Activation marker analysis of mononuclear cell infiltrates of oral lichen planus in situ

Kilpi, Anu

doi:10.1111/j.1600-0722.1987.tb01826.x

Cited by 32 publications

(34 citation statements)

References 24 publications

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“…Many of the local inflammatory cells in the infiltrate of the oral lichen planus lesions were the immunocompetent Tlymphocytes, which findings are in line with other authors [51][52][53][54]. Therefore, a hypothesis has been proposed about the interaction between cellular and molecular signals in the local immune response.…”

Section: Discussionsupporting

confidence: 77%

Role of Humoral Mechanisms in Etiology of Lichen Planus

Поповска¹,

Mitik²,

Grchevska³

et al. 2014

Prilozi

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Aim: To examine the role of IgA, CIC and component C3 as indicators of humoral immune response in the etiopathogenesis of oral erosive lichen planus (OELP). Material and method:The study comprised 19 patients with OELP whose samples of blood, saliva and tissue were obtained after carefully taken medical history and clinical examination. Samples of oral mucosa were taken from the site of lesion, i.e. exclusively from buccal mucosa (1 cm in width and length), and from the deep epithelium as well as a segment from the lamina propria. Determination of immunoglobulins in serum and saliva, and determination of component C3, was done using the micro-elisa technique by Rook&Cameron, Engvall and Ulman. Determination of CIC in serum and mixed saliva was done with the PEG (polyethylene glycol) method. Determination of immunoglobulin A and component C3 in biopsy material was done with direct immunofluorescence. Results: Levels of immunoglobulin A in serum in OELP during exacerbation were decreased (1.04 ± 0.49 gr/l) and during remission increased (5.92 ± 0.62) in comparison with the control group (p < 0.001). Levels of CIC during exacerbation and remission were increased (p < 0.001), and component C3 levels were increased in both examined phases in the examined group compared with the control group (p < 0.05). Deposits of IgA were registered in one (5.88%) patient with OELP and component C3 was registered in 3 (17.64%) patients. Conclusion: Changes in IgA values, as well as CIC and component C3, may correlate with changes in oral mucosa emphasizing the role of humoral immune response in the pathogenesis of oral lichen planus.

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Section: Discussionsupporting

confidence: 77%

Role of Humoral Mechanisms in Etiology of Lichen Planus

Поповска¹,

Mitik²,

Grchevska³

et al. 2014

Prilozi

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“…The lymphocytic infiltrate in OLP is composed almost exclusively of T-cells, and the majority of T-cells within the epithelium and adjacent to damaged basal keratinocytes are activated CD8 + lymphocytes (Matthews et al, 1984;Kilpi, 1987Kilpi, , 1988Jungell et al, 1989b). In our recent studies, the majority of subepithelial and intra-epithelial lymphocytes in OLP were CD8 + (Khan et al, 2001, submitted).…”

Section: Cd8 + T-cellsmentioning

confidence: 99%

The Pathogenesis of Oral Lichen Planus

Sugerman

Savage²,

Walsh³

et al. 2002

Critical Reviews in Oral Biology & Medicine

646

584

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Both antigen-specific and non-specific mechanisms may be involved in the pathogenesis of oral lichen planus (OLP). Antigen-specific mechanisms in OLP include antigen presentation by basal keratinocytes and antigen-specific keratinocyte killing by CD8 + cytotoxic T-cells. Non-specific mechanisms include mast cell degranulation and matrix metalloproteinase (MMP) activation in OLP lesions. These mechanisms may combine to cause T-cell accumulation in the superficial lamina propria, basement membrane disruption, intra-epithelial T-cell migration, and keratinocyte apoptosis in OLP. OLP chronicity may be due, in part, to deficient antigen-specific TGF-␤1-mediated immunosuppression. The normal oral mucosa may be an immune privileged site (similar to the eye, testis, and placenta), and breakdown of immune privilege could result in OLP and possibly other autoimmune oral mucosal diseases. Recent findings in mucocutaneous graft-versus-host disease, a clinical and histological correlate of lichen planus, suggest the involvement of TNF-␣, CD40, Fas, MMPs, and mast cell degranulation in disease pathogenesis. Potential roles for oral Langerhans cells and the regional lymphatics in OLP lesion formation and chronicity are discussed. Carcinogenesis in OLP may be regulated by the integrated signal from various tumor inhibitors (TGF-␤1, TNF-␣, IFN-␥, IL-12) and promoters (MIF,. We present our recent data implicating antigen-specific and non-specific mechanisms in the pathogenesis of OLP and propose a unifying hypothesis suggesting that both may be involved in lesion development. The initial event in OLP lesion formation and the factors that determine OLP susceptibility are unknown.

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“…The lesional lymphocytic infiltrate in LP is comprised principally of T-cells, including CD4+ and CD8+ lymphocytes (Bhan et al, 1981;De Panfilis et al, 1983;Buechner, 1984;Matthews et al, 1984;Ishii, 1987;Takeuchi et al, 1988;Walsh et al, 1990a,b;Akasu et al, 1993;Robertson and Wray, 1993;Eversole et al, 1994). There may be a gradual CD8+ accumulation with disease progression, and there is also a variation in the distribution of T-cells within the lesions, the majority of intraepithelial T-cells being CD8+ and the proportion of CD8+ being higher in the superficial than in the deep lamina propria (Kilpi, 1987;Jungell et al, 1989). Immunohistochemical studies indicate that activated Tcells (e.g., expressing HLA-DR) can lie close to the damaged epithelial basement membrane and sometimes close to areas of epithelial erosion (Gabriel et at., 1985;Kilpi, 1987).…”

Section: Pathogenesismentioning

confidence: 99%

“…It is assumed that an antigenic modification of the cellular surface triggers a tissue reaction, via the dendritic antigen-presenting cells in the epithelium and mesenchyme, in which CD4+ T-lymphocytes play a pivotal role. Indeed, these lymphocytes are the main component of the inflammatory infiltrate so clearly observed in early lesions of LP, with long-standing lesions containing a greater number of CD8+ T-lymphocytes (Matthews et al, 1984;Kilpi, 1987;Sugerman et al, 1994). The lesional lymphocytic infiltrate in LP is comprised principally of T-cells, including CD4+ and CD8+ lymphocytes (Bhan et al, 1981;De Panfilis et al, 1983;Buechner, 1984;Matthews et al, 1984;Ishii, 1987;Takeuchi et al, 1988;Walsh et al, 1990a,b;Akasu et al, 1993;Robertson and Wray, 1993;Eversole et al, 1994).…”

Section: Pathogenesismentioning

confidence: 99%

Update On Oral Lichen Planus: Etiopathogenesis and Management

Scully

Beyli²,

Ferreiro

et al. 1998

Critical Reviews in Oral Biology & Medicine

471

461

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Lichen planus (LP) is a relatively common disorder of the stratified squamous epithelia, which is, in many ways, an enigma. This paper is the consensus outcome of a workshop held in Switzerland in 1995, involving a selection of clinicians and scientists with an interest in the condition and its management. The oral (OLP) eruptions usually have a distinct clinical morphology and characteristic distribution, but OLP may also present a confusing array of patterns and forms, and other disorders may clinically simulate OLP. Lesions may affect other mucosae and/or skin. Lichen planus is probably of multifactorial origin, sometimes induced by drugs or dental materials, often idiopathic, and with an immunopathogenesis involving T-cells in particular. The etiopathogenesis appears to be complex, with interactions between and among genetic, environmental, and lifestyle factors, but much has now been clarified about the mechanisms involved, and interesting new associations, such as with liver disease, have emerged. The management of lichen planus is still not totally satisfactory, and there is as yet no definitive treatment, but there have been advances in the control of the condition. There is no curative treatment available; immunomodulation, however, can control the condition. Based on the observed increased risk of malignant development, OLP patients should be offered regular follow-up examination from two to four times annually and asked to report any changes in their lesions and/or symptoms. Follow-up may be particularly important in patients with atrophic/ulcerative/erosive affections of the tongue, the gingiva, or the buccal mucosa. Much more research is required into the genetic and environmental aspects of lichen planus, into the premalignant potential, and into the possible associations with chronic liver, and other, disorders. More clinical studies are required into the possible efficacy of immunomodulatory drugs such as pentoxifylline and thalidomide.

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Activation marker analysis of mononuclear cell infiltrates of oral lichen planus in situ

Cited by 32 publications

References 24 publications

Role of Humoral Mechanisms in Etiology of Lichen Planus

Role of Humoral Mechanisms in Etiology of Lichen Planus

The Pathogenesis of Oral Lichen Planus

Update On Oral Lichen Planus: Etiopathogenesis and Management

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