Inflammasome activation and vitiligo/nonsegmental vitiligo progression
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M. Picardo | T. Jouary | M. Cario-André | K. Ezzedine | C. Cota | A. Taieb | D. Kovacs | C. Pain | B. Vergier | Alain Taïeb | J. Marié | Carlo Cota
[1] M. Mansuri,et al. Association of NLRP1 genetic variants and mRNA overexpression with generalized vitiligo and disease activity in a Gujarat population , 2013, The British journal of dermatology.
[2] A. Alkhateeb,et al. Polymorphisms in NLRP1 gene and susceptibility to autoimmune thyroid disease , 2013, Autoimmunity.
[3] R. Spritz,et al. NLRP1 haplotypes associated with vitiligo and autoimmunity increase interleukin-1β processing via the NLRP1 inflammasome , 2013, Proceedings of the National Academy of Sciences.
[4] Shi Weimin,et al. Global Activation of CD8+ Cytotoxic T Lymphocytes Correlates with an Impairment in Regulatory T Cells in Patients with Generalized Vitiligo , 2012, PloS one.
[5] M. Picardo,et al. Revised classification/nomenclature of vitiligo and related issues: the Vitiligo Global Issues Consensus Conference , 2012, Pigment cell & melanoma research.
[6] A. Taïeb. Vitiligo as an inflammatory skin disorder: a therapeutic perspective , 2012, Pigment cell & melanoma research.
[7] T. Jouary,et al. Multivariate analysis of factors associated with early‐onset segmental and nonsegmental vitiligo: a prospective observational study of 213 patients , 2011, The British journal of dermatology.
[8] S. Deo,et al. GENETIC VARIATIONS IN NALP1 MRNA EXPRESSIONS IN HUMAN VITILIGO , 2011, Indian journal of dermatology.
[9] Dariush Moussai,et al. Th17 Cells and Activated Dendritic Cells Are Increased in Vitiligo Lesions , 2011, PloS one.
[10] G. Girolomoni,et al. The Role of Innate Immunity in Vitiligo , 2010 .
[11] B. Lie,et al. A coding polymorphism in NALP1 confers risk for autoimmune Addison's disease and type 1 diabetes , 2009, Genes and Immunity.
[12] J. Tschopp,et al. The inflammasome: a danger sensing complex triggering innate immunity. , 2007, Current opinion in immunology.
[13] A. Taïeb. NALP1 and the inflammasomes: challenging our perception of vitiligo and vitiligo-related autoimmune disorders. , 2007, Pigment cell research.
[14] S. Werner,et al. The Inflammasome Mediates UVB-Induced Activation and Secretion of Interleukin-1β by Keratinocytes , 2007, Current Biology.
[15] F. Martinon,et al. Inflammasome Components NALP 1 and 3 Show Distinct but Separate Expression Profiles in Human Tissues Suggesting a Site-specific Role in the Inflammatory Response , 2007, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.
[16] Sheri L. Riccardi,et al. NALP1 in vitiligo-associated multiple autoimmune disease. , 2007, The New England journal of medicine.
[17] M. Picardo,et al. The definition and assessment of vitiligo: a consensus report of the Vitiligo European Task Force. , 2007, Pigment cell research.
[18] R. Boissy,et al. 4-Tertiary butyl phenol exposure sensitizes human melanocytes to dendritic cell-mediated killing: relevance to vitiligo. , 2005, The Journal of investigative dermatology.
[19] W. Westerhof,et al. Local Immune Response in Skin of Generalized Vitiligo Patients , 2000, Laboratory Investigation.
[20] T. Egelrud,et al. Biologically active, alternatively processed interleukin‐1β in psoriatic scales , 1997 .
[21] T. Egelrud,et al. Biologically active, alternatively processed interleukin-1 beta in psoriatic scales. , 1997, European journal of immunology.
[22] J. Garioch,et al. An immunohistological study of cutaneous lymphocytes in vitiligo , 1993, The Journal of pathology.
[23] J. Bystryn,et al. Relation between the incidence and level of pigment cell antibodies and disease activity in vitiligo. , 1991, The Journal of investigative dermatology.
[24] G. Naughton,et al. Correlation between vitiligo antibodies and extent of depigmentation in vitiligo. , 1986, Journal of the American Academy of Dermatology.
[25] G. Naughton,et al. Detection of antibodies to melanocytes in vitiligo by specific immunoprecipitation. , 1983, The Journal of investigative dermatology.