IL-4 Suppresses UVB-induced Apoptosis in Skin

Hwang, Ha Young; Choi, Soo Young; Kim, Tae Yoon

doi:10.5483/bmbrep.2007.40.1.036

Cited by 7 publications

(6 citation statements)

References 20 publications

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“…Interestingly, the UVB-irradiated HaCaT cells did not release significant quantities of representative Th2 cytokines such as IL-4 and IL-10. In relation to this, Hwang et al (2007) have demonstrated that IL-4 suppresses UVB-induced apoptosis in murine skin irradiated at 200 mJ/cm 2 . It is also been known that an imbalance between Th1 and Th2 cytokines may induce abnormal immunological responses (Jacobson et al, 1997;Thompson, 1995).…”

Section: Discussionmentioning

confidence: 96%

Release of cytokines/chemokines and cell death in UVB‐irradiated human keratinocytes, HaCaT

Yoshizumi

Nakamura

Katô

et al. 2008

Cell Biology International

126

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Ultraviolet (UV) B can lead to inflammatory responses such as sunburn, which involves the production of various inflammatory cytokines and chemokines, and the induction of cell death. Keratinocytes in the skin has one of the highest risks of exposure to UV. However, the detailed mechanisms underlying UVB irradiation-induced inflammation and cell death are not well known. Thus, we investigated the effect of UVB irradiation on the production of various cytokines/chemokines and the induction of cell death in UVB-irradiated human keratinocytes (HaCaT cells). We evaluated 11 cytokines/chemokines in cell culture supernatants from HaCaT cells exposed to 0-400 mJ/cm(2) UVB irradiation. UVB at a dose 400 mJ/cm(2) induced the release of various cytokines; interleukin (IL)-1beta, IL-6, IL-8, interferon (IFN)-gamma, granulocyte-colony stimulating factor (G-CSF), macrophage inflammatory protein (MIP)-1beta, and tumor necrosis factor (TNF)-alpha. These results suggest that UVB irradiation-induced the release of several cytokines/chemokines and led to cell death in human keratinocytes. UV exposure may be associated with multiple physiological events in the human skin.

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Section: Discussionmentioning

confidence: 96%

Release of cytokines/chemokines and cell death in UVB‐irradiated human keratinocytes, HaCaT

Yoshizumi

Nakamura

Katô

et al. 2008

Cell Biology International

126

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“…This may be attributed to the anti-apoptotic role of IL4 signalling [35]. Overexpression of IL4 in mouse keratinocytes prevented UVB-irradiation induced apoptosis, and in vitro treatment of normal human epithelial cells with IL4 induced the expression of anti-apoptotic proteins and reduced apoptosis by cytotoxic drugs [36], [37]. Increased apoptosis of keratinocytes in Sharpin cpdm-Dem , Il4ra −/− mice may lead to greater release of pro-inflammatory danger molecules and increased dermatitis.…”

Section: Discussionmentioning

confidence: 99%

Chronic Proliferative Dermatitis in Sharpin Null Mice: Development of an Autoinflammatory Disease in the Absence of B and T Lymphocytes and IL4/IL13 Signaling

et al. 2014

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SHARPIN is a key regulator of NFKB and integrin signaling. Mice lacking Sharpin develop a phenotype known as chronic proliferative dermatitis (CPDM), typified by progressive epidermal hyperplasia, apoptosis of keratinocytes, cutaneous and systemic eosinophilic inflammation, and hypoplasia of secondary lymphoid organs. Rag1−/− mice, which lack mature B and T cells, were crossed with Sharpin−/− mice to examine the role of lymphocytes in CDPM. Although inflammation in the lungs, liver, and joints was reduced in these double mutant mice, dermatitis was not reduced in the absence of functional lymphocytes, suggesting that lymphocytes are not primary drivers of the inflammation in the skin. Type 2 cytokine expression is increased in CPDM. In an attempt to reduce this aspect of the phenotype, Il4ra−/− mice, unresponsive to both IL4 and IL13, were crossed with Sharpin−/− mice. Double homozygous Sharpin−/−, Il4ra−/− mice developed an exacerbated granulocytic dermatitis, acute system inflammation, as well as hepatic necrosis and mineralization. High expression of CHI3L4, normally seen in CPDM skin, was abolished in Sharpin−/−, Il4ra−/− double mutant mice indicating the crucial role of IL4 and IL13 in the expression of this protein. Cutaneous eosinophilia persisted in Sharpin−/−, Il4ra−/− mice, although expression of Il5 mRNA was reduced and the expression of Ccl11 and Ccl24 was completely abolished. TSLP and IL33 were both increased in the skin of Sharpin−/− mice and this was maintained in Sharpin−/−, Il4ra−/− mice suggesting a role for TSLP and IL33 in the eosinophilic dermatitis in SHARPIN-deficient mice. These studies indicate that cutaneous inflammation in SHARPIN-deficient mice is autoinflammatory in nature developing independently of B and T lymphocytes, while the systemic inflammation seen in CPDM has a strong lymphocyte-dependent component. Both the cutaneous and systemic inflammation is enhanced by loss of IL4 and IL13 signaling indicating that these cytokines normally play an anti-inflammatory role in SHARPIN-deficient mice.

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“…Previous studies demonstrated the occurrence of UVB-stimulated apoptosis in the mouse skin (Chun et al 2007, Hwang et al 2007). Therefore, we investigated the expression pattern Figure 2.…”

Section: Phloroglucinol Down-regulates the Expression Of Apoptotic Mementioning

confidence: 98%

Phloroglucinol inhibits ultraviolet B radiation-induced oxidative stress in the mouse skin

Piao¹,

Ahn²,

Kang³

et al. 2014

International Journal of Radiation Biology

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IL-4 Suppresses UVB-induced Apoptosis in Skin

Cited by 7 publications

References 20 publications

Release of cytokines/chemokines and cell death in UVB‐irradiated human keratinocytes, HaCaT

Release of cytokines/chemokines and cell death in UVB‐irradiated human keratinocytes, HaCaT

Chronic Proliferative Dermatitis in Sharpin Null Mice: Development of an Autoinflammatory Disease in the Absence of B and T Lymphocytes and IL4/IL13 Signaling

Phloroglucinol inhibits ultraviolet B radiation-induced oxidative stress in the mouse skin

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