Disease relevance of Lichen Planus

• Primary biliary cirrhosis, penicillamine, and lichen planus [1].
• A significantly greater proportion of HCV-infected patients had PCT, vitiligo, lichen planus, and cryoglobulinemia [2].
• Cytoid bodies in lichen planus (LP) and discoid lupus erythematosus (DLE) were strongly stained with AE1, AE3, EKH4, and EKH1 antibodies but were negative with AE2 [3].
• To reexamine the tissue distribution of human C5aR expression, transcription of the C5aR gene was investigated in normal and pathologically affected human lung (bronchopneumonia, tuberculosis), large intestine (acute appendicitis, Crohn's disease), and skin (pyogenic granuloma, lichen planus) using in situ hybridization [4].
• Skin biopsies from lichen planus, chronic discoid lupus erythematosus, allergic patch test reactions, psoriasis, and Jessner's lymphocytic infiltration of the skin were investigated for chemokine expression using RNA in situ hybridization, and for the expression of CXCR3 using immunohistochemistry [5].

High impact information on Lichen Planus

• Treatment of lichen planus with temarotene [6].
• Only scattered CD8+ cells in lichen planus expressed a significant amount of KIR3DL2 [7].
• In addition, some samples of dysplastic lesions, benign tumors, lichen planus and normal mucosa exhibiting poor telomerase activity revealed weak expression of hTRT [8].
• Autoantibodies in lichen planus pemphigoides react with a novel epitope within the C-terminal NC16A domain of BP180 [9].
• Two lichen planus pemphigoides sera, in addition, reacted with the immunodominant antigenic region associated with bullous pemphigoid [9].

Chemical compound and disease context of Lichen Planus

• The hemidesmosome-associated complex, alpha 6 beta 4 integrin, was localized at the basal aspect of basal epithelial cells of nonaffected sites, but was diffuse and discontinuous in lichen planus lesions [10].
• Kalinin staining was discontinuous in lichen planus lesions [10].
• In all five cases of lichen planus, the deposits contained IgM and C3, and in addition, IgA was present in four, IgG and fibrinogen in three [11].
• A case of lichen planus attributed to exposure to hydroxyethyl starch has been reported previously [12].
• Treatment of severe lichen planus with cyclosporine [13].

Biological context of Lichen Planus

• The phenotype of the cutaneous immunocompetent cells in lesions of cutaneous T cell lymphoma (mycosis fungoides, Sézary syndrome), lichen planus, and chronic graft-vs.-host reaction infiltrates, was examined by the use of monoclonal antibodies directed against T cell populations and Langerhans cells (OKT3, OKT4, OKT5, OKT6, OKT8) (BL2, BL6) [14].
• The keratin profile in lichen planus is analogous to the wound healing response [15].
• The dissimilarities between the various groups are expressed in terms of gene and haplotype frequencies, as well as in HLA-disease associations (as for example rheumatoid arthritis, erosive lichen planus, primary Sjögren's syndrome, pemphigus vulgaris) [16].
• Ultrastructural localization of the binding sites of antibasement membrane zone antibodies in lichen planus pemphigoides on 1.0 M sodium chloride-separated skin [17].
• Comparisons between the allele frequencies in patients and controls showed a positive association with cutaneous idiopathic lichen planus for the DRB1*0101 allele (RR = 5.8, P = 0.0097), DRB1*0101 and DRB1*0102 are associated with the same DQA1 and DQB1 alleles and are different only for two amino acids in positions 85 and 86 of the DRB1 gene [18].

Anatomical context of Lichen Planus

• We found distinct patterns of intercellular adhesion molecule-1 (ICAM-1) expression in three diseases characterized by interface dermatitis with mononuclear infiltrates and keratinocyte cytotoxicity: lichen planus (LP), subacute cutaneous lupus erythematosus (SCLE), and erythema multiforme (EM) [19].
• To determine the phenotypic and functional characteristics of the infiltrating lymphocytes, T-cell lines from normal and lesional skin from the same patients with lichen planus were established by culture with interleukin 2 followed by stimulation every 14 d with phytohemagglutinin and irradiated allogeneic feeder cells [20].
• Altered expression of basement membrane proteins and their integrin receptors in lichen planus: possible pathogenetic role of gelatinases A and B [21].
• Donor toxicity in granulocyte collections: association of lichen planus with the use of hydroxyethyl starch leukapheresis [22].
• Our results are compatible with the hypothesis that the inhibition of CD4 T cells by cyclosporine might explain the drug's therapeutic action and that the interaction between antigen-presenting cells and CD4 T cells is important in the pathogenesis of lichen planus [23].

Gene context of Lichen Planus

• MIG is a dominant lymphocyte-attractant chemokine in lichen planus lesions [24].
• Phenylethanolamine N-methyltransferase (PNMT)-like immunoreactivity has been found in psoriatic skin and in this study, PNMT-like immunoreactivity was investigated in the involved and uninvolved skin of six patients with lichen planus and four patients with lichen simplex [25].
• In our case report predisposition to cutaneous idiopathic lichen planus is correlated with a valine in position 85 and a glycine in position 86 at the second exon of the DRB1 gene [18].
• The number of keratinocytes in per mm2 of epidermis stained for RANTES were 116.79+/-98.42 in psoriatic tissues compared to 32.00+/-46.05 (p<0.05), 6.39+/-3.59 (p<0.01), 2.64 +/-1.15 (p<0.01) and 3.53+/-5.26 (p<0.01), respectively, in the non-lesional, lichen planus, eczematous lesions and normal skin [26].
• In the present study, an analysis was made of the expression pattern of thrombospondin-1 (TSP1) and its receptor (CD36) in skin biopsies obtained from healthy volunteers and from patients with lichen planus, lupus erythematosus, cutaneous T-cell lymphoma and psoriasis vulgaris [27].

Analytical, diagnostic and therapeutic context of Lichen Planus

• Frozen sections of skin lesions of systemic lupus erythematosus and lichen planus, and patients' sera known to have pemphigus or pemphigoid antibodies were used for IF procedures [28].
• Examples of chemokines and chemokine receptors being involved in mediating autoimmune disease exist for rheumatoid arthritis, multiple sclerosis, allograft rejection, systemic lupus erythematosus, psoriasis, atopic dermatitis, lichen planus, and graft-versus-host-disease [29].
• Over 10 years ago a series of indirect immunofluorescence researches with patients' lesional skin and serum disclosed the presence of lichen planus specific antigens (LPSA) [30].
• The reliability of immunofluorescence and histopathology in the diagnosis of discoid lupus erythematosus and lichen planus [31].
• A study of forty patients with active lichen planus and a negative family history for diabetes showed that 42% had unequivocally abnormal oral glucose tolerance [32].

References