Tumour necrosis factor receptor II (p75) signalling is required for the migration of Langerhans' cells

Wang, B.; Kondo, Seiji; Shivji, Gulnar M.; Fujisawa, Hiroshi; Mak, Tak W.; Sauder, Daniel N.

doi:10.1111/j.1365-2567.1996.tb00016.x

Cited by 94 publications

(51 citation statements)

References 21 publications

(1 reference statement)

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“…Recently, in order to confirm the role of TNF-␣ in LC migration and to examine which type of TNF receptor signaling is involved in such an event, we have utilized mutant mice deficient in TNF receptor I (p55) or II (p75). Our studies demonstrated that although LC migration was normal in TNF receptor p55-deficient mice, the migration was markedly depressed in TNF receptor p75-deficient mice compared to the wild-type mice [76,77]. TNF receptor p75-deficient mice also demonstrated a hyporesponsiveness in CHS.…”

Section: Studies Using Gene Knockout Micementioning

confidence: 90%

Role of cytokines in epidermal Langerhans cell migration

Wang

Amerio

Sauder

1999

Journal of Leukocyte Biology

151

107

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Section: Studies Using Gene Knockout Micementioning

confidence: 90%

Role of cytokines in epidermal Langerhans cell migration

Wang

Amerio

Sauder

1999

Journal of Leukocyte Biology

151

107

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“…Briefly, LNs were gently disrupted by rubbing between the frosted ends of two microscope slides, and then filtered through a nylon mesh cell strainer. LNCs were washed with HBSS and resuspended in complete RPMI 1640 medium (33).…”

Section: Preparation Of Lncsmentioning

confidence: 99%

CD4+ Th1 and CD8+ Type 1 Cytotoxic T Cells Both Play a Crucial Role in the Full Development of Contact Hypersensitivity

Wang

Fujisawa

Zhuang

et al. 2000

The Journal of Immunology

213

176

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The role of CD4+ vs CD8+ T cells in contact hypersensitivity (CHS) remains controversial. In this study, we used gene knockout (KO) mice deficient in CD4+ or CD8+ T cells to directly address this issue. Mice lacking either CD4+ or CD8+ T cells demonstrated depressed CHS responses to dinitrofluorobenzene and oxazolone compared with wild-type C57BL/6 mice. The depression of CHS was more significant in CD8 KO mice than in CD4 KO mice. Furthermore, in vivo depletion of either CD8+ T cells from CD4 KO mice or CD4+ T cells from CD8 KO mice virtually abolished CHS responses. Lymph node cells (LNCs) from hapten-sensitized CD4 and CD8 KO mice showed a decreased capacity for transferring CHS. In vitro depletion of either CD4+ T cells from CD8 KO LNCs or CD8+ T cells from CD4 KO LNCs resulted in a complete loss of CHS transfer. LNCs from CD4 and CD8 KO mice produced significant amounts of IFN-γ, indicating that both CD4+ and CD8+ T cells are able to secrete IFN-γ. LNCs from CD8, but not CD4, KO mice were able to produce IL-4 and IL-10, suggesting that IL-4 and IL-10 are mainly derived from CD4+ T cells. Intracellular cytokine staining of LNCs confirmed that IFN-γ-positive cells consisted of CD4+ (Th1) and CD8+ (type 1 cytotoxic T) T cells, whereas IL-10-positive cells were exclusively CD4+ (Th2) T cells. Collectively, these results suggest that both CD4+ Th1 and CD8+ type 1 cytotoxic T cells are crucial effector cells in CHS responses to dinitrofluorobenzene and oxazolone in C57BL/6 mice.

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“…To prepare single-cell suspensions, LN were gently disrupted by rubbing between the frosted ends of two microscope slides. The stromal fragments were digested with a collagenase IV/DNase I solution at room temperature for 25 min, and the cells were filtered through nylon mesh (44).…”

Section: Preparation Of Lncmentioning

confidence: 99%

Contribution of Langerhans Cell-Derived IL-18 to Contact Hypersensitivity

Wang

Feliciani

Howell

et al. 2002

The Journal of Immunology

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The epidermal Langerhans cells (LC), a member of the dendritic cell family, and the LC-derived cytokine IL-12 play a pivotal role in the initiation of contact hypersensitivity (CHS), a Th1 immune response in the skin. Because IL-18, another LC-derived cytokine, shares functional and biological properties with IL-12, we examined a potential role for IL-18 in CHS initiation. Our studies demonstrated that during the induction phase of murine CHS, IL-18 mRNA was significantly up-regulated in the skin-draining lymph nodes (LN). Migratory hapten-modified LC in LN expressed high levels of IL-18 mRNA and secreted functional IL-18 protein. LN cells produced significant amounts of IFN-γ following in vitro IL-12 stimulation, which could be partially blocked by anti-IL-18 Ab, suggesting a synergistic role for endogenous IL-18 in IFN-γ production by LN cells. Because mature IL-18 requires cleavage of immature precursors by caspase-1, we further examined IL-12-induced IFN-γ production in caspase-1−/− LN cells. An impaired IFN-γ production was seen in caspase-1−/− LN cells, which could be restored by addition of exogenous IL-18, supporting a role for caspase-1-cleaved, mature IL-18 in IFN-γ production. Finally, in vivo studies showed that CHS responses were significantly inhibited in mice treated with neutralizing IL-18 Ab as well as in caspase-1−/− mice deficient in mature IL-18, indicating functional relevance for IL-18 in CHS. Taken together, our studies demonstrate that LC-derived IL-18 significantly contributes to CHS initiation.

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Tumour necrosis factor receptor II (p75) signalling is required for the migration of Langerhans' cells

Cited by 94 publications

References 21 publications

Role of cytokines in epidermal Langerhans cell migration

Role of cytokines in epidermal Langerhans cell migration

CD4+ Th1 and CD8+ Type 1 Cytotoxic T Cells Both Play a Crucial Role in the Full Development of Contact Hypersensitivity

Contribution of Langerhans Cell-Derived IL-18 to Contact Hypersensitivity

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