The selective triggering of CD40 on keratinocytes in vivo enhances cell-mediated immunity

Fuller, Bruce W.; Nishimura, Toshihide; Noelle, Randolph J.

doi:10.1002/1521-4141(200203)32:3<895::aid-immu895>3.0.co;2-a

Cited by 10 publications

(4 citation statements)

References 18 publications

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“…These mechanisms presumably promote migration into the area of activated T-cells, which may interact with epithelial cells and bind CD40. These effects would synergize to produce more chemokines and exacerbate the inflammatory status of conditions such as OLP (34)(35)(36).…”

Section: Discussionmentioning

confidence: 91%

Immune receptors CD40 and CD86 in oral keratinocytes and implications for oral lichen planus

et al. 2017

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Lichen planus (LP) is a chronic T-cell-mediated mucocutaneous inflammatory disease that targets stratified epithelia, including those lining the oral cavity. The intraoral variant of LP (OLP) is associated with interferon (IFN)-γ production by infiltrating T lymphocytes; however, the role of epithelial cells in the etiopathogenesis OLP is not completely understood. There is however a growing body of evidence regarding the involvement of epithelial-derived cytokines, immune receptors, and costimulatory molecules in the pathobiological processes that promote and sustain OLP. In the present study, we used a reverse transcriptase-polymerase chain reaction assay to assess whether CD40-a receptor found mainly on antigen presenting cells-and the costimulatory molecule CD86 were expressed in oral keratinocytes (three strains of primary normal oral keratinocytes and the H357 cell line) in the presence or absence of IFN-γ. To further characterize the involvement of CD40 in OLP, expression and distribution of receptor and ligand (CD40/CD154) in tissues from OLP were evaluated by immunohistochemistry. The present results are the first to show that both CD40 and CD86 are constitutively expressed at low levels in oral keratinocytes and that their expression was enhanced by IFN-γ stimulation. The intensity of CD40 staining in OLP tissues was strong. Taken together, the results strongly suggest that CD40 and CD86 play a role in the pathophysiology of oral inflammatory diseases such as OLP.

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Section: Discussionmentioning

confidence: 91%

Immune receptors CD40 and CD86 in oral keratinocytes and implications for oral lichen planus

et al. 2017

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“…Thus, other methods should be used to establish that lesional keratinocytes are already programmed by the inflammatory environment of the lesion to release chemokines in response to CD154. These may include engagement of CD40 by sCD154 in animals transgenically expressing human CD40 in keratinocytes 32 or in situ hybridization for chemokines in lesional skin transplanted into SCID mice that are infused with psoriatic T cells or sCD154.…”

Section: Discussionmentioning

confidence: 99%

In situ demonstration of CD40‐ and CD154‐positive cells in psoriatic lesions and keratinocyte production of chemokines by CD40 ligation in vitro

Pasch

Timár

Meurs

et al. 2004

The Journal of Pathology

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In psoriatic lesions, T cells and keratinocytes are in an activated state. Ligation of CD40 expressed on activated keratinocytes with CD154 expressed on activated T cells is thought to be involved in the pathogenesis of psoriasis. However, the presence of CD40(+) and CD154(+) cells in psoriatic skin has not been thoroughly studied. The present study has therefore examined their presence by immunohistochemistry in the lesional and non-lesional skin of ten patients. The influence of CD154-CD40 ligation on the release of chemokines (IL-8, RANTES, and MCP-1) and complement components (C3 and factor B) from keratinocytes was also investigated in vitro. Studies using single and double staining showed that clusters of CD40(+) keratinocytes were present in both lesional and non-lesional skin; CD40(+)CD1a(+) Langerhans cells in lesional, non-lesional, and normal skin; and numerous CD40(+)CD83(+) cells in lesional skin. CD1a(+) and CD83(+) cells always expressed CD40 strongly. Numerous T cells were seen in lesional skin. A small number of T cells expressed CD154. CD154(+) T cells were seen in the lesional epidermis of seven of ten patients-in six, in juxtaposition to CD40(+) cells including keratinocytes. In non-lesional epidermis, CD154(+) T cells were seen in two patients-in one, in juxtaposition to CD40(+) keratinocytes. In vitro studies showed that IFN-gamma-treated keratinocytes released small amounts of IL-8, RANTES, and MCP-1; ligation of these cells with CD154-transfected J558 cells or soluble CD154 greatly enhanced the release. This ligation did not enhance the release of C3 and factor B. These results warrant further studies on the role of CD40 ligation in the pathogenesis of psoriasis.

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“…Based on the coexpression of CD40, ICAM‐1 and Bcl‐x in keratinocytes, which colocalized with the influx of CD3+ T cells in psoriasis, these authors suggested that CD40 on keratinocytes may have implications for the pathogenesis of T‐cell‐mediated skin diseases. More recently, Fuller et al 31 . found evidence that CD40 engagement on keratinocytes, during the contact hypersensitivity response, exacerbated and prolonged the cutaneous immune reaction.…”

Section: Discussionmentioning

confidence: 99%

Evidence for modulation of human epidermal differentiation and remodelling by CD40

Concha¹,

Vidal²,

Moreno³

et al. 2003

Br J Dermatol

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The selective triggering of CD40 on keratinocytes in vivo enhances cell-mediated immunity

Cited by 10 publications

References 18 publications

Immune receptors CD40 and CD86 in oral keratinocytes and implications for oral lichen planus

Immune receptors CD40 and CD86 in oral keratinocytes and implications for oral lichen planus

In situ demonstration of CD40‐ and CD154‐positive cells in psoriatic lesions and keratinocyte production of chemokines by CD40 ligation in vitro

Evidence for modulation of human epidermal differentiation and remodelling by CD40

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