TIM-4 is differentially expressed in the distinct subsets of dendritic cells in skin and skin-draining lymph nodes and controls skin Langerhans cell homeostasis

Zhang, Xilin; Liu, Queping; Wang, Jie; Liu, Guihua; Weiland, Matthew; Yu, Fei; Mi, Qing Sheng; Gu, Jun; Zhou, Li

doi:10.18632/oncotarget.9546

Cited by 15 publications

(16 citation statements)

References 76 publications

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“…8 During sensitization, allergens (or haptens) are topically applied to the skin, where they gain immunogenicity after internalization by skin-resident antigen-presenting cells (APCs), notably dermal DCs (dDC1 and dDC2s) and Langerhans cells (LCs). 17,[29][30][31] Hapten-activated APCs traffic to skin-draining lymph nodes (sdLNs), where they activate CD4 1 and CD8 1 T cells. During elicitation, reexposure to the same hapten at a neutral skin site triggers a robust activation of this primed T-cell response, resulting in localized inflammation, irritation, and edema.…”

Section: Resultsmentioning

confidence: 99%

RETRACTED: Noncanonical autophagy in dermal dendritic cells mediates immunosuppressive effects of UV exposure

Sil

Suwanpradid

Muse

et al. 2020

Journal of Allergy and Clinical Immunology

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Immunosuppression by UV exposure requires Rubcn. Background: Control of the inflammatory response is critical to maintaining homeostasis, and failure to do so contributes to the burden of chronic inflammation associated with several disease states. The mechanisms that underlie immunosuppression, however, remain largely unknown. Although defects in autophagy machinery have been associated with inflammatory pathologic conditions, we now appreciate that autophagic components participate in noncanonical pathways distinct from classical autophagy. We have previously demonstrated that LC3-associated phagocytosis (LAP), a noncanonical autophagic

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Section: Resultsmentioning

confidence: 99%

RETRACTED: Noncanonical autophagy in dermal dendritic cells mediates immunosuppressive effects of UV exposure

Sil

Suwanpradid

Muse

et al. 2020

Journal of Allergy and Clinical Immunology

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“…Recently, Zhang et al (52) found that the expression of Tim-4 was variable in the different subsets of DCs in skin and skindraining LNs that were studied. Dermal CD207 + DCs and LNs resident CD207 − CD4 + DCs highly expressed Tim-4.…”

Section: Dendritic Cellsmentioning

confidence: 99%

Tim-4 in Health and Disease: Friend or Foe?

Liang

et al. 2020

Front. Immunol.

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T-cell immunoglobulin and mucin domain containing 4 (Tim-4) is a phosphatidylserine receptor and is selectively expressed on antigen presenting cells. Recently, Tim-4 was reported to be expressed on iNKT cells, B1 cells, and tumor cells, suggesting it has multiple biological functions. In this review, we mainly summarize the expression and regulation of Tim-4 in immune cells including T cells, macrophages, dendritic cells, NKT cells, B cells, and mast cells. The expression of Tim-4 in these cells implies that Tim-4 might participate in immune related diseases. Emerging evidence emphasizes a substantial role for Tim-4 in maintaining homeostasis by regulating various immune responses, including viral infection, allergy, autoimmunity, and tumor immunity. Here, we collectively evaluated the role of Tim-4 in health and diseases. This summary will be extremely useful to fully understand the function of Tim-4 in the pathogenesis of immune related diseases, which would provide novel clues for the diagnosis and treatment of diseases.

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“…We have previously shown that ectopic expression of human and mouse TIM-4 in HEK 293T cells enhances rVSV/EBOV GP entry [50,51]. While it is appreciated that tissue macrophage and dendritic cell populations express endogenous TIM-4 in both humans and mice [91,92], the role of this receptor in filovirus infection of those primary populations has not been previously reported. Two lines of evidence indicated that TIM-4 is important for EBOV infection of pmacs.…”

Section: Discussionmentioning

confidence: 99%

IL-4/IL-13 polarization of macrophages enhances Ebola virus glycoprotein-dependent infection

et al. 2019

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BackgroundEbolavirus (EBOV) outbreaks, while sporadic, cause tremendous morbidity and mortality. No therapeutics or vaccines are currently licensed; however, a vaccine has shown promise in clinical trials. A critical step towards development of effective therapeutics is a better understanding of factors that govern host susceptibility to this pathogen. As macrophages are an important cell population targeted during virus replication, we explore the effect of cytokine polarization on macrophage infection.Methods/Main findingsWe utilized a BSL2 EBOV model virus, infectious, recombinant vesicular stomatitis virus encoding EBOV glycoprotein (GP) (rVSV/EBOV GP) in place of its native glycoprotein. Macrophages polarized towards a M2-like anti-inflammatory state by combined IL-4 and IL-13 treatment were more susceptible to rVSV/EBOV GP, but not to wild-type VSV (rVSV/G), suggesting that EBOV GP-dependent entry events were enhanced by these cytokines. Examination of RNA expression of known surface receptors that bind and internalize filoviruses demonstrated that IL-4/IL-13 stimulated expression of the C-type lectin receptor DC-SIGN in human macrophages and addition of the competitive inhibitor mannan abrogated IL-4/IL-13 enhanced infection. Two murine DC-SIGN-like family members, SIGNR3 and SIGNR5, were upregulated by IL-4/IL-13 in murine macrophages, but only SIGNR3 enhanced virus infection in a mannan-inhibited manner, suggesting that murine SIGNR3 plays a similar role to human DC-SIGN. In vivo IL-4/IL-13 administration significantly increased virus-mediated mortality in a mouse model and transfer of ex vivo IL-4/IL-13-treated murine peritoneal macrophages into the peritoneal cavity of mice enhanced pathogenesis.SignificanceThese studies highlight the ability of macrophage polarization to influence EBOV GP-dependent virus replication in vivo and ex vivo, with M2a polarization upregulating cell surface receptor expression and thereby enhancing virus replication. Our findings provide an increased understanding of the host factors in macrophages governing susceptibility to filoviruses and identify novel murine receptors mediating EBOV entry.

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TIM-4 is differentially expressed in the distinct subsets of dendritic cells in skin and skin-draining lymph nodes and controls skin Langerhans cell homeostasis

Cited by 15 publications

References 76 publications

RETRACTED: Noncanonical autophagy in dermal dendritic cells mediates immunosuppressive effects of UV exposure

RETRACTED: Noncanonical autophagy in dermal dendritic cells mediates immunosuppressive effects of UV exposure

Tim-4 in Health and Disease: Friend or Foe?

IL-4/IL-13 polarization of macrophages enhances Ebola virus glycoprotein-dependent infection

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