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Nor Fazila Che Mat

Researcher at RMIT University

Publications -  30
Citations -  740

Nor Fazila Che Mat is an academic researcher from RMIT University. The author has contributed to research in topics: Medicine & Proinflammatory cytokine. The author has an hindex of 8, co-authored 24 publications receiving 564 citations. Previous affiliations of Nor Fazila Che Mat include Universiti Sains Malaysia & Queen's University.

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Journal ArticleDOI

The IL-12 family of cytokines in infection, inflammation and autoimmune disorders.

TL;DR: The biological properties of the IL-12 family of cytokines, the signalling pathways mediated by these cytokines and their role in infection, inflammation, and autoimmune diseases will be the focus of this review.
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A single mass gathering resulted in massive transmission of COVID-19 infections in Malaysia with further international spread.

TL;DR: From this cluster, 1701 samples have been tested positive out of 21 920 tests carried out, thus, mass gathering during COVID-19 pandemic period should be banned to curb disease transmission.
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Interleukin-27 induces a STAT1/3- and NF-κB-dependent proinflammatory cytokine profile in human monocytes.

TL;DR: IL-27 is a strong inducer of proinflammatory cytokine and chemokine expression, including enhancement of IL-6, IP-10, MIP-1α, Mip-1β, and TNF-α expression in human primary monocytes, and it is observed that IL-27-induced cytokines and Chemokine production was mediated by STAT1, STAT3, and NF-κB activation.
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Impact of HIV infection, highly active antiretroviral therapy, and hepatitis C coinfection on serum interleukin-27.

TL;DR: It is found that clinical characteristics, including HIV viral load, hepatitis C virus coinfection, and CD4 T cell counts, were associated with changes in serum IL-27, suggesting circulating HIV may suppress IL- 27, a critical concept in treatment development with this cytokine.
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Interleukin-23-induced interleukin-23 receptor subunit expression is mediated by the Janus kinase/signal transducer and activation of transcription pathway in human CD4 T cells.

TL;DR: It is demonstrated that inhibition of the Janus kinase/signal transducer and activation of transcription (JAK/STAT) pathway by SD-1029, a JAK2 inhibitor, 5'-deoxy-5'-(methylthio) adenosine, and STAT3 VII, a STAT3 inhibitor, were able to blockIL-23-induced expression of IL-23 receptor subunits in the human SUPT-1 T cell line and in primary CD