2021
DOI: 10.1016/j.intimp.2020.107331
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The role of Th17 cells in viral infections

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Cited by 46 publications
(28 citation statements)
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“…There is some evidence showing that human viruses can initiate the activation of immune system responses, in which CD4 helper T cells (Th) are differentiated into cytokinesecreting effector subpopulations, such as IL-17-producing Th17 cells [14]. Despite their key role in suppressing certain viral infections, Th17 cells are also involved in the induction of detrimental conditions since they can promote tissue damage and mediate chronic inflammation in a wide range of target organs [15]. Th17 cells are a subset of CD4 T cells, and naive CD4 T cell differentiation into effector Th17 cells is dependent on the transcription factor retinoic acid-related (RAR) orphan gamma receptor (RORC2) expression and on the presence of the cytokines IL-6, TGF-β and IL-1β [16][17][18].…”
Section: Introductionmentioning
confidence: 99%
“…There is some evidence showing that human viruses can initiate the activation of immune system responses, in which CD4 helper T cells (Th) are differentiated into cytokinesecreting effector subpopulations, such as IL-17-producing Th17 cells [14]. Despite their key role in suppressing certain viral infections, Th17 cells are also involved in the induction of detrimental conditions since they can promote tissue damage and mediate chronic inflammation in a wide range of target organs [15]. Th17 cells are a subset of CD4 T cells, and naive CD4 T cell differentiation into effector Th17 cells is dependent on the transcription factor retinoic acid-related (RAR) orphan gamma receptor (RORC2) expression and on the presence of the cytokines IL-6, TGF-β and IL-1β [16][17][18].…”
Section: Introductionmentioning
confidence: 99%
“…severity of the disease is distinguished by the host immune response to the virus infection. [15][16][17] To date, several instances of SARS-CoV and MERS-CoV mixed infection have been reported; however, in the case of COVID-19, coinfection is less frequent. 18 The prevalence of coinfection in different individuals with COVID-19 is thought to vary to a significant extent as only 50% of deaths associated with COVID-19 are suspected to stem from mixed infection.…”
mentioning
confidence: 99%
“…Even worse, SARS-CoV-2 as a catastrophic pandemic, emerged worldwide, surpassing any former coronavirus epidemics, and resulting in severe clinical symptoms leading to death [ 7 ]. Moreover, the interactions between the host and this virus can mediate the induction of a “cytokine storm”, resulting in various immunopathological consequences, including immunothrombosis [ 8 , 9 ]. For example, the lowered secretion of IFNs reduces the uptake of neutrophils into the infected area, making their presence more abundant in the blood stream.…”
Section: Introductionmentioning
confidence: 99%
“…The human innate immune system plays an essential role as the first immune barrier in the inflammatory consequences that COVID-19 imposes [ 93 ]. A severe COVID-19 infection can be observed due to the increased pro-inflammatory cytokines, including interleukin‐6 and tumor necrosis factor‐alpha [ 9 , 15 ]. The primary source of these cytokines is dependent on the toll‐like receptors (TLRs) signaling pathways [ 28 ].…”
Section: Introductionmentioning
confidence: 99%