Signal transducer and activator of transcription signals in allergic disease

Chen, Weiguo; Hershey, Gurjit K. Khurana

doi:10.1016/j.jaci.2007.01.004

Cited by 27 publications

(15 citation statements)

References 204 publications

(192 reference statements)

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“…10,11,26 In addition, the strong negative correlation (R 5 20.82, P 5 .0007) between the 2 activated transcription factors among the entire asthmatic cohort further supports the notion that these 2 STAT isoforms function, at least in part, in an antagonistic fashion. Furthermore, our results identified age at onset as correlating positively with phospho-STAT1 levels and negatively with phospho-STAT6 levels.…”

Section: Discussionmentioning

confidence: 63%

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Altered phosphorylated signal transducer and activator of transcription profile of CD4+CD161+ T cells in asthma: Modulation by allergic status and oral corticosteroids

Gernez

Tirouvanziam

Nguyen

et al. 2007

Journal of Allergy and Clinical Immunology

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Section: Discussionmentioning

confidence: 63%

“…Moreover, within asthmatic patients, phospho-STAT1 and phospho-STAT6 levels measured in combination provide excellent discrimination between allergic and nonallergic asthmatic patients and between asthmatic patients taking or not taking OCSs, confirming the importance of functional STAT polarization in asthma pathophysiology and response to treatment. 26 …”

mentioning

confidence: 99%

Altered phosphorylated signal transducer and activator of transcription profile of CD4+CD161+ T cells in asthma: Modulation by allergic status and oral corticosteroids

Gernez

Tirouvanziam

Nguyen

et al. 2007

Journal of Allergy and Clinical Immunology

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“…The discovery that cytokine programming of the immune responses is mediated by a family of intracellular signaling factors, the protein tyrosine kinases, known as Janus kinase (JAK), and the signal transducer and activator of transcription (STAT) molecules, over 15 years ago, has come up with new potential targets for the pharmaceutical modulation of the immune responses [59]. This family comprises four JAKs molecules (JAK1 to 3, and Tyk-2) and seven STAT molecules (STAT1 to 6, including STAT5A and STAT5B).…”

Section: Modifying the Immune Responses?mentioning

confidence: 99%

An overview of the immunopathology of human paracoccidioidomycosis

2008

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We review here the advances in the understanding of the immunopathology of human paracoccidioidomycosis (PCM). Its investigation must take in account the intriguing natural history of the mycosis and its agent, providing clues to the mechanisms that lead to development of disease (unbalanced host-parasite relationship?) or to the clinically silent, chronic carrier state (balanced hostparasite relationship?), in exposed people living in endemic areas. Although the literature on this subject has progressed notably, the overall picture of what are the mechanisms of susceptibility or resistance continues to be fragmentary. Major advances were seen in the description of both the cytokines/chemokines associated to the different outcomes of the hostparasite interaction, and the fungus-monocyte/macrophage interaction, and cytokines released thereof by these cells. However, relatively few studies have attempted to modify, even in vitro, the patients' unbalanced immune reactivity. Consequently, the benefits of this improved knowledge did not yet reach clinical practice. Fortunately, the previous notion of the immune system as having two nearly independent arms, the innate and adaptive immunities, leaving a large gap between them, is now being overcome.Immunologists are now trying to dissect the connections between these two arms. This will certainly lead to more productive results. Current investigations should address the innate immunity events that trigger the IL-12/IFN-c axis and confer protection against PCM in those individuals living in endemic areas, who have been infected, but did not develop the mycosis.

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“…2). Studies in STAT6-knockout mice have revealed that IL-13 signaling utilizes the Jak-STAT pathway and specifically STAT6 [2,29]. Jaks are tyrosine kinases that each contains a true catalytic domain and a pseudokinase domain.…”

Section: Il-13 Signalingmentioning

confidence: 99%

IL-13 receptor isoforms: Breaking through the complexity

Tabata¹,

Hershey

2007

Curr Allergy Asthma Rep

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Interleukin (IL)-13 is an immunoregulatory cytokine secreted predominantly by activated T-helper type 2 (Th2) cells, and it has been identified as crucial in developing allergic inflammatory responses. Its diverse functions are mediated by a complex receptor system including IL-4 receptor alpha (IL-4Ralpha; CD124) and two other cognate cell surface proteins, IL-13Ralpha1 (CD213a1) and IL-13Ralpha2 (CD213a2). IL-13Ralpha1 forms a heterodimer with IL-4Ralpha that is a signaling IL-13 receptor. In contrast, IL-13Ralpha2 has been thought to be a decoy receptor due to its short cytoplasmic tail. IL-13Ralpha2 exists on the cell membrane, intracellularly, and in soluble form. Recent reports revealed that membrane IL-13Ralpha2 may have some signaling capabilities, and soluble IL-13Ralpha2 is a critical endogenous modulator for IL-13 responses. The receptor has more complicated functions than a simple decoy receptor. In this review, we describe the isoforms of IL-13Ralpha2 and discuss newly revealed functions of IL-13Ralpha2.

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Signal transducer and activator of transcription signals in allergic disease

Cited by 27 publications

References 204 publications

Altered phosphorylated signal transducer and activator of transcription profile of CD4+CD161+ T cells in asthma: Modulation by allergic status and oral corticosteroids

Altered phosphorylated signal transducer and activator of transcription profile of CD4+CD161+ T cells in asthma: Modulation by allergic status and oral corticosteroids

An overview of the immunopathology of human paracoccidioidomycosis

IL-13 receptor isoforms: Breaking through the complexity

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