Mitochondria as Oxidative Signaling Organelles in T-cell Activation: Physiological Role and Pathological Implications

Kamiński, Marcin M.; Röth, Daniel; Krammer, Peter H.; Gülow, Karsten

doi:10.1007/s00005-013-0235-0

Cited by 59 publications

(65 citation statements)

References 221 publications

(265 reference statements)

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“…In this context, Sena et al showed that ETC complex III-originating ROS, produced upon T-cell activation, are essential for NFAT activation as well as IL-2 production (Murphy and Siegel, 2013;Sena et al, 2013). The findings of Sena et al are in line with a study by Kaminski and colleagues who, a few years earlier, reported that complex-I-oxidants control IL-2 and IL-4 production and activation of NF-κB and AP-1 (Kaminski et al, 2010(Kaminski et al, , 2013. The authors of the latter study further supported their conclusions by examining T cells isolated from atopic dermatitis patients.…”

Section: When and Where Are Ros Generated?supporting

confidence: 68%

“…The authors of the latter study further supported their conclusions by examining T cells isolated from atopic dermatitis patients. Blockade of mitochondrial complex-I in these cells reduced disease-associated hyper-expression of IL-4 (Kaminski et al, 2010(Kaminski et al, , 2013. In addition, a number of recent studies identified novel molecular players, which all affect mitochondrial ROS production and thereby T-cell activation as well as apoptosis (Kaminski et al, 2007(Kaminski et al, , 2013Silic-Benussi et al, 2010).…”

Section: When and Where Are Ros Generated?mentioning

confidence: 98%

“…Also mitochondria produce O 2 ·-and H 2 O 2 , which appear to play an important function in T cells [for the interested reader we recommend a recently published review on the role of mitochondrial oxidative signaling in T-cell activation, Kaminski et al (2013)]. The functional role of these organelles and their oxidant production in T cells was reported some decades ago.…”

Section: When and Where Are Ros Generated?mentioning

confidence: 98%

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Redox regulation of T-cell receptor signaling

Simeoni

Bogeski

2015

Biological Chemistry

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T-cell receptor (TCR) triggering by antigens activates a sophisticated intracellular signaling network leading to transcriptional activation, proliferation and differentiation of T cells. These events ultimately culminate in adaptive immune responses. Over recent years it has become evident that reactive oxygen species (ROS) play an important role in T-cell activation. It is now clear that ROS are involved in the regulation of T-cell mediated physiological and pathological processes. Upon TCR triggering, T cells produce oxidants, which originate from different cellular sources. In addition, within inflamed tissues, T cells are exposed to exocrine ROS produced by activated phagocytes or other ROS-producing cells. Oxidative modifications can have different effects on T-cell function. Indeed, they can stimulate T-cell activation but they can be also detrimental. These opposite effects of oxidation likely depend on different factors such as ROS concentration and source and also on the differentiation status of the T cells. Despite the well-stablished fact that ROS represent important modulators of T-cell activation, the precise molecular mechanisms of their action are far from clear. Here, we summarize the present knowledge on redox regulation of T-cell function with a particular emphasis on the redox regulation of TCR signaling.

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Section: When and Where Are Ros Generated?supporting

confidence: 68%

Section: When and Where Are Ros Generated?mentioning

confidence: 98%

Section: When and Where Are Ros Generated?mentioning

confidence: 98%

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Redox regulation of T-cell receptor signaling

Simeoni

Bogeski

2015

Biological Chemistry

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“…However, if immune system either fails to be properly activated or is persistently activated it can contribute to multiple diseases including autoimmunity, cardiovascular disease, and accelerate the normal aging process. In the past two decades, there is substantial evidence that ROS are essential second messengers in innate and adaptive immune cells [73, 74]. Yet, increased levels of ROS within immune cells can result in hyperactivation of inflammatory responses resulting in tissue damage and pathology [75].…”

Section: Redox Signaling and Oxidative Stress: Regulation Of Inflammamentioning

confidence: 99%

ROS Function in Redox Signaling and Oxidative Stress

2014

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Oxidative stress refers to elevated intracellular levels of reactive oxygen species (ROS) that cause damage to lipids, proteins and DNA. Oxidative stress has been linked to a myriad of pathologies. However, elevated ROS are also signaling molecules i.e. redox biology that maintain physiological functions. In this review we discuss the two faces of ROS, redox signaling and oxidative stress, and their contribution to both physiological and pathological conditions. Redox biology refers to low levels of ROS that activate signaling pathways to initiate biological processes while oxidative stress denotes high levels of ROS that incur damage to DNA, protein or lipids. Thus, the response to ROS displays hormesis. The In this review, we argue that redox biology, rather than oxidative stress, underlies physiological and pathological conditions.

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“…Mitochondria are indeed involved in apoptosis induction during activation-induced cell death caused by TCR stimulation and aimed at restricting further clonal expansion to prevent autoimmune disorders [35,36]. Finally, mitochondria produce ROS, which accompany upregulation of nuclear factor kappa B (NFκB) and nuclear factor of activated T cells (NFAT), two master regulators of TCR-stimulated transcription changes [37–41]. These three processes are stimulated by an increase in mitochondrial Ca 2+ , as this ion stimulates the tricarbon acid (TCA) cycle in the mitochondrial matrix, leading to an increase in proton pumping, ATP synthesis and ROS production [42,43] (figure 1).…”

Section: Introductionmentioning

confidence: 99%

Computational properties of mitochondria in T cell activation and fate

2016

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In this article, we review how mitochondrial Ca2+ transport (mitochondrial Ca2+ uptake and Na+/Ca2+ exchange) is involved in T cell biology, including activation and differentiation through shaping cellular Ca2+ signals. Based on recent observations, we propose that the Ca2+ crosstalk between mitochondria, endoplasmic reticulum and cytoplasm may form a proportional–integral–derivative (PID) controller. This PID mechanism (which is well known in engineering) could be responsible for computing cellular decisions. In addition, we point out the importance of analogue and digital signal processing in T cell life and implication of mitochondrial Ca2+ transport in this process.

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Mitochondria as Oxidative Signaling Organelles in T-cell Activation: Physiological Role and Pathological Implications

Abstract: Early scientific reports limited the cell biological role of reactive oxygen species (ROS)

Cited by 59 publications

References 221 publications

Redox regulation of T-cell receptor signaling

Redox regulation of T-cell receptor signaling

ROS Function in Redox Signaling and Oxidative Stress

Computational properties of mitochondria in T cell activation and fate

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