Expression and localization of proteins of the complement system in human skin.

Dovezenski, Nebojša; Billetta, Rosario; Gigli, Irma

doi:10.1172/jci116080

Cited by 52 publications

(35 citation statements)

References 49 publications

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“…In control tissue, C3d was found diffuse in the epidermis as has been described earlier 21,22 ( Figure 1A, arrow I). Also, C3d positivity was found in the horn layer ( Figure 1A, arrow II).…”

Section: Resultssupporting

confidence: 80%

Acute Inflammation is Persistent Locally in Burn Wounds: A Pivotal Role for Complement and C-Reactive Protein

Goot

Krijnen

Begieneman

et al. 2009

Journal of Burn Care & Research

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Severe burns can cause major complications, such as infection and deforming scar formation. Burn wounds induce an excessive inflammatory response. Serum levels of complement and the acute phase reactant C-reactive protein (CRP) are upregulated in response to burn injury and have been shown to be related to the severity of burn trauma and to the clinical outcome. However, complement and CRP have not been investigated on a tissue level locally at the site of the burn trauma. Protein levels and localization of complement activation product C3d and CRP were determined semi-quantitatively in burn eschar between 2 and 46 days after injury, using immunohistochemistry. CD68 and myeloperoxidase (MPO), markers for macrophages and neutrophilic granulocytes, respectively, were also analyzed on these biopsies. Skin biopsies of very recent surgical wounds (seconds old) served as controls. C3d and CRP are present at high levels in the burn wound. Protein levels of both mediators are significantly elevated up to at least 46 days after injury in comparison with control wounds. In line with this, neutrophils and macrophages infiltrate the burn wound in high numbers up to at least 46 days after injury. The excessive presence of the inflammatory mediators, complement and CRP, and the increased infiltration of neutrophils and macrophages in burn woundsup to 46 days after injury implicate a persistent ongoing acute inflammation locally in the burn wound up to weeks after the initial trauma. (J Burn Care Res 2009;30:274 -280)

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Section: Resultssupporting

confidence: 80%

Acute Inflammation is Persistent Locally in Burn Wounds: A Pivotal Role for Complement and C-Reactive Protein

Goot

Krijnen

Begieneman

et al. 2009

Journal of Burn Care & Research

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“…DAF, MCP, and CD59 are present on keratinocytes in the human skin as seen in situ in previous immunohistochemical studies (Dovezenski et al, 1992;Venneker et al, 1994). This study shows surface expression of DAF, MCP, and CD59 on cultured keratinocytes.…”

Section: Discussionsupporting

confidence: 80%

“…Keratinocytes have C-regulatory proteins embedded in their membranes to prevent this damage (Sayama et al, 1991;Dovezenski et al, 1992;Venneker et al, 1994). These include decay accelerating factor (DAF; CD55), membrane cofactor protein (MCP; CD46), and CD59 (Liszewski et al, 1996).…”

mentioning

confidence: 99%

Effects of UVB on the Synthesis of Complement Proteins by Keratinocytes

Pasch

Okada

Bos³

et al. 1998

Journal of Investigative Dermatology

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UVB exposure of the skin results in increased production of several cytokines by keratinocytes and infiltration of inflammatory cells. We hypothesized that UVB may increase the expression of complement (C) components and C-regulatory proteins by keratinocytes. In vivo, UVB may upregulate these proteins by direct effects or via cytokines released by keratinocytes or infiltrating inflammatory cells. In vitro, UVB may upregulate these proteins only directly, because of dilution of released cytokines in the medium. To test this, we exposed cultured human keratinocytes to UVB (0-64 J per m2) and monitored C3 and Factor B release in the medium by enzyme-linked immunosorbent assay, and surface expression of decay accelerating factor, membrane cofactor protein, and CD59 by flow cytometry. Keratinocytes produced small amounts of C3 and Factor B, which remained unaffected by UVB. UVB (32 J per m2) caused a transient upregulation of all three C-regulatory proteins. Decay accelerating factor expression was maximal at 48 h (1.81 +/- 0.06-fold increase in mean fluorescence intensity over nonexposed cells), membrane cofactor protein at 72 h (2.13 +/- 0.09-fold increase in mean fluorescence intensity), and CD59 at 120 h (1.96 +/- 0.09-fold increase in mean fluorescence intensity), returning to baseline values within 96, 192, and 192 h, respectively. Exposure to 64 J per m2 resulted in significant cell death; cells surviving this dose up to 48 h expressed a higher level of all the three proteins than those surviving 32 J per m2. In conclusion, UVB upregulated membrane cofactor protein, decay accelerating factor, and CD59 on keratinocytes without affecting the constitutive release of C3 and Factor B. Thus, UVB can increase the resistance of keratinocytes against their own C known to be produced excessively in response to cytokines of inflammatory cells that infiltrate the skin following UVB exposure.

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“…This ability to activate complement has been suggested as a mechanism responsible for the inflammation associated with seborrheic dermatitis (SD). The proteins involved in the initial steps of the alternative complement pathway are known to be present in the skin (117), and complement-mediated inflammation is associated with many dermatoses, including bullous pemphigoid (198), acne vulgaris (390), and psoriasis (410). Immunohistochemical studies of SD have found that deposits of C3 are present in the lesions, localized solely around the collections of Malassezia cells, and are absent from uninvolved skin (334).…”

Section: Activation Of the Complement Cascadementioning

confidence: 99%

Immunology of Diseases Associated withMalasseziaSpecies

2002

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SUMMARY Malassezia species are members of the human cutaneous commensal flora, in addition to causing a wide range of cutaneous and systemic diseases in suitably predisposed individuals. Studies examining cellular and humoral immune responses specific to Malassezia species in patients with Malassezia-associated diseases and healthy controls have generally been unable to define significant differences in their immune response. The use of varied antigenic preparations and strains from different Malassezia classifications may partly be responsible for this, although these problems can now be overcome by using techniques based on recent work defining some important antigens and also a new taxonomy for the genus. The finding that the genus Malassezia is immunomodulatory is important in understanding its ability to cause disease. Stimulation of the reticuloendothelial system and activation of the complement cascade contrasts with its ability to suppress cytokine release and downregulate phagocytic uptake and killing. The lipid-rich layer around the yeast appears to be pivotal in this alteration of phenotype. Defining the nonspecific immune response to Malassezia species and the way in which the organisms modulate it may well be the key to understanding how Malassezia species can exist as both commensals and pathogens.

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Expression and localization of proteins of the complement system in human skin.

Cited by 52 publications

References 49 publications

Acute Inflammation is Persistent Locally in Burn Wounds: A Pivotal Role for Complement and C-Reactive Protein

Acute Inflammation is Persistent Locally in Burn Wounds: A Pivotal Role for Complement and C-Reactive Protein

Effects of UVB on the Synthesis of Complement Proteins by Keratinocytes

Immunology of Diseases Associated withMalasseziaSpecies

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