Evaluation of ATPase-positive Langerhans' cells in skin lesions of lupus erythematosus and experimentally induced inflammations

Kanauchi, Hideo; Furukawa, Fukumi; Imamura, Sadao

doi:10.1007/bf00412976

Cited by 10 publications

(7 citation statements)

References 21 publications

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“…CD40/CD40L interactions may play an important role in this cross-talk [41]. In this regard, we found that skin dendritic cells including Langerhans cells, which are known to infiltrate the dermis during the active stages of spontaneous skin lesions in SLE [3,33], were significantly increased in CD1d KO MRL-lpr mice (Fig. 1D, E).…”

Section: Discussionmentioning

confidence: 70%

“…Organ weights and cellularity of thymus (A), liver (B) and spleen, axillary lymph nodes (ALN) and mesenteric lymph nodes (MLN) (C) are shown as the mean ± SE in CD1d-deficient and WT MRL-lpr mice. [3,33]. To investigate if exacerbation of skin disease in CD1d KO mice is associated with an expansion of these cell types, we performed immunohistochemistry to detect resident skin dendritic cells (Fig.…”

Section: Figmentioning

confidence: 99%

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CD1d deficiency exacerbates inflammatory dermatitis in MRL‐lpr/lpr mice

et al. 2004

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Mechanisms responsible for the development of autoimmune skin disease in humans and animal models with lupus remain poorly understood. In this study, we have investigated the role of CD1d, an antigen-presenting molecule known to activate natural killer T cells, in the development of inflammatory dermatitis in lupus-susceptible MRL-lpr/lpr mice. In particular, we have established MRL-lpr/lpr mice carrying a germ-line deletion of the CD1d genes. We demonstrate that CD1d-deficient MRL-lpr/lpr mice, as compared with wild-type littermates, have more frequent and more severe skin disease, with increased local infiltration with mast cells, lymphocytes and dendritic cells, including Langerhans cells. CD1d-deficient MRL-lpr/ lpr mice had increased prevalence of CD4 + T cells in the spleen and liver and of TCR § g + B220 + cells in lymph nodes. Furthermore, CD1d deficiency was associated with decreased T cell production of type 2 cytokines and increased or unchanged type 1 cytokines. These findings indicate a regulatory role of CD1d in inflammatory dermatitis. Understanding the mechanisms by which CD1d deficiency results in splenic T cell expansion and cytokine alterations, with increased dermal infiltration of dendritic cells and lymphocytes in MRL-lpr/lpr mice, will have implications for the pathogenesis of inflammatory skin diseases.

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Section: Discussionmentioning

confidence: 70%

Section: Figmentioning

confidence: 99%

CD1d deficiency exacerbates inflammatory dermatitis in MRL‐lpr/lpr mice

et al. 2004

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“…CD4 and CD8 cells in skin lesions of SLE patients. Cells were counted according to a method described previously (18]. Results are expressed as the mean + I SD from 24 cases.…”

Section: Resultsmentioning

confidence: 99%

Susceptibility to UVB Light in Cultured Keratinocytes of Cutaneous Lupus erythematosus

1994

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In this study, we investigated UVB-light-induced cytotoxicity and the binding of antibodies to extractable nuclear antigens on cultured keratinocytes from patients with cutaneous lupus erythematosus (LE). Keratinocytes from cutaneous LE patients showed a higher susceptibility to single-dose UVB light irradiation compared to keratinocytes from normal controls. The binding of antibodies to U1RNP and Ro/SS-A antigens on cultured keratinocytes was induced by UVB light and more up-regulated when cultured keratinocytes were reacted with autologous sera. Antibody-dependent cellular cytotoxicity (ADCC) was induced when cultured keratinocytes irradiated with UVB light were combined with autologous sera, using peripheral mononuclear cells of normal controls. Immunohistochemical studies of skin biopsy specimens from patients with systemic LE revealed an increased number of epidermal Langerhans cells at the peripheral sites of skin lesions and a relative dominance of infiltrative CD8-positive lymphocytes in the central area of skin lesions. Based on these findings we suggested that ADCC mechanisms were involved in the development of skin lesions, and the distribution of Langerhans cells and infiltrated CD8 cells were responsible for the expansion and persistence of lesions.

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“…The unique APC subsets present in different organs, which may be differentially regulated by NKT cells, may contribute to the differential effect on various tissues in the MRL-lpr model. For example, Langerhans cells, the unique APC subset in the skin, infiltrate the dermis during the active and early stages of spontaneous skin lesions in humans with SLE and MRL-lpr mice (3,32). These cells as well as macrophages and keratinocytes are activated in the skin lesions of MRL-lpr mice, as evidenced by increased expression of MHC class II Ags (3,33).…”

Section: Treatment With ␣-Galcer Ameliorates Lupus Dermatitismentioning

confidence: 99%

Repeated α-Galactosylceramide Administration Results in Expansion of NK T Cells and Alleviates Inflammatory Dermatitis in MRL-lpr/lpr Mice

Yang

Saxena

et al. 2003

The Journal of Immunology

117

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NK T (NKT) cells expressing the invariant Vα14-Jα18 TCR α-chain recognize glycolipid Ags such as α-galactosylceramide (α-GalCer) presented by the MHC class I-like molecule CD1d. Upon activation by α-GalCer, invariant NKT cells secrete multiple cytokines and confer protection in certain immune-mediated disorders. Here we have investigated the role of NKT cells in the development of inflammatory dermatitis in MRL-lpr/lpr mice, which shares features with lupus in humans. Our results show that the numbers Sand functions of NKT (TCRβ+CD1d/α-GalCer tetramer+) cells, particularly of the NK1.1− subset, are reduced in MRL-lpr/lpr mice compared with MRL-fas/fas and/or nonautoimmune C3H/Hej and BALB/c mice. Repeated treatments with α-GalCer result in the expansion of NKT cells and alleviate dermatitis in MRL-lpr/lpr mice. Our results indicate that NKT cell deficiency can be corrected by repeated α-GalCer treatment and that NKT cells may play a protective role in inflammatory dermatitis of lupus-prone mice.

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Evaluation of ATPase-positive Langerhans' cells in skin lesions of lupus erythematosus and experimentally induced inflammations

Cited by 10 publications

References 21 publications

CD1d deficiency exacerbates inflammatory dermatitis in MRL‐lpr/lpr mice

CD1d deficiency exacerbates inflammatory dermatitis in MRL‐lpr/lpr mice

Susceptibility to UVB Light in Cultured Keratinocytes of Cutaneous Lupus erythematosus

Repeated α-Galactosylceramide Administration Results in Expansion of NK T Cells and Alleviates Inflammatory Dermatitis in MRL-lpr/lpr Mice

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