Lymphocyte activation in the pathogenesis of psoriasis.

[1]  S. Ziegler,et al.  The repertoire of T cell antigen receptor beta-chain variable regions associated with psoriasis vulgaris. , 1997, The Journal of investigative dermatology.

[2]  I. Eperon,et al.  Selective amplification of T-cell receptor variable region species is demonstrable but not essential in early lesions of psoriasis vulgaris: analysis by anchored polymerase chain reaction and hypervariable region size spectratyping. , 1997, The Journal of investigative dermatology.

[3]  M. Detmar,et al.  Murine psoriasis-like disorder induced by naive CD4+ T cells , 1997, Nature Medicine.

[4]  B. Nickoloff,et al.  Dermal injection of immunocytes induces psoriasis. , 1996, The Journal of clinical investigation.

[5]  D. Leung,et al.  Staphylococcal toxins and protein A differentially induce cytotoxicity and release of tumor necrosis factor-alpha from human keratinocytes. , 1996, The Journal of investigative dermatology.

[6]  T. Zollner,et al.  Pulling the trigger on psoriasis , 1996, Nature.

[7]  J. Travers,et al.  Evidence for a streptococcal superantigen-driven process in acute guttate psoriasis. , 1995, The Journal of clinical investigation.

[8]  A. Menssen,et al.  Evidence for an antigen-specific cellular immune response in skin lesions of patients with psoriasis vulgaris. , 1995, Journal of immunology.

[9]  D. Carlo,et al.  CD8+ T‐Cells in Psoriatic Lesions Preferentially Use T‐Cell Receptors Vβ3 and/or Vβ13.1 Genes , 1995 .

[10]  J. Travers,et al.  The role of superantigens in skin disease. , 1995, The Journal of investigative dermatology.

[11]  B. Böhm,et al.  T-Cell-Receptor Repertoire in Chronic Plaque-Stage Psoriasis Is Restricted and Lacks Enrichment of Superantigen-Associated Vβ Regions , 1995 .

[12]  James G. Krueger,et al.  Response of psoriasis to a lymphocyte-selective toxin (DAB389IL-2) suggests a primary immune, but not keratinocyte, pathogenic basis , 1995, Nature Genetics.

[13]  I. Jónsdóttir,et al.  Psoriasis: a T-cell-mediated autoimmune disease induced by streptococcal superantigens? , 1995, Immunology today.

[14]  L. Picker,et al.  Bacterial superantigens induce T cell expression of the skin-selective homing receptor, the cutaneous lymphocyte-associated antigen, via stimulation of interleukin 12 production , 1995, The Journal of experimental medicine.

[15]  A. Menssen,et al.  T lymphocytes derived from skin lesions of patients with psoriasis vulgaris express a novel cytokine pattern that is distinct from that of T helper type 1 and T helper type 2 cells , 1994, European journal of immunology.

[16]  D. Carlo,et al.  CD8+ T cells in psoriatic lesions preferentially use T-cell receptor V beta 3 and/or V beta 13.1 genes. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[17]  H. Dvorak,et al.  Overexpression of vascular permeability factor/vascular endothelial growth factor and its receptors in psoriasis , 1994, The Journal of experimental medicine.

[18]  A. Gottlieb,et al.  PUVA bath therapy strongly suppresses immunological and epidermal activation in psoriasis: a possible cellular basis for remittive therapy , 1994, The Journal of experimental medicine.

[19]  James T. Elder,et al.  GRO-alpha mRNA is selectively overexpressed in psoriatic epidermis and is reduced by cyclosporin A in vivo, but not in cultured keratinocytes. , 1993, The Journal of investigative dermatology.

[20]  J. Garioch,et al.  Restricted T‐cell receptor Vβ gene usage in the skin of patients with guttate and chronic plaque psoriasis , 1993, The British journal of dermatology.

[21]  M. Yamamura,et al.  The cytokine network in lesional and lesion-free psoriatic skin is characterized by a T-helper type 1 cell-mediated response. , 1993, The Journal of investigative dermatology.

[22]  J. Voorhees,et al.  T-lymphocyte clones initiated from lesional psoriatic skin release growth factors that induce keratinocyte proliferation. , 1993, The Journal of investigative dermatology.

[23]  J. Garioch,et al.  Group A streptococcal antigen‐specific T lymphocytes in guttate psoriatic lesions , 1993, The British journal of dermatology.

[24]  D. Leung,et al.  A potential role for superantigens in the pathogenesis of psoriasis. , 1993, The Journal of investigative dermatology.

[25]  W. Sterry,et al.  Type I and type II psoriasis show a similar usage of T-cell receptor variable regions. , 1991, The Journal of investigative dermatology.

[26]  V. Dixit,et al.  Detection of interferon-gamma mRNA in psoriatic epidermis by polymerase chain reaction. , 1991, Journal of dermatological science.

[27]  K. L. Johnson,et al.  Enrichment and function of urushiol (poison ivy)-specific T lymphocytes in lesions of allergic contact dermatitis to urushiol. , 1990, Journal of immunology.

[28]  B. Bernard,et al.  Spreading of psoriatic plaques: alteration of epidermal differentiation precedes capillary leakiness and anomalies in vascular morphology. , 1990, The Journal of investigative dermatology.

[29]  J. Voorhees,et al.  Oral cyclosporine in the treatment of inflammatory and noninflammatory dermatoses. A clinical and immunopathologic analysis. , 1990, Archives of dermatology.

[30]  H. Valdimarsson,et al.  Epidermal T lymphocytes and HLA‐DR expression in psoriasis , 1984, The British journal of dermatology.

[31]  H. Valdimarsson,et al.  T‐cell subpopulations in the blood and skin of patients with psoriasis , 1984, The British journal of dermatology.

[32]  B. Benacerraf,et al.  Studies on the specificity of the cellular infiltrate of delayed hypersensitivity reactions. , 1963, Journal of immunology.