming, additional, and Ritchie, Rebecca H., additional

Published
2017
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224. Low-dose interleukin-2 treatment selectively modulates CD4+ T cell subsets in patients with systemic lupus erythematosus

Author

He, Jing, primary, Zhang, Xia, additional, Wei, Yunbo, additional, Sun, Xiaolin, additional, Chen, Yaping, additional, Deng, Jun, additional, Jin, Yuebo, additional, Gan, Yuzhou, additional, Hu, Xin, additional, Jia, Rulin, additional, Xu, Chuanhui, additional, Hou, Zhaohua, additional, Leong, Yew Ann, additional, Zhu, Lei, additional, Feng, Jinhong, additional, An, Yuan, additional, Jia, Yuan, additional, Li, Chun, additional, Liu, Xu, additional, Ye, Hua, additional, Ren, Limin, additional, Li, Ru, additional, Yao, Haihong, additional, Li, Yuhui, additional, Chen, Shi, additional, Zhang, Xuewu, additional, Su, Yin, additional, Guo, Jianping, additional, Shen, Nan, additional, Morand, Eric F, additional, Yu, Di, additional, and Li, Zhanguo, additional

Published
2016
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226. Macrophage migration inhibitory factor is essential for osteoclastogenic mechanisms in vitro and in vivo mouse model of arthritis

Author

Gu, Ran, Santos, Leilani L., Ngo, Devi, Fan, HuaPeng, Singh, Preetinder P., Fingerle-Rowson, Gunter, Bucala, Richard, Xu, Jiake, Quinn, Julian M. W., Morand, Eric F., Gu, Ran, Santos, Leilani L., Ngo, Devi, Fan, HuaPeng, Singh, Preetinder P., Fingerle-Rowson, Gunter, Bucala, Richard, Xu, Jiake, Quinn, Julian M. W., and Morand, Eric F.

Abstract

Macrophage migration inhibitory factor (MIF) enhances activation of leukocytes, endothelial cells and fibroblast-like synoviocytes (FLS), thereby contributing to the pathogenesis of rheumatoid arthritis (RA). A MIF promoter polymorphism in RA patients resulted in higher serum MIF concentration and worsens bone erosion; controversially current literature reported an inhibitory role of MIF in osteoclast formation. The controversial suggested that the prease role of MIF and its putative receptor CD74 in osteoclastogenesis and RA bone erosion, mediated by locally formed osteoclasts in response to receptor activator of NF-kappa B ligand (RANKL), is unclear. We reported that in an in vivo K/BxN serum transfer arthritis, reduced clinical and histological arthritis in MIF-/- and CD74(-/-) mice were accompanied by a virtual absence of osteoclasts at the synovium-bone interface and reduced osteoclast-related gene expression. Furthermore, in vitro osteoclast formation and osteoclast-related gene expression were significantly reduced in MIF-/- cells via decreasing RANKL-induced phosphorylation of NF-kappa B-p65 and ERK1/2. This was supported by a similar reduction of osteoclastogenesis observed in CD74(-/-) cells. Furthermore, a MIF blockade reduced RANKL-induced osteoclastogeriesis via deregulating RANKL-mediated NF-kappa B and NFATc1 transcription factor activation. These data indicate that MIF and CD74 facilitate RANKL-induced osteoclastogenesis, and suggest that MIF contributes directly to bone erosion, as well as inflammation, in RA. (C) 2014 Elsevier Ltd. All rights reserved.

Published
2015

228. Correction: Targeting DORIS Remission and LLDAS in SLE: A Review.

Author

Parra Sánchez, Agner R., van Vollenhoven, Ronald F., Morand, Eric F., Bruce, Ian N., Kandane-Rathnayake, Rangi, Weiss, Gudrun, Tummala, Raj, Al-Mossawi, Hussein, and Sorrentino, Alessandro

Subjects
*INVESTIGATIONAL drugs, *IMMUNOSUPPRESSIVE agents, *SYSTEMIC lupus erythematosus, *PHYSICIANS
Abstract

This correction notice addresses minor errors in the original article titled "Targeting DORIS Remission and LLDAS in SLE: A Review." The errors pertain to the definition of DORIS remission and the data presented in Tables 1 and 3. The corrected definition of DORIS remission includes achieving a clinical SLEDAI-2K = 0 and a Physician's Global Assessment (PGA) < 0.5, irrespective of serology, with the use of antimalarials, low-dose glucocorticoids, and/or stable doses of immunosuppressants. The updated data in Table 3 shows changes in the number and percentage of patients achieving DORIS remission in the placebo group, as well as updated odds ratios and p-values for the comparison between treatment groups. The original article has been corrected. [Extracted from the article]

Published
2024
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229. MIF receptor CD74 mediates alphavirus-induced arthritis and myositis

Author

Herrero, Lara J., Sheng, Kuo-Ching, Jian, Peng, Taylor, Adam, Her, Zhisheng, Herring, Belinda L., Chow, Angela, Leo, Yee-Sin, Hickey, Michael J., Morand, Eric F., Ng, Lisa F.P., Bucala, Richard, and Mahalingam, Suresh

Subjects
Male, Mice, Knockout, Arthritis, Infectious, Myositis, Alphavirus Infections, Histocompatibility Antigens Class II, Apoptosis, Severity of Illness Index, Article, Monocytes, Antigens, Differentiation, B-Lymphocyte, Mice, Inbred C57BL, Disease Models, Animal, Mice, Ross River virus, Animals, Cytokines, Humans, Female, Chemokines, Receptors, Immunologic, Chikungunya virus, Cells, Cultured
Abstract

Arthrogenic alphaviruses such as Ross River virus (RRV) and chikungunya virus (CHIKV) circulate worldwide. This virus class causes debilitating illnesses that are characterized by arthritis, arthralgia, and myalgia. In previous studies, we identified macrophage migration inhibitory factor (MIF) as a critical inflammatory factor in the pathogenesis of alphaviral diseases. The present study was undertaken to characterize the role of CD74, a cell surface receptor of MIF, in both RRV- and CHIKV-induced alphavirus arthritides.Mouse models of RRV and CHIKV infection were used to investigate the immunopathogenesis of arthritic alphavirus infection. The role of CD74 was assessed using histologic analysis, real-time polymerase chain reaction, flow cytometry, and plaque assay.In comparison to wild-type mice, CD74-/- mice developed only mild clinical features and had low levels of tissue damage. Leukocyte infiltration, characterized predominantly by inflammatory monocytes and natural killer cells, was substantially reduced in the infected tissue of CD74-/- mice, but production of proinflammatory cytokines and chemokines was not decreased. CD74 deficiency was associated with increased monocyte apoptosis, but had no effect on monocyte migratory capacity. Consistent with these findings, alphaviral infection resulted in a dose-dependent up-regulation of CD74 expression in human peripheral blood mononuclear cells, and serum MIF levels were significantly elevated in patients with RRV or CHIKV infection.CD74 appears to regulate immune responses to alphaviral infection through its effects on cellular recruitment and survival. These findings suggest that both MIF and CD74 play a critical role in mediating alphaviral disease, and blocking these factors with novel therapeutic agents could substantially ameliorate the pathologic manifestations.

Published
2013

230. Genetic contributions to lupus nephritis in a multi-ethnic cohort of systemic lupus erythematous patients.

Author

Lanata, Cristina M., Nititham, Joanne, Taylor, Kimberly E., Chung, Sharon A., Torgerson, Dara G., Seldin, Michael F., Pons-Estel, Bernardo A., Tusié-Luna, Teresa, Tsao, Betty P., Morand, Eric F., Alarcón-Riquelme, Marta E., and Criswell, Lindsey A.

Subjects
SYSTEMIC lupus erythematosus, HUMAN genetic variation, NEPHRITIS, ETIOLOGY of diseases, SINGLE nucleotide polymorphisms, GENETICS
Abstract

Objective: African Americans, East Asians, and Hispanics with systemic lupus erythematous (SLE) are more likely to develop lupus nephritis (LN) than are SLE patients of European descent. The etiology of this difference is not clear, and this study was undertaken to investigate how genetic variants might explain this effect. Methods: In this cross-sectional study, 1244 SLE patients from multiethnic case collections were genotyped for 817,810 single-nucleotide polymorphisms (SNPs) across the genome. Continental genetic ancestry was estimated utilizing the program ADMIXTURE. Gene-based testing and pathway analysis was performed within each ethnic group and meta-analyzed across ethnicities. We also performed candidate SNP association tests with SNPs previously established as risk alleles for SLE, LN, and chronic kidney disease (CKD). Association testing and logistic regression models were performed with LN as the outcome, adjusted for continental ancestries, sex, disease duration, and age. Results: We studied 255 North European, 263 South European, 238 Hispanic, 224 African American and 264 East Asian SLE patients, of whom 606 had LN (48.7%). In genome-wide gene-based and candidate SNP analyses, we found distinct genes, pathways and established risk SNPs associated with LN for each ethnic group. Gene-based analyses showed significant associations between variation in ZNF546 (p = 1.0E-06), TRIM15 (p = 1.0E-06), and TRIMI0 (p = 1.0E-06) and LN among South Europeans, and TTC34 (p = 8.0E-06) was significantly associated with LN among Hispanics. The SNP rs8091180 in NFATC1 was associated with LN (OR 1.43, p = 3.3E-04) in the candidate SNP meta-analysis with the highest OR among African-Americans (OR 2.17, p = 0.0035). Conclusion: Distinct genetic factors are associated with the risk of LN in SLE patients of different ethnicities. CKD risk alleles may play a role in the development of LN in addition to SLE-associated risk variants. These findings may further explain the clinical heterogeneity of LN risk and response to therapy observed between different ethnic groups. [ABSTRACT FROM AUTHOR]

Published
2018
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231. Macrophage migration inhibitory factor is required for NLRP3 inflammasome activation.

Author

Lee, Jacinta P. W., Fan, Huapeng, Deen, Nadia S., Morand, Eric F., Harris, James, Tali Lang, Pinar, Anita A., Mueller, Ivo, Stanisic, Danielle, Baiwog, Francesca S., Skene, Colin, Elgass, Kirstin, Creed, Sarah J., Tate, Michelle D., Mansell, Ashley, Aitken, Elizabeth H., Wilce, Matthew C. J., and Traore, Daouda A. K.

Subjects
MACROPHAGE migration inhibitory factor, CELLS, IMMUNE system, CYTOKINES, VIMENTIN
Abstract

Macrophage migration inhibitory factor (MIF) exerts multiple effects on immune cells, as well as having functions outside the immune system. MIF can promote inflammation through the induction of other cytokines, including TNF, IL-6, and IL-1 family cytokines. Here, we show that inhibition of MIF regulates the release of IL-1α, IL-1β, and IL-18, not by affecting transcription or translation of these cytokines, but via activation of the NLRP3 inflammasome. MIF is required for the interaction between NLRP3 and the intermediate filament protein vimentin, which is critical for NLRP3 activation. Further, we demonstrate that MIF interacts with NLRP3, indicating a role for MIF in inflammasome activation independent of its role as a cytokine. These data advance our understanding of how MIF regulates inflammation and identify it as a factor critical for NLRP3 inflammasome activation. [ABSTRACT FROM AUTHOR]

Published
2018
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232. Analysis of Serum Interleukin (IL)-iβ and IL-18 in Systemic Lupus Erythematosus.

Author

Mende, Rachel, Vincent, Fabien B., Kandane-Rathnayake, Rangi, Koelmeyer, Rachel, Lin, Emily, Janet Chang, Hoi, Alberta Y., Morand, Eric F., Harris, James, and Tali Lang

Subjects
SYSTEMIC lupus erythematosus, INTERLEUKIN-1, INTERLEUKIN-18
Abstract

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disease characterized by biological and clinical heterogeneity. The interleukin (IL)-1 superfamily is a group of innate cytokines that contribute to pathogenesis in many autoimmune diseases. IL-1β and IL-18 are two members that have been shown to play a role in murine lupus-like models, but their role in human SLE remains poorly understood. Here, IL-1β and IL-18 were quantified by enzyme-linked immunosorbent assay in the serum of healthy controls (HCs) and SLE patients from a prospectively followed cohort. Disease activity and organ damage were assessed using SLE disease activity index 2000 (SLEDAI-2K) and SLE damage index scores (SDI), respectively. 184 SLE patients (mean age 44.9 years, 91% female, 56% double-stranded deoxyribonucleic acid positive) were compared to 52 HC. SLE patients had median [IQR] SLEDAI-2K of 4 [2,6], and SDI of 1 [0-2]. Serum IL-18 levels were statistically significantly higher in SLE patients compared to HCs. Univariable linear regression analyses showed that patients with active renal disease or irreversible organ damage had statistically significantly elevated serum IL-18 levels. The association between serum IL-18 and active renal disease was confirmed in multivariable analysis after adjusting for ethnicity and organ damage. High baseline serum IL-18 levels were associated with organ damage at the subsequent visit. Serum IL-1β levels were not significantly elevated in SLE patients when compared to HCs and had no association with overall or organ-specific disease activity or organ damage in cross-sectional and longitudinal analyses. Our data suggest that serum IL-18 and IL-1β have different clinical implications in SLE, with IL-18 being potentially associated with active renal disease. [ABSTRACT FROM AUTHOR]

Published
2018
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233. Lupus Low Disease Activity State (LLDAS) attainment discriminates responders in a systemic lupus erythematosus trial: analysis of the Phase IIb MUSE trial of anifrolumab.

Author

Morand, Eric F., Trasieva, Teodora, Berglind, Anna, Illei, Gabor G., and Tummala, Raj

Subjects
THERAPEUTIC use of monoclonal antibodies, IMMUNOSUPPRESSIVE agents, PREDNISOLONE, COMPARATIVE studies, RESEARCH methodology, MEDICAL cooperation, RESEARCH, STATISTICAL sampling, SYSTEMIC lupus erythematosus, EVALUATION research, RANDOMIZED controlled trials, TREATMENT effectiveness, SEVERITY of illness index, THERAPEUTICS
Abstract

Objectives: In a post-hoc analysis, we aimed to validate the Lupus Low Disease Activity State (LLDAS) definition as an endpoint in an systemic lupus erythematosus (SLE) Phase IIb randomised controlled trial (RCT) (MUSE [NCT01438489]) and then utilize LLDAS to discriminate between anifrolumab and placebo.Methods: Patients received intravenous placebo (n=102) or anifrolumab (300 mg, n=99; 1,000 mg, n=104) Q4W plus standard of care for 48 weeks. LLDAS attainment (SLE Disease Activity Index 2000 ≤4 without major organ activity, no new disease activity, Physician's Global Assessment ≤1, prednisolone ≤7.5 mg/d and standard immunosuppressant dosage tolerance) was assessed. Associations with endpoints and LLDAS attainment differences between treatments were explored.Results: LLDAS attainment at Week 52 was associated with SLE Responder Index 4 (SRI[4]) and British Isles Lupus Assessment Group-based Composite Lupus Assessment (BICLA) (74/85[87%] and 62/84[74%] were also SRI[4] and BICLA responders, respectively; both nominal p<0.001). Only 74/159 (47%) of SRI(4) and 62/121 (51%) of BICLA responders reached LLDAS.Anifrolumab-treated patients achieved earlier LLDAS, and more spent at least half their observed time in LLDAS (OR vs. placebo; 300 mg: 3.04, 95% CI 1.34 to 6.92, nominal p=0.008; 1,000 mg: 2.17, 95% CI 0.93 to 5.03, nominal p=0.072) vs placebo-treated patients. At Week 52, 17/102 (17%), 39/99 (39%) and 29/104 (28%) of patients on placebo, anifrolumab 300 and 1,000 mg, respectively, attained LLDAS (OR vs. placebo; 300 mg: 3.41, 95% CI 1.73 to 6.76, p<0.001; 1,000 mg: 2.03, 95% CI 1.01 to 4.07, nominal p=0.046).Conclusions: LLDAS attainment represents a clinically meaningful SLE outcome measure, and anifrolumab is associated with more patients who met LLDAS criteria versus placebo. These data support LLDAS as an SLE RCT endpoint.Trial Registration Number: NCT1438489; Post-results. [ABSTRACT FROM AUTHOR]

Published
2018
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234. Easy-BILAG: as easy as ABC?

Author

Connelly, Kathryn and Morand, Eric F

Subjects
*SYSTEMIC lupus erythematosus diagnosis, *RELIABILITY (Personality trait), *DISEASE progression, *RESEARCH methodology evaluation, *MULTITRAIT multimethod techniques
Abstract

The authors discuss a study by L. M. Carter and colleagues, published in the issue which describe the development and initial accuracy and usability testing of Easy-BILAG, a more streamlined version of the BILAG-2004, which is regarded as the most comprehensive disease activity index used in systemic lupus erythematosus (SLE). They discuss the changes made to BILAG-2004 and issues on the update of the instrument

Published
2022
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235. Identification of NURR1 as a Mediator of MIF Signaling During Chronic Arthritis : Effects on Glucocorticoid-Induced MKP1

Author

Ralph, Jennifer A., Ahmed, Afsar U., Santos, Leilani L., Clark, Andrew R., McMorrow, Jason, Murphy, Evelyn P., and Morand, Eric F.

Subjects
Mice, Knockout, Dual Specificity Phosphatase 1, Response Elements, Arthritis, Experimental, Arthritis, Rheumatoid, Mice, Chronic Disease, Nuclear Receptor Subfamily 4, Group A, Member 2, NIH 3T3 Cells, Animals, Humans, RNA Interference, RNA, Small Interfering, Glucocorticoids, Macrophage Migration-Inhibitory Factors, Regular Articles, Signal Transduction
Abstract

Elucidation of factors regulating glucocorticoid (GC) sensitivity is required for the development of "steroid-sparing" therapies for chronic inflammatory diseases, including rheumatoid arthritis (RA). Accumulating evidence suggests that macrophage migration inhibitory factor (MIF) counterregulates the GC-induction of anti-inflammatory mediators, including mitogen-activated protein kinase phosphatase 1 (MKP1), a critical mitogen-activated protein kinase signaling inhibitor. This observation has yet to be extended to human disease; the molecular mechanisms remain unknown. We investigated NURR1, a GC-responsive transcription factor overexpressed in RA, as a MIF signaling target. We reveal abrogation by recombinant MIF (rMIF) of GC-induced MKP1 expression in RA fibroblast-like synoviocytes (FLS). rMIF enhanced NURR1 expression, artificial NBRE (orphan receptor DNA-binding site) reporter transactivation, and reversed GC-inhibition of NURR1. NURR1 expression was reduced during experimental arthritis in MIF-/- synovium, and silencing MIF reduced RA FLS NURR1 mRNA. Consistent with NBRE identification on the MKP1 gene, MKP1 mRNA was reduced in FLS that ectopically express NURR1, and silencing NURR1 enhanced MKP1 mRNA in RA FLS. rMIF enhanced NBRE binding on the MKP1 gene, and the absence of the NBRE prevented NURR1-repressive effects on basal and GC-induced MKP1 transactivation. This study defines NURR1 as a novel MIF target in chronic inflammation and demonstrates a role for NURR1 in regulating the anti-inflammatory mediator, MKP1. We propose a MIF-NURR1 signaling axis as a regulator of the GC sensitivity of MKP1.

Published
2010

236. Glucocorticoid-induced leucine zipper (GILZ) inhibits B cell activation in systemic lupus erythematosus

Author

Jones, Sarah A, primary, Toh, Andrew E J, additional, Odobasic, Dragana, additional, Oudin, Marie-Anne Virginie, additional, Cheng, Qiang, additional, Lee, Jacinta P W, additional, White, Stefan J, additional, Russ, Brendan E, additional, Infantino, Simona, additional, Light, Amanda, additional, Tarlinton, David M, additional, Harris, James, additional, and Morand, Eric F, additional

Published
2015
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239. Definition and initial validation of a Lupus Low Disease Activity State (LLDAS)

Author

Franklyn, Kate, primary, Lau, Chak Sing, additional, Navarra, Sandra V, additional, Louthrenoo, Worawit, additional, Lateef, Aisha, additional, Hamijoyo, Laniyati, additional, Wahono, C Singgih, additional, Chen, Shun Le, additional, Jin, Ou, additional, Morton, Susan, additional, Hoi, Alberta, additional, Huq, Molla, additional, Nikpour, Mandana, additional, and Morand, Eric F, additional

Published
2015
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242. The Role and Effects of Glucocorticoid-Induced Leucine Zipper in the Context of Inflammation Resolution

Author

Vago, Juliana P., primary, Tavares, Luciana P., additional, Garcia, Cristiana C., additional, Lima, Kátia M., additional, Perucci, Luiza O., additional, Vieira, Érica L., additional, Nogueira, Camila R. C., additional, Soriani, Frederico M., additional, Martins, Joilson O., additional, Silva, Patrícia M. R., additional, Gomes, Karina B., additional, Pinho, Vanessa, additional, Bruscoli, Stefano, additional, Riccardi, Carlo, additional, Beaulieu, Elaine, additional, Morand, Eric F., additional, Teixeira, Mauro M., additional, and Sousa, Lirlândia P., additional

Published
2015
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243. Manipulation of B-cell responses with histone deacetylase inhibitors

Author

Waibel, Michaela, primary, Christiansen, Ailsa J., additional, Hibbs, Margaret L., additional, Shortt, Jake, additional, Jones, Sarah A., additional, Simpson, Ian, additional, Light, Amanda, additional, O’Donnell, Kristy, additional, Morand, Eric F., additional, Tarlinton, David M., additional, Johnstone, Ricky W., additional, and Hawkins, Edwin D., additional

Published
2015
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247. Bcl-2 Antagonists Kill Plasmacytoid Dendritic Cells From Lupus-Prone Mice and Dampen Interferon-α Production

Author

Zhan, Yifan, primary, Carrington, Emma M., additional, Ko, Hyun-Ja, additional, Vikstrom, Ingela B., additional, Oon, Shereen, additional, Zhang, Jian-Guo, additional, Vremec, David, additional, Brady, Jamie L., additional, Bouillet, Philippe, additional, Wu, Li, additional, Huang, David C. S., additional, Wicks, Ian P., additional, Morand, Eric F., additional, Strasser, Andreas, additional, and Lew, Andrew M., additional

Published
2015
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249. Macrophage Migration Inhibitory Factor Inhibits the Antiinflammatory Effects of Glucocorticoids via Glucocorticoid-Induced Leucine Zipper

Author

Fan, Huapeng, Kao, Wenping, Yang, Yuan H., Gu, Ran, Harris, James, Fingerle-Rowson, Guenter, Bucala, Richard, Ngo, Devi, Beaulieu, Elaine, Morand, Eric F., Fan, Huapeng, Kao, Wenping, Yang, Yuan H., Gu, Ran, Harris, James, Fingerle-Rowson, Guenter, Bucala, Richard, Ngo, Devi, Beaulieu, Elaine, and Morand, Eric F.

Abstract

Objective. Glucocorticoids remain a mainstay in the treatment of rheumatoid arthritis (RA). Dose-dependent adverse effects highlight the need for therapies that regulate glucocorticoid sensitivity to enable dosage reduction. Macrophage migration inhibitory factor (MIF) is a proinflammatory protein that has been implicated in the pathogenesis of RA; it impairs glucocorticoid sensitivity via MAPK phosphatase 1 (MKP-1) inhibition. The intracellular protein glucocorticoid-induced leucine zipper (GILZ) mimics the effects of glucocorticoids in models of RA, but whether it represents a target for the modulation of glucocorticoid sensitivity remains unknown. We undertook this study to investigate whether GILZ is involved in the regulation of glucocorticoid sensitivity by MIF. Methods. GILZ expression was studied in the presence and absence of MIF, and the role of GILZ in the MIF-dependent regulation of the glucocorticoid sensitivity mediator MKP-1 was studied at the level of expression and function. Results. GILZ expression was significantly inhibited by endogenous MIF, both basally and during responses to glucocorticoid treatment. The effects of MIF on GILZ were dependent on the expression and Akt-induced nuclear translocation of the transcription factor FoxO3A. GILZ was shown to regulate the expression of MKP-1 and consequent MAPK phosphorylation and cytokine release. Conclusion. MIF exerts its effects on MKP-1 expression and MAPK activity through inhibitory effects on GILZ. These findings suggest a previously unsuspected interaction between MIF and GILZ and identify GILZ as a potential target for the therapeutic regulation of glucocorticoid sensitivity.

Published
2014

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