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Titolo:
Ultraviolet-radiation-induced keratinocyte apoptosis in C1q-deficient mice
Autore:
Pickering, MC; Fischer, S; Lewis, MR; Walport, MJ; Botto, M; Cook, HT;
Indirizzi:
Hammersmith Hosp, Imperial Coll, Sch Med, Div Med,Rheumatol Sect, London W12 0NN, England Hammersmith Hosp London England W12 0NN ol Sect, London W12 0NN, England Hammersmith Hosp, Imperial Coll, Sch Med, Dept Histopathol, London W12 0NN, England Hammersmith Hosp London England W12 0NN opathol, London W12 0NN, England
Titolo Testata:
JOURNAL OF INVESTIGATIVE DERMATOLOGY
fascicolo: 1, volume: 117, anno: 2001,
pagine: 52 - 58
SICI:
0022-202X(200107)117:1<52:UKAICM>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN EPIDERMAL-KERATINOCYTES; SYSTEMIC LUPUS-ERYTHEMATOSUS; NECROSIS-FACTOR-ALPHA; IN-VIVO; LANGERHANS CELLS; COMPLEMENT PROTEINS; INTERFERON-GAMMA; UV-RADIATION; SUNBURN CELL; A-431 CELLS;
Keywords:
autoimmunity; complement; skin; sunburn cell; systemic lupus erythematosus;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Pickering, MC Hammersmith Hosp, Imperial Coll, Sch Med, Div Med,Rheumatol Sect, Hammersmith Campus,Du Cane Rd, London W12 0NN, England Hammersmith Hosp Hammersmith Campus,Du Cane Rd London England W12 0NN
Citazione:
M.C. Pickering et al., "Ultraviolet-radiation-induced keratinocyte apoptosis in C1q-deficient mice", J INVES DER, 117(1), 2001, pp. 52-58

Abstract

Exposure to ultraviolet B radiation is an important trigger of both systemic and cutaneous disease flares in individuals with systemic lupus erythematosus, More than 90% of individuals with homozygous C1q deficiency develop a systemic-lupus-erythematosus-like illness, which is typically associated with a severe photosensitive rash, Apoptotic, human keratinocytes have beenshown in vitro to bind C1q, in the absence of antibody, These observations, together with the hypothesis that a major source of the autoantigens driving the immune response in systemic lupus erythematosus comes from apoptotic cells, led us to investigate the effects of murine C1q deficiency on ultraviolet-radiation-induced keratinocyte apoptosis in vivo. In this work, we demonstrated C1q binding to apoptotic murine keratinocytes in vitro and showed for the first time that C1q is also present on sunburn cells in vivo. In addition to C1q, we detected C3 deposition on sunburn cells in both wild-type and C1q-deficient mice, suggesting activation of the alternative pathway, Following acute ultraviolet exposure in vivo, no difference in the rateof clearance of sunburn cells was found ill C1q-deficient mice from three different genetic backgrounds, compared with strain-matched wild-type controls, Furthermore, chronic ultraviolet exposure did not result in the production of autoantibodies or the development of glomerulonephritis. Our findings suggest that C1q does not play a critical role in the physiologic clearance of apoptotic murine keratinocytes in vivo.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 16:07:14