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Article ; Online: The Pathogenesis, Molecular Mechanisms, and Therapeutic Potential of the Interferon Pathway in Systemic Lupus Erythematosus and Other Autoimmune Diseases.

Ramaswamy, Madhu / Tummala, Raj / Streicher, Katie / Nogueira da Costa, Andre / Brohawn, Philip Z

International journal of molecular sciences

2021 Volume 22, Issue 20

Abstract: Therapeutic success in treating patients with systemic lupus erythematosus (SLE) is limited by the multivariate disease etiology, multi-organ presentation, systemic involvement, and complex immunopathogenesis. Agents targeting B-cell differentiation and ... ...

Abstract	Therapeutic success in treating patients with systemic lupus erythematosus (SLE) is limited by the multivariate disease etiology, multi-organ presentation, systemic involvement, and complex immunopathogenesis. Agents targeting B-cell differentiation and survival are not efficacious for all patients, indicating a need to target other inflammatory mediators. One such target is the type I interferon pathway. Type I interferons upregulate interferon gene signatures and mediate critical antiviral responses. Dysregulated type I interferon signaling is detectable in many patients with SLE and other autoimmune diseases, and the extent of this dysregulation is associated with disease severity, making type I interferons therapeutically tangible targets. The recent approval of the type I interferon-blocking antibody, anifrolumab, by the US Food and Drug Administration for the treatment of patients with SLE demonstrates the value of targeting this pathway. Nevertheless, the interferon pathway has pleiotropic biology, with multiple cellular targets and signaling components that are incompletely understood. Deconvoluting the complexity of the type I interferon pathway and its intersection with lupus disease pathology will be valuable for further development of targeted SLE therapeutics. This review summarizes the immune mediators of the interferon pathway, its association with disease pathogenesis, and therapeutic modalities targeting the dysregulated interferon pathway.
MeSH term(s)	Animals ; Antiviral Agents/pharmacology ; Autoimmune Diseases/drug therapy ; Autoimmune Diseases/pathology ; Humans ; Immunity, Innate/drug effects ; Interferon Type I/pharmacology ; Lupus Erythematosus, Systemic/drug therapy ; Lupus Erythematosus, Systemic/pathology ; Signal Transduction
Chemical Substances	Antiviral Agents ; Interferon Type I
Language	English
Publishing date	2021-10-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms222011286
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Article ; Online: Type I interferon blockade with anifrolumab in patients with systemic lupus erythematosus modulates key immunopathological pathways in a gene expression and proteomic analysis of two phase 3 trials.

Baker, Tina / Sharifian, Hoda / Newcombe, Paul J / Gavin, Patrick G / Lazarus, Mark N / Ramaswamy, Madhu / White, Wendy I / Ferrari, Nicola / Muthas, Daniel / Tummala, Raj / Morand, Eric F / Furie, Richard / Vital, Edward M / Chamberlain, Chris / Platt, Adam / Al-Mossawi, Hussein / Brohawn, Philip Z / Csomor, Eszter

Annals of the rheumatic diseases

2024

Abstract: Introduction: Anifrolumab is a type I interferon (IFN) receptor 1 (IFNAR1) blocking antibody approved for treating patients with systemic lupus erythematosus (SLE). Here, we investigated the immunomodulatory mechanisms of anifrolumab using longitudinal ... ...

Abstract	Introduction: Anifrolumab is a type I interferon (IFN) receptor 1 (IFNAR1) blocking antibody approved for treating patients with systemic lupus erythematosus (SLE). Here, we investigated the immunomodulatory mechanisms of anifrolumab using longitudinal transcriptomic and proteomic analyses of the 52-week, randomised, phase 3 TULIP-1 and TULIP-2 trials. Methods: Patients with moderate to severe SLE were enrolled in TULIP-1 and TULIP-2 and received intravenous anifrolumab or placebo alongside standard therapy. Whole-blood expression of 18 017 genes using genome-wide RNA sequencing (RNA-seq) (pooled TULIP; anifrolumab, n=244; placebo, n=258) and 184 plasma proteins using Olink and Simoa panels (TULIP-1; anifrolumab, n=124; placebo, n=132) were analysed. We compared treatment groups via gene set enrichment analysis using MetaBase pathway analysis, blood transcriptome modules, in silico deconvolution of RNA-seq and longitudinal linear mixed effect models for gene counts and protein levels. Results: Compared with placebo, anifrolumab modulated >2000 genes by week 24, with overlapping results at week 52 and 41 proteins by week 52. IFNAR1 blockade with anifrolumab downregulated multiple type I and II IFN-induced gene modules/pathways and type III IFN-λ protein levels, and impacted apoptosis-associated and neutrophil extracellular trap-associated transcriptional pathways, innate cell activating chemokines and receptors, proinflammatory cytokines and B-cell activating cytokines. In silico deconvolution of RNA-seq data indicated an increase from baseline of mucosal-associated invariant and γδT cells and a decrease of monocytes following anifrolumab treatment. Discussion: Type I IFN blockade with anifrolumab modulated multiple inflammatory pathways downstream of type I IFN signalling, including apoptotic, innate and adaptive mechanisms that play key roles in SLE immunopathogenesis.
Language	English
Publishing date	2024-04-03
Publishing country	England
Document type	Journal Article
ZDB-ID	7090-7
ISSN	1468-2060 ; 0003-4967
ISSN (online)	1468-2060
ISSN	0003-4967
DOI	10.1136/ard-2023-225445
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Article ; Online: The Pathogenesis, Molecular Mechanisms, and Therapeutic Potential of the Interferon Pathway in Systemic Lupus Erythematosus and Other Autoimmune Diseases

Madhu Ramaswamy / Raj Tummala / Katie Streicher / Andre Nogueira da Costa / Philip Z. Brohawn

International Journal of Molecular Sciences, Vol 22, Iss 11286, p

2021 Volume 11286

Abstract	Therapeutic success in treating patients with systemic lupus erythematosus (SLE) is limited by the multivariate disease etiology, multi-organ presentation, systemic involvement, and complex immunopathogenesis. Agents targeting B-cell differentiation and survival are not efficacious for all patients, indicating a need to target other inflammatory mediators. One such target is the type I interferon pathway. Type I interferons upregulate interferon gene signatures and mediate critical antiviral responses. Dysregulated type I interferon signaling is detectable in many patients with SLE and other autoimmune diseases, and the extent of this dysregulation is associated with disease severity, making type I interferons therapeutically tangible targets. The recent approval of the type I interferon-blocking antibody, anifrolumab, by the US Food and Drug Administration for the treatment of patients with SLE demonstrates the value of targeting this pathway. Nevertheless, the interferon pathway has pleiotropic biology, with multiple cellular targets and signaling components that are incompletely understood. Deconvoluting the complexity of the type I interferon pathway and its intersection with lupus disease pathology will be valuable for further development of targeted SLE therapeutics. This review summarizes the immune mediators of the interferon pathway, its association with disease pathogenesis, and therapeutic modalities targeting the dysregulated interferon pathway.
Keywords	interferon ; systemic lupus erythematosus ; autoimmunity ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2021-10-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Autoimmunity: twenty years in the Fas lane.

Ramaswamy, Madhu / Siegel, Richard M

Journal of immunology (Baltimore, Md. : 1950)

2012 Volume 189, Issue 11, Page(s) 5097–5100

MeSH term(s)	Animals ; Lupus Erythematosus, Systemic/history ; Lymphatic Diseases/history ; Lymphoproliferative Disorders/history ; fas Receptor/history
Chemical Substances	Fas protein, mouse ; fas Receptor
Language	English
Publishing date	2012-11-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Comment
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1202833
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Article ; Online: Determination of apoptosis sensitivity in specific T cell subsets from human peripheral blood by utilizing a multiparameter fluorescence-activated cell sorting-based technique.

Lo, Bernice / Ramaswamy, Madhu

Methods in molecular biology (Clifton, N.J.)

2013 Volume 979, Page(s) 33–41

Abstract: Among the different techniques available for determining physiological cell death or apoptosis in immune cells, fluorescence-activated cell sorting-based approaches prove to be one of the most efficient and quantitative assays in capturing cells that are ...

Abstract	Among the different techniques available for determining physiological cell death or apoptosis in immune cells, fluorescence-activated cell sorting-based approaches prove to be one of the most efficient and quantitative assays in capturing cells that are actively undergoing apoptosis elicited by either extrinsic or intrinsic forms of cell death. The key advantage of the technique is to allow the user to determine apoptotic responses of multiple immune cell types or subsets of the same lineage of immune cells without the prior requirement for cell separation. Here, we describe a "multiparameter" flow method to rapidly determine apoptosis-sensitivity induced by the Fas receptor pathway within different CD4 T cell subsets in a mixed pool of analyzed ex vivo peripheral blood mononuclear cells.
MeSH term(s)	Apoptosis ; CD4-Positive T-Lymphocytes/cytology ; CD4-Positive T-Lymphocytes/metabolism ; Ficoll/chemistry ; Flow Cytometry/methods ; Humans ; T-Lymphocyte Subsets/cytology ; T-Lymphocyte Subsets/metabolism ; fas Receptor/metabolism
Chemical Substances	fas Receptor ; Ficoll (25702-74-3)
Language	English
Publishing date	2013
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-62703-290-2_4
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Article ; Online: Immunomodulation of T- and NK-cell Responses by a Bispecific Antibody Targeting CD28 Homolog and PD-L1.

Ramaswamy, Madhu / Kim, Taeil / Jones, Des C / Ghadially, Hormas / Mahmoud, Tamer I / Garcia, Andrew / Browne, Gareth / Zenonos, Zenon / Puplampu-Dove, Yvonne / Riggs, Jeffrey M / Bhat, Geetha K / Herbst, Ronald / Schofield, Darren J / Carlesso, Gianluca

Cancer immunology research

2021 Volume 10, Issue 2, Page(s) 200–214

Abstract: Checkpoint blockade therapies targeting PD-1/PD-L1 and CTLA-4 are clinically successful but also evoke adverse events due to systemic T-cell activation. We engineered a bispecific, mAb targeting CD28 homolog (CD28H), a newly identified B7 family receptor ...

Abstract	Checkpoint blockade therapies targeting PD-1/PD-L1 and CTLA-4 are clinically successful but also evoke adverse events due to systemic T-cell activation. We engineered a bispecific, mAb targeting CD28 homolog (CD28H), a newly identified B7 family receptor that is constitutively expressed on T and natural killer (NK) cells, with a PD-L1 antibody to potentiate tumor-specific immune responses. The bispecific antibody led to T-cell costimulation, induced NK-cell cytotoxicity of PD-L1-expressing tumor cells, and activated tissue-resident memory CD8
MeSH term(s)	Antibodies, Bispecific/metabolism ; B7-H1 Antigen/metabolism ; CD28 Antigens/metabolism ; CD8-Positive T-Lymphocytes ; Cell Line, Tumor ; Humans ; Immunotherapy ; Killer Cells, Natural ; Lymphocyte Activation ; Neoplasms/metabolism ; Programmed Cell Death 1 Receptor/metabolism
Chemical Substances	Antibodies, Bispecific ; B7-H1 Antigen ; CD28 Antigens ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2021-12-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-21-0218
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Article: A FAScinating receptor in self-tolerance.

Ramaswamy, Madhu / Siegel, Richard M

Immunity

2007 Volume 26, Issue 5, Page(s) 545–547

Abstract: In this issue of Immunity,Stranges et al. (2007) ablate expression of the death receptor Fas in T cells, B cells, and DC. Fas deficiency in any of these lineages is sufficient to break self-tolerance. ...

Abstract	In this issue of Immunity,Stranges et al. (2007) ablate expression of the death receptor Fas in T cells, B cells, and DC. Fas deficiency in any of these lineages is sufficient to break self-tolerance.
MeSH term(s)	Animals ; Antigen Presentation/immunology ; Cell Death ; Humans ; Self Tolerance/immunology ; fas Receptor/immunology
Chemical Substances	fas Receptor
Language	English
Publishing date	2007-05
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2007.05.004
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Article ; Online: Extracellular flux analysis to monitor glycolytic rates and mitochondrial oxygen consumption.

Pelletier, Martin / Billingham, Leah K / Ramaswamy, Madhu / Siegel, Richard M

Methods in enzymology

2014 Volume 542, Page(s) 125–149

Abstract: Evidence accumulating over the past decade has linked alterations in bioenergetic metabolism to the pathogenesis of several diseases, including inflammatory conditions and cancer. However, the mutual relationship between the effector functions and the ... ...

Abstract	Evidence accumulating over the past decade has linked alterations in bioenergetic metabolism to the pathogenesis of several diseases, including inflammatory conditions and cancer. However, the mutual relationship between the effector functions and the metabolism of immune cells has begun to emerge only recently. Similar to malignant cells, both innate and adaptive immune cells undergo a metabolic reprogramming that is required for effector functions, de facto underlying the elicitation of a robust immune response. These changes allow immune cells not only to rapidly respond to pathogens or (pre)malignant cells but also to adapt to changing microenvironmental conditions. Targeting the metabolic alterations of malignant cells has been the subject of an intense wave of investigation, resulting in the identification of promising therapeutic strategies. Since the inflammatory milieu and the tumor microenvironment are similar, the metabolism of immune cells and its regulation has recently come under renewed interest as a target for immunotherapy. Here, we describe different tools and techniques to study the bioenergetic metabolism of cultured cells, using immune cells as a model. Our methodological approach relies on an extracellular flux analyzer, an instrument that enables the real-time measurement of the two central pathways used by living cells to generate adenosine triphosphate: glycolysis and oxidative phosphorylation. This instrument and similar technological innovations have transformed the study of cellular metabolism, unveiling its profound impact on various immunologic and oncological disorders.
MeSH term(s)	Biochemistry/instrumentation ; Biochemistry/methods ; Cells, Cultured ; Energy Metabolism ; Extracellular Space/metabolism ; Glycolysis ; Humans ; Immune System/cytology ; Immune System/metabolism ; Jurkat Cells ; Lymphocytes/metabolism ; Metabolome ; Mitochondria/metabolism ; Myeloid Cells/metabolism ; Oxidative Phosphorylation ; Oxygen/metabolism ; Tissue Array Analysis
Chemical Substances	Oxygen (S88TT14065)
Language	English
Publishing date	2014
Publishing country	United States
Document type	Journal Article
ISSN	1557-7988 ; 0076-6879
ISSN (online)	1557-7988
ISSN	0076-6879
DOI	10.1016/B978-0-12-416618-9.00007-8
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Article ; Online: Harnessing programmed cell death as a therapeutic strategy in rheumatic diseases.

Ramaswamy, Madhu / Deng, Min / Siegel, Richard M

Nature reviews. Rheumatology

2011 Volume 7, Issue 3, Page(s) 152–160

Abstract: Programmed cell death (PCD) is a key process in the regulation of immune cell development and peripheral immune homeostasis. Caspase-dependent apoptosis, as well as a number of alternative cell death mechanisms, account for immune cell PCD induced by ... ...

Abstract	Programmed cell death (PCD) is a key process in the regulation of immune cell development and peripheral immune homeostasis. Caspase-dependent apoptosis, as well as a number of alternative cell death mechanisms, account for immune cell PCD induced by cell-intrinsic and extrinsic pathways. In animal models, compelling evidence has emerged that genetic defects in PCD can result in autoimmune disease. Autoimmune disease can arise from single-gene mutations that affect PCD, and defective PCD has been observed in some tissues and cells from patients with rheumatic disease. Selectively inducing PCD in autoreactive B and T cells is very attractive as a therapeutic strategy because it offers the possibility of permanent elimination of these pathogenic cell subsets. In addition, the anti-inflammatory effects of apoptotic cells may add to the therapeutic benefit of induced PCD. Immune cell subsets vary widely in their sensitivity to specific inducers of cell death, and understanding these differences is key to predicting the outcome of inducing apoptosis for therapeutic means. Here, we review approaches that have been used to induce PCD in the treatment of autoimmune disease, and describe the prospects of bringing these experimental strategies into clinical practice.
MeSH term(s)	Animals ; Apoptosis/physiology ; Autoimmune Diseases/drug therapy ; Autoimmune Diseases/physiopathology ; Caspases/physiology ; Humans ; Models, Animal ; Rheumatic Diseases/drug therapy ; Rheumatic Diseases/physiopathology
Chemical Substances	Caspases (EC 3.4.22.-)
Language	English
Publishing date	2011-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	2491532-4
ISSN	1759-4804 ; 1759-4790
ISSN (online)	1759-4804
ISSN	1759-4790
DOI	10.1038/nrrheum.2010.225
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Article ; Online: Fibroblast-derived CXCL12 promotes breast cancer metastasis by facilitating tumor cell intravasation.

Ahirwar, Dinesh K / Nasser, Mohd W / Ouseph, Madhu M / Elbaz, Mohamad / Cuitiño, Maria C / Kladney, Raleigh D / Varikuti, Sanjay / Kaul, Kirti / Satoskar, Abhay R / Ramaswamy, Bhuvaneswari / Zhang, Xiaoli / Ostrowski, Michael C / Leone, Gustavo / Ganju, Ramesh K

Oncogene

2018 Volume 37, Issue 32, Page(s) 4428–4442

Abstract: The chemokine CXCL12 has been shown to regulate breast tumor growth, however, its mechanism in initiating distant metastasis is not well understood. Here, we generated a novel conditional allele of Cxcl12 in mice and used a fibroblast-specific Cre ... ...

Abstract	The chemokine CXCL12 has been shown to regulate breast tumor growth, however, its mechanism in initiating distant metastasis is not well understood. Here, we generated a novel conditional allele of Cxcl12 in mice and used a fibroblast-specific Cre transgene along with various mammary tumor models to evaluate CXCL12 function in the breast cancer metastasis. Ablation of CXCL12 in stromal fibroblasts of mice significantly delayed the time to tumor onset and inhibited distant metastasis in different mouse models. Elucidation of mechanisms using in vitro and in vivo model systems revealed that CXCL12 enhances tumor cell intravasation by increasing vascular permeability and expansion of a leaky tumor vasculature. Furthermore, our studies revealed CXCL12 enhances permeability by recruiting endothelial precursor cells and decreasing endothelial tight junction and adherence junction proteins. High expression of stromal CXCL12 in large cohort of breast cancer patients was directly correlated to blood vessel density and inversely correlated to recurrence and overall patient survival. In addition, our analysis revealed that stromal CXCL12 levels in combination with number of CD31+ blood vessels confers poorer patient survival compared to individual protein level. However, no correlation was observed between epithelial CXCL12 and patient survival or blood vessel density. Our findings describe the novel interactions between fibroblasts-derived CXCL12 and endothelial cells in facilitating tumor cell intrvasation, leading to distant metastasis. Overall, our studies indicate that cross-talk between fibroblast-derived CXCL12 and endothelial cells could be used as novel biomarker and strategy for developing tumor microenvironment based therapies against aggressive and metastatic breast cancer.
MeSH term(s)	Animals ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line ; Cell Line, Tumor ; Cell Movement/physiology ; Chemokine CXCL12/metabolism ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Female ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Mammary Neoplasms, Animal ; Mice ; Mice, Transgenic ; Neoplasm Invasiveness/pathology ; Neoplasm Metastasis/pathology ; Tumor Microenvironment/physiology
Chemical Substances	Chemokine CXCL12 ; Cxcl12 protein, mouse
Language	English
Publishing date	2018-05-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-018-0263-7
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