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16. Making inroads to precision medicine for the treatment of autoimmune diseases: Harnessing genomic studies to better diagnose and treat complex disorders.

Author

Baglaenko, Yuriy, Wagner, Catriona, Bhoj, Vijay G., Brodin, Petter, Gershwin, M. Eric, Graham, Daniel, Invernizzi, Pietro, Kidd, Kenneth K., Korsunsky, Ilya, Levy, Michael, Mammen, Andrew L., Nizet, Victor, Ramirez-Valle, Francisco, Stites, Edward C., Williams, Marc S., Wilson, Michael, Rose, Noel R., Ladd, Virginia, and Sirota, Marina

Subjects
AUTOIMMUNE diseases, INDIVIDUALIZED medicine, THERAPEUTICS, DIAGNOSIS, PREVENTIVE medicine
Abstract

Precision Medicine is an emerging approach for disease treatment and prevention that takes into account individual variability in genes, environment, and lifestyle. Autoimmune diseases are those in which the body's natural defense system loses discriminating power between its own cells and foreign cells, causing the body to mistakenly attack healthy tissues. These conditions are very heterogeneous in their presentation and therefore difficult to diagnose and treat. Achieving precision medicine in autoimmune diseases has been challenging due to the complex etiologies of these conditions, involving an interplay between genetic, epigenetic, and environmental factors. However, recent technological and computational advances in molecular profiling have helped identify patient subtypes and molecular pathways which can be used to improve diagnostics and therapeutics. This review discusses the current understanding of the disease mechanisms, heterogeneity, and pathogenic autoantigens in autoimmune diseases gained from genomic and transcriptomic studies and highlights how these findings can be applied to better understand disease heterogeneity in the context of disease diagnostics and therapeutics. [ABSTRACT FROM AUTHOR]

Published
2023
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30. IL-12 overexpression in mice as a model for Sjogren lung disease

Author

McGrath-Morrow, Sharon, Laube, Beth, Tzou, Shey-Cherng, Cho, Cecilia, Cleary, Jeffrey, Kimura, Hiroaki, Rose, Noel R., and Caturegli, Patrizio

Subjects
Sjogren's syndrome -- Physiological aspects, Sjogren's syndrome -- Causes of, Interleukin-12 -- Physiological aspects, Biological sciences
Abstract

Interleukin-12 (IL-12), a Th1 proinflammatory cytokine, is reported to be increased in Sjogren syndrome. To evaluate the effects of local Th1/Th2 deregulation, we generated a transgenic mouse model that overexpresses IL-12 in the lungs. IL-12 transgenic mice developed bronchial and alveolar abnormalities strikingly similar to those found in the lungs of Sjogren patients. Pathologically, lung abnormalities began at ~4 mo of age and were characterized by lymphocytic infiltrates around the bronchi, intraluminal periodic acid Schiff-positive debris, increased cell proliferation in the alveolar region, and increased interstitial and alveolar macrophages. Functionally, these abnormalities translated into decreased mucociliary clearance (P < 0.05 vs. wild-type littermates) and increased oxidative stress (P < 0.01). The pathological and functional abnormalities were accompanied by significant changes in lung natural killer (NK) cells. The number of NK cells was fourfold higher in IL-12 transgenic than wild-type lungs (20% of all lymphoid cells vs. 5%) during the first month of life. NK cells then decreased within a narrow window of time (from 30 to 50 days of age), reaching a nadir of ~2% on day 50, and remained at these low levels thereafter. This new mouse model highlights the role of IL-12 in the initiation of Sjogren syndrome. autoimmunity; transgenic mice; inflammation; natural killer cells

Published
2006

31. Impaired up-regulation of CD25 on CD[4.sup.+] T cells in IFN-[gamma] knockout mice is associated with progression of myocarditis to heart failure

Author

Afanasyeva, Marina, Georgakopoulos, Dimitrios, Belardi, Diego F., Bedja, Djahida, Fairweather, DeLisa, Wang, Yan, Kaya, Ziya, Gabrielson, Kathleen L., Rodriguez, E. Rene, Caturegli, Patrizio, Kass, David A., and Rose, Noel R.

Subjects
Cell death -- Research, Heart diseases -- Research, Science and technology
Abstract

Inflammation has been recognized increasingly as a critical pathologic component of a number of heart diseases. A mouse model of autoimmune myocarditis was developed to study the role of immune mediators in the development of cardiac dysfunction. We have found previously that IFN-[gamma] deficiency promotes inflammation in murine myocarditis, it has been unclear, however, how IFN-[gamma] deficiency in myocarditis affects cardiac function and what underlying immune mechanisms are responsible for these effects. In this work, we show that IFN-[gamma] knockout (KO) mice have more pronounced systolic and diastolic dysfunction and greater frequency of progression to dilated cardiomyopathy and heart failure compared with WT mice. Cardiac dysfunction in the KO mice is associated with the expansion of activated (CD[44.sup.high]) CD[3.sup.+] T cells due to reduced apoptosis of CD[4.sup.+], but not CD[8.sup.+], T cells. CD[4.sup.+] T cells in the KO mice show impaired up-regulation of CD25 upon activation, resulting in the expansion of CD[4.sup.+]CD[44.sup.+]CD[25.sup.-] T cells and their infiltration into the heart. CD[4.sup.+]CD[25.sup.-] T cells are less apoptosis-prone compared with the CD[25.sup.+] population, and their infiltration into the heart is associated with greater severity of myocarditis. We conclude that IFN-[gamma] deficiency in autoimmune myocarditis is associated with preferential expansion of CD[4.sup.+]CD[44.sup.+]CD[25.sup.-] T cells resulting in increased cardiac inflammation. An exaggerated inflammatory response in IFN-[gamma] KO mice causes cardiac dysfunction, leading to dilated cardiomyopathy and heart failure. activation-induced cell death | autoimmunity | pressure-volume relations

Published
2005

32. Women and autoimmune diseases

Author

Fairweather, DeLisa and Rose, Noel R.

Subjects
Communicable diseases -- Causes of, Autoimmune diseases -- Causes of, Autoimmune diseases -- Demographic aspects, Autoimmune diseases -- Research, Autoimmune diseases -- Genetic aspects
Abstract

Autoimmune diseases affect approximately 8% of the population, 78% of whom are women. The reasons for the high prevalence in women are unknown, but circumstantial evidence links autoimmune diseases with [...]

Published
2004

49. Preface

Author

ROSE, NOEL R.

Published
2008

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