MFV3D Book Archive > Nonfiction 9 > Download Cutaneous Lupus Erythematosus by Thomas M. Herndon, George C. Tsokos (auth.), Priv.-Doz. Dr. PDF

Download Cutaneous Lupus Erythematosus by Thomas M. Herndon, George C. Tsokos (auth.), Priv.-Doz. Dr. PDF

By Thomas M. Herndon, George C. Tsokos (auth.), Priv.-Doz. Dr. Annegret Kuhn, Prof. Dr. Percy Lehmann, Prof. Dr. Dr. H.C. Thomas Ruzicka (eds.)

Lupus erythematosus is a prolonged inflammatory autoimmune disorder characterised by means of a large spectrum of manifestations with a variable evolution. there was a long-standing desire for a booklet with a unifying thought at the cutaneous manifestations of this illness. The booklet relies on multidisciplinary wisdom and is written by means of top clinicians and scientists. It offers not just a entire description of the big number of cutaneous abnormalities but additionally a synthesis of the connection among cutaneous and systemic alterations, together with chapters on type and scientific points, pathogenesis and pathologic beneficial properties, and therapy and administration of lupus erythematosus. In precis, the publication is a crucial source for clinicians and scientists operating within the box of autoimmune diseases.

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1996, Schmitt et al. 2000). On the other hand, one should not forget the evidence of extranuclear cellular UVB targets involved in photoimmunology. UVB radiation effects the release Photoimmunology 27 of many cytokines, which can modulate immune responses and may also interfere with the biological activities of immune mediators, whether they be depletion or alteration of the functionality of antigen-presenting or T cells. For example, UVB irradiation interferes with the signal transduction pathway of interferon-γ and IL-2, both important immunomodulatory cytokines (Aragane et al.

1996, Ullrich 1994). These findings are in agreement with the observation that spleen cells from UVBtreated mice are unable to present antigen to Th1 cells, whereas antigen presentation to Th2 cells was even enhanced (Ullrich 1994). Abrogation of both effects was achieved by application of neutralizing anti-IL-10 antibodies. To directly address the role of IL-10 in UV-induced systemic immunosuppression, IL-10-deficient mice were used (Beissert et al. 1996). The induction of DTH responses in IL-10-deficient mice could not be suppressed by UVB irradiation, whereas the induction of CHS responses was suppressed after UVB exposure.

Further supporting data were provided by studies in which the release of the cytokines IL-10 and TNF-α triggered by UV irradiation of keratinocytes was considerably suppressed after treatment with T4N5 (Kibitel et al. 1991, Nishigori et al. 1996). Further evidence was made available by studies conducted in a mouse model in which essential components of the nucleotide excision repair system, the endogenous repair system, were knocked out (Boonstra et al. 2001). These animals are more susceptible to UV-induced immunosuppression, and these studies underlined that both global and transcription-coupled repair are needed to mitigate immunomodulation by UVB.

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