The pathogenic role of tissue-resident immune cells in psoriasis

被引:106
作者
Boyman, Onur [1 ]
Conrad, Curdin
Tonel, Giulia
Gilliet, Michel
Nestle, Frank O.
机构
[1] Univ Lausanne Hosp CHUV, Div Immunol & Allergy, CH-1011 Lausanne, Switzerland
[2] Univ Zurich Hosp, Dept Dermatol, CH-8091 Zurich, Switzerland
[3] Univ Texas, MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA
[4] Kings Coll London, Sch Med, Div Med & Mol Genet, St Johns Inst Dermatol, London SE1 9RT, England
基金
英国惠康基金; 美国国家卫生研究院;
关键词
NECROSIS-FACTOR-ALPHA; CHRONIC PLAQUE PSORIASIS; DERMAL DENDRITIC CELLS; NORMAL HUMAN-SKIN; T-CELLS; RHEUMATOID-ARTHRITIS; RANDOMIZED-TRIAL; AUTOIMMUNE-DISEASE; IMPROVES PSORIASIS; INTERFERON-GAMMA;
D O I
10.1016/j.it.2006.12.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Psoriasis is a common chronic inflammatory skin disease, the study of which might also be of considerable value to the understanding of other inflammatory and autoimmune-type diseases, such as rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis and diabetes mellitus. There is clear evidence that T cells and dendritic cells have a central role in psoriasis. Based on recent data from humans and animal models, we propose that a psoriasis lesion can be triggered and sustained by the local network of skin-resident immune cells. This concept focuses attention on local, rather than systemic, components of the immune system for rationalized therapeutic approaches of psoriasis and possibly also other chronic inflammatory diseases.
引用
收藏
页码:51 / 57
页数:7
相关论文
共 79 条
[1]  
Albanesi Cristina, 2005, Current Drug Targets - Inflammation and Allergy, V4, P329, DOI 10.2174/1568010054022033
[2]   The major psoriasis susceptibility locus PSORS1 is not a risk factor for late-onset psoriasis [J].
Allen, MH ;
Ameen, H ;
Veal, C ;
Evans, J ;
Ramrakha-Jones, VS ;
Marsland, AM ;
Burden, AD ;
Griffiths, CEM ;
Trembath, RC ;
Barker, JNWN .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2005, 124 (01) :103-106
[3]   The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-γ, interleukin-2, and tumor necrosis factor-α, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations:: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients [J].
Austin, LM ;
Ozawa, M ;
Kikuchi, T ;
Walters, IB ;
Krueger, JG .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1999, 113 (05) :752-759
[4]   Treatment of recalcitrant plaque psoriasis with a humanized non-depleting antibody to CD4 [J].
Bachelez, H ;
Flageul, B ;
Dubertret, L ;
Fraitag, S ;
Grossman, R ;
Brousse, N ;
Poisson, D ;
Knowles, RW ;
Wacholtz, MC ;
Haverty, TP ;
Chatenoud, L ;
Bach, JF .
JOURNAL OF AUTOIMMUNITY, 1998, 11 (01) :53-62
[5]   Anti-E-selectin is ineffective in the treatment of psoriasis: a randomized trial [J].
Bhushan, M ;
Bleiker, TO ;
Ballsdon, AE ;
Allen, MH ;
Sopwith, M ;
Robinson, MK ;
Clarke, C ;
Weller, RPJB ;
Graham-Brown, RAC ;
Keefe, M ;
Barker, JNWN ;
Griffiths, CEM .
BRITISH JOURNAL OF DERMATOLOGY, 2002, 146 (05) :824-831
[6]   Psoriasis: dysregulation of innate immunity [J].
Bos, JD ;
de Rie, MA ;
Teunissen, MBM ;
Piskin, G .
BRITISH JOURNAL OF DERMATOLOGY, 2005, 152 (06) :1098-1107
[7]   THE SKIN IMMUNE-SYSTEM (SIS) - DISTRIBUTION AND IMMUNOPHENOTYPE OF LYMPHOCYTE SUBPOPULATIONS IN NORMAL HUMAN-SKIN [J].
BOS, JD ;
ZONNEVELD, I ;
DAS, PK ;
KRIEG, SR ;
VANDERLOOS, CM ;
KAPSENBERG, ML .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1987, 88 (05) :569-573
[8]   The immunological and genetic basis of inflammatory bowel disease [J].
Bouma, G ;
Strober, W .
NATURE REVIEWS IMMUNOLOGY, 2003, 3 (07) :521-533
[9]   Selective stimulation of T cell subsets with antibody-cytokine immune complexes [J].
Boyman, O ;
Kovar, M ;
Rubinstein, MP ;
Surh, CD ;
Sprent, J .
SCIENCE, 2006, 311 (5769) :1924-1927
[10]   Spontaneous development of psoriasis in a new animal model shows an essential role for resident T cells and tumor necrosis factor-α [J].
Boyman, O ;
Hefti, HP ;
Conrad, C ;
Nickoloff, BJ ;
Suter, M ;
Nestle, FO .
JOURNAL OF EXPERIMENTAL MEDICINE, 2004, 199 (05) :731-736