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2. Decay-Accelerating Factor

Author

Christy, Joseph M., primary, Toomey, Christopher B., additional, Cauvi, David M., additional, and Pollard, Kenneth M., additional

Published
2018
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3. List of Contributors

Author

Agarwal, Atul, primary, Atkinson, John P., additional, Barlow, Paul N., additional, Barnum, Scott R., additional, Bettuzzi, Saverio, additional, Blom, Anna M., additional, Boackle, Susan A., additional, Bohlson, Suzanne, additional, Bullard, Daniel C., additional, Cauvi, David M., additional, Cedzyński, Maciej, additional, Christy, Joseph M., additional, Coulthard, Liam G., additional, DiScipio, Richard G., additional, Drouet, Christian, additional, Ferreira, Viviana P., additional, Fishelson, Zvi, additional, Gaboriaud, Christine, additional, Ghannam, Arije, additional, Ghebrehiwet, Berhane, additional, Ghiran, Ionita, additional, Hawksworth, Owen ​A., additional, Huang, Mingjun, additional, Isenman, David E., additional, Jensenius, Jens C., additional, Kemper, Claudia, additional, Kilpatrick, David C., additional, Laskowski, Jennifer, additional, Liszewski, M. Kathryn, additional, Manne, Kartik, additional, Matsushita, Misao, additional, Morgan, Paul, additional, Naponelli, Valeria, additional, Narayana, Sthanam V.L., additional, Nicholson-Weller, Anne, additional, Ohtani, Katsuki, additional, Okrój, Marcin, additional, Orozco, Luz D., additional, Pangburn, Michael K., additional, Pihl, Ramus, additional, Podos, Steven D., additional, Pollard, Kenneth M., additional, Ponard, Denise, additional, Riesbeck, Kristian, additional, Rossi, Véronique, additional, Schein, Theresa N., additional, Su, Yu-Ching, additional, Świerzko, Anna S., additional, Thielens, Nicole M., additional, Thiel, Steffen, additional, Thurman, Joshua M., additional, Toomey, Christopher B., additional, van Lookeren Campagne, Menno, additional, Wakamiya, Nobutaka, additional, Wetsel, Rick A., additional, and Woodruff, Trent ​M., additional

Published
2018
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6. The Role of Decay Accelerating Factor in Environmentally Induced and Idiopathic Systemic Autoimmune Disease

Author

Toomey, Christopher B., Cauvi, David M., and Pollard, Kenneth M.

Subjects
Article Subject, fungi, chemical and pharmacologic phenomena
Abstract

Decay accelerating factor (DAF) plays a complex role in the immune system through complement-dependent and -independent regulation of innate and adaptive immunity. Over the past five years there has been accumulating evidence for a significant role of DAF in negatively regulating adaptive T-cell responses and autoimmunity in both humans and experimental models. This review discusses the relationship between DAF and the complement system and highlights major advances in our understanding of the biology of DAF in human disease, particularly systemic lupus erythematosus. The role of DAF in regulation of idiopathic and environmentally induced systemic autoimmunity is discussed including studies showing that reduction or absence of DAF is associated with autoimmunity. In contrast, DAF-mediated T cell activation leads to cytokine expression consistent with T regulatory cells. This is supported by studies showing that interaction between DAF and its molecular partner, CD97, modifies expression of autoimmunity promoting cytokines. These observations are used to develop a hypothetical model to explain how DAF expression may impact T cell differentiation via interaction with CD97 leading to T regulatory cells, increased production of IL-10, and immune tolerance.

Published
2014
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8. beta 2-microglobulin is required for the full expression of xenobiotic-induced systemic autoimmunity

Author

Pollard, Kenneth M, Hultman, Per, Toomey, Christopher B, Cauvi, David M, Konoc, Dwight H, Pollard, Kenneth M, Hultman, Per, Toomey, Christopher B, Cauvi, David M, and Konoc, Dwight H

Abstract

ercury exposure in both humans and mice is associated with features of systemic autoimmunity. Murine HgCl(2)-induced autoimmunity (mHgIA) requires MHC Class II, CD4(+) T-cells, co-stimulatory molecules, and interferon-gamma (IFN-gamma), similar to spontaneous models of systemic lupus erythematosus (SLE). beta(2)-microglobulin (B2m) is required for functional MHC Class I molecules and the neonatal F(c) receptor (F(c)Rn). Deficiency of B2m in lupus-prone strains is consistently associated with reduced IgG levels, but with variable effects on other manifestations. Herein, we examined the role of B2m in mHgIA and show that in the absence of B2m, mercury-exposed mice failed to exhibit hypergammaglobulinemia, had reduced anti-nucleolar autoantibodies (ANoA), and had a lower incidence of immune complex deposits in splenic blood vessels, whereas IgG anti-chromatin autoantibodies and renal immune deposits were largely unaffected. Subclass analysis of the IgG anti-chromatin, however, revealed a significant reduction in the IgG(1) subtype. Examination of IFN gamma, IL-4, and IL-2 in exposed skin, draining lymph nodes, and spleen following mercury exposure showed reduced IL-4 in the spleen and skin in B2m-deficient mice, consistent with the lower IgG(1) anti-chromatin levels, and reduced IFN-gamma expression in the skin. These findings demonstrate how a single genetic alteration can partially but significantly modify the clinical manifestations of systemic autoimmunity induced by exposure to xenobiotics.

Published
2011
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11. Interferon-γ and systemic autoimmunity.

Author

Pollard KM, Cauvi DM, Toomey CB, Morris KV, and Kono DH

Subjects
Animals, Gene Expression Regulation immunology, Humans, Lupus Erythematosus, Systemic pathology, Adaptive Immunity, Autoimmunity, Immunity, Innate, Interferon-gamma immunology, Lupus Erythematosus, Systemic immunology
Abstract

The term interferon describes a family of proteins consisting of three major types (I, II, and III) which differ in their primary protein sequences, cognate receptors, genetic loci, and cell types responsible for their production. The interferons, including types I and II, overlap significantly in the genes they control resulting in a shared spectrum of diverse biological effects which includes regulation of both the innate and adaptive immune responses. As such, the interferons are major effectors in the pathogenesis of autoimmunity, especially systemic autoimmunity. The type I IFNs, because they are produced during the early stages of the innate immune response, are thought to play the foremost role in autoimmune responses. However, numerous studies have found that the single type II IFN, IFN-γ, plays an essential role in the development and severity of systemic autoimmunity, particularly systemic lupus erythematosus. This is supported by animal studies where IFN-γ is uniformly required in both spontaneous and induced models of lupus. Although expression of IFN-γ in cells of the innate immune system is almost immediate after activation, expression in adaptive immunity requires a complex orchestration of cellular interactions, signaling events, and epigenetic modifications. The multifaceted nature of IFN-γ in adaptive immunity identifies numerous possible therapeutic targets that, because of the essential contribution of IFN-γ to systemic autoimmunity, have the potential for producing benefits.

Published
2013

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