TWEAK/Fn14 Activation Participates in Skin Inflammation

Table 1

The action of TWEAK in different skin diseases.

Diseases	Effect on target cells or animal models	References
Psoriasis	KC: to enhance chemokine expression and cell proliferation	[22, 65]
	Murine model: to induce immune cell infiltrates in lesional skin
AD	KC: to increase TNF-α expression and induce apoptosis	[28, 65]
	Dermal fibroblast: to regulate chemokine expression
	Murine model: to induce cellular infiltrates, migration of immune cells, and chemokine expression
Cutaneous vasculitis	HMEC: to regulate NF-κB activation and chemokine production	[71, 92]
	Murine model: to induce endothelial damage and perivascular leukocyte infiltrates
HPV infection	KC: to enhance TNFR2 expression and cell proliferation	[64]
Carcinogenesis	Various tumor cells: to induce cell proliferation or apoptosis in a cytokine-dependent way	[64, 112, 113]
	Glioma cells: to promote cell migration and invasion
	KC: to induce cell proliferation
	Vascular ECs: to upregulate FGF-2 and VEGF-A expression and to promote angiogenesis
Cutaneous lupus erythematosus	KC: to enhance Ro52 and proinflammatory cytokine expression and induce apoptosis	[70, 109]
	Macrophage: to enhance chemoattraction and cytokine expression (including TWEAK)
	MRL/lpr mice: to induce chemokine production, cell infiltration, and apoptosis
Systemic sclerosis	Monocytes/macrophages: to lead to greater extent of skin fibrosis or to exert as a protective role against fibrosis	[111, 114]
Polymyositis & dermatomyositis	Myoblast: to induce degradation of myosin heavy chain, to affect cell proliferation and differentiation, and to induce metabolic abnormalities	[107, 115, 116]
	Murine model: to induce muscle atrophy and interstitial fibrosis
Bullous pemphigoid	KC: to reduce BP180 expression and suppresses cell adhesion	[8]