The pathophysiology of photosensitivity in lupus erythematosus

Orteu, Catherine H.; Sontheimer, Richard D.; Dutz, Jan P.

doi:10.1034/j.1600-0781.2001.170301.x

Cited by 43 publications

(30 citation statements)

References 271 publications

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“…Within the skin, these cytokines are thought to be produced predominately by keratinocytes and activated T cells (8,17,18). LT␣3, defined as having similar biological activity as TNF-␣, is also found to be expressed on activated keratinocytes and T cells in skin tissue, suggesting that the interaction of LT␣3 singling may also be involved in the induction of keratinocyte destruction (24).…”

Section: Discussionmentioning

confidence: 99%

“…Regulation by members of the TNF superfamily of the expression of adhesion molecules has been well established (8,27,28). Both LT␣3 and TNF-␣ can up-regulate the expression of adhesion molecules such as ICAM-1 in vitro (8).…”

Section: Discussionmentioning

confidence: 99%

“…Local primary inflammatory cytokines such as TNF-␣ and IL-1 can play important roles in the induction of keratinocyte destruction via directly damaging local tissues and attracting inflammatory cells (5,8,17,18,23). Within the skin, these cytokines are thought to be produced predominately by keratinocytes and activated T cells (8,17,18).…”

Section: Discussionmentioning

confidence: 99%

“…Keratinocyte apoptosis can be induced by autoreactive T cells and local inflammatory cytokines (8,(17)(18)(19). The presence of apoptotic keratinocytes is a useful early diagnostic criterion for GVHD.…”

Section: Lt␤r-ig Treatment Inhibits Epidermal Keratinocyte Apoptosismentioning

confidence: 99%

“…TNF-␣, a member of the TNF superfamily, plays a crucial enhancing role in the expression of adhesion molecules on dermal microvessels during the development of lichenoid cutaneous lesions (5,8). However, blockade of the TNF pathway with anti-TNF Abs has been unable to completely prevent the expression of GVHSD, suggesting that other inflammatory cytokines could be involved in the pathogenesis of lichenoid cutaneous lesions.…”

mentioning

confidence: 99%

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Blockade of Lymphotoxin Signaling Inhibits the Clinical Expression of Murine Graft-versus-Host Skin Disease

Sontheimer

2004

The Journal of Immunology

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Adhesion molecules are essential for the recruitment of T cells into the skin during the development of graft-vs-host skin disease (GVHSD). However, the mechanisms responsible for the regulation of expression of cutaneous adhesion molecules in this setting are still poorly understood. In this study we blocked lymphotoxin (LT) signaling in a murine model of minor histocompatibility Ag system mismatch GVHSD by using an LTβ receptor-Ig fusion protein (LTβR-Ig). The recipient mice treated with control human Ig developed clinically apparent, severe skin lesions. However, none of the mice treated with LTβR-Ig developed clinical skin disease. The expression of ICAM-1 in cutaneous tissue was also much lower in mice treated with LTβR-Ig than in mice treated with human Ig. Thus, the inhibition of LT signaling via LTβR-Ig treatment appears to be capable of markedly ameliorating the development of GVHSD, possibly by inhibiting the expression of adhesion molecules.

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