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Year : 2006  |  Volume : 72  |  Issue : 5  |  Page : 350-352

Indirect immunofluorescence to demonstrate lichen planus specific antigen (LPSA) in lichen planus

Department of Skin and STD, Kasturba Medical College, Manipal, India

Correspondence Address:
Raghavendra Rao
Department of Skin and STD, Kasturba Medical College, Manipal - 576 104
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0378-6323.27750

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Background: Current evidence suggests that lichen planus is an immunological disease. Cytotoxic CD8+ cells in the lesional epidermis recognize a unique antigen called lichen planus specific antigen. This antigen could be demonstrated by indirect immunofluorescence using the patient's serum and autologous lesional skin. Aim: To study indirect immunofluorescence pattern in lichen planus, among Indian patients. Methods: Twenty-five consecutive patients with the clinical diagnosis of lichen planus were enrolled in the study. Direct immunofluorescence was done in all patients. Indirect immunofluorescence using lesional skin as substrate was done in all 25 patients and five patients with other dermatoses. Results: A specific fluorescence pattern corresponding to the distribution of lichen planus specific antigen was observed in the stratum spinosum and granulosum in 22 (88%) patients. It was absent from other parts of the epidermis, dermis and in patients with other dermatoses. Conclusion: Indirect immunofluorescence is a useful adjuvant test in lichen planus, particularly in atypical cases.

Keywords: Indirect immunofluorescence, Lichen planus, Lichen planus specific antigen

How to cite this article:
Rao R, Shenoi S D. Indirect immunofluorescence to demonstrate lichen planus specific antigen (LPSA) in lichen planus. Indian J Dermatol Venereol Leprol 2006;72:350-2

How to cite this URL:
Rao R, Shenoi S D. Indirect immunofluorescence to demonstrate lichen planus specific antigen (LPSA) in lichen planus. Indian J Dermatol Venereol Leprol [serial online] 2006 [cited 2019 Oct 14];72:350-2. Available from: http://www.ijdvl.com/text.asp?2006/72/5/350/27750

  Introduction Top

The histopathological criteria for the diagnosis of lichen planus are well established in textbooks of dermatopathology. Briefly, they consist of hyperkeratosis, wedge-shaped hypergranulosis, irregular acanthosis, vacuolar degeneration of basal layer with the presence of intraepidermal or subepidermal colloid bodies, saw-toothing of rete-ridges and papillary dermal band-like infiltrate.[1] Direct immunofluorescence (DIF) of lesional skin further supports the diagnosis. It shows ragged fibrin band at basement membrane zone (BMZ) and clusters of colloid bodies (with IgM and C 3 ; to a lesser extent with other classes of immunoglobulin) in almost all patients.[2] Though histopathological and DIF findings are highly characteristic of lichen planus, they are not specific. Transitional histopathological and DIF features could be seen in various other dermatoses such as lupus erythematosus and dermatomyositis.[3] Previous studies have reported the usefulness of indirect immunofluorescence findings in lichen planus.[4],[5] Our aim was to establish its role in Indian patients.

  Methods Top

Twenty-five patients with the clinical diagnosis of lichen planus were enrolled in the study. A 4-mm punch biopsy was taken from the lesional skin, snap frozen and stored in the deep freezer at -70C. Using cryostat, 4 mm sections were taken. Patient's serum was obtained after collecting 5 ml of blood. Serum (1:10 and 1: 80 dilutions) was incubated with lesional skin sections for one hour. Later it was washed in phosphate buffer saline (PBS) and incubated with various fluorescein isothiocyanate conjugates for one hour. It was once again washed in PBS, mounted in buffered glycerol and examined under fluorescent microscope. DIF of lesional skin was done in all patients. Five patients with other dermatoses were used as controls (two patients with SLE, one case each of scleroderma, MCTD and atopic dermatitis) and indirect immunofluorescence was done using the same technique.

  Results Top

Among 25 patients 13 were males and 12 females. Average age of the patients in the study group was 39.72 years (range 13 - 63 years). Mean duration of illness was 2.72 years (range 15 days - 5 years). Various clinical types of lichen planus encountered are shown in [Table - 1]. Oral lesion in the form of lacy reticular net-like pattern was seen in three patients. Results of DIF are shown in [Table - 2].

Indirect immunofluorescence using autologous lesional skin showed characteristic fluorescent IgG deposits in the upper epidermis, at the level of the stratum granulosum and stratum spinosum in 22 (88%) patients [Figure - 1]. Such findings were not seen in other parts of the epidermis, BMZ or in the dermis. Direct immunofluorescence did not reveal any such finding. The test was negative in one patient who was on oral steroid therapy; however it was positive in two others, who were also on oral steroids at the time of the test. Among the patients with negative test, one had classical lichen planus (LP) lesions and was on steroid while the other two were not on any medication and had hypertrophic and generalized type of LP respectively. The test was negative in the control group.

  Discussion Top

LP is a papulo-squamous disease of the skin and mucous membrane of worldwide distribution. The exact etiology of LP remains unknown. There is little evidence to support the older hypothesis of viral origin, neurological changes or psychological stress as sole causative factors.[6] Recent studies have shown that LP represents a cell-mediated immune response to an induced antigenic change in the epidermal cells in a genetically predisposed individual.[7] CD8+ infiltrates in the lesional skin recognize a MHC Class I antigen called lichen planus specific antigen (LPSA). The exact nature of this antigen is unknown. It may be an auto-reactive peptide or exogenous antigen such as altered protein, drug, contact allergen and viral or other infectious agent.[8] In 1983, Olsen et al . demonstrated LPSA by indirect immunofluorescence technique using autologous lesional skin.[4] It was present only in the stratum granulosum and stratum spinosum and absent from other parts of the epidermis, BMZ and dermis. Lichen planus specific antigen (LPSA) is specific for LP and found in about 80% of the patients with or without oral lesions.[5] In our study, we found LPSA in 88% of patients. Though the test was negative in one patient who was being treated with systemic corticosteroids, it was positive in the other two who were also receiving steroid therapy. We feel that corticosteroid therapy was not responsible for the negative finding. Olsen et al . made a similar observation. They suggest that LPSA is not produced in all LP lesions or absent in the lesion during some stages of the disease or that it may not always be detectable by this method.[5]

Earlier studies have demonstrated LPSA in patients belonging to diverse ethnic backgrounds such as Caucasians, Negroes and Koreans.[5],[6] Our study revealed LPSA among Indian patients with LP. LPSA can be demonstrated in various clinical types of LP such as hypertrophic, vesicular, actinic and eruptive, as shown in our study. Camisa et al . have shown LPSA in bullous LP,[9] while Olsen et al . have demonstrated the usefulness of this technique in LP / LE overlap syndrome. They concluded that this technique could help to differentiate atypical cases of LP from other dermatoses such as lupus erythematosus where DIF shows equivocal results.[10]

LPSA is unique to lichen planus and is expressed in the stratum granulosum and stratum spinosum of patients with LP. It can be demonstrated by indirect immunofluorescence using the patient's serum and autologous lesional skin. This test is of particular help to differentiate atypical cases of lichen planus from other dermatoses.

  References Top

1.Toussaint S, Kamino H. Non infectious erythematous papular and squamous diseases of the skin. In : Elder D, Elenitsas, Jawrsky C, Johnson Jr B, editors. Lever's histopathology of the skin. 8th ed. J B Lipponcott Raven Publishers: Philadelphia; 1999. p. 167-71.  Back to cited text no. 1    
2.de la Faille-Kuyper EH, de la Faille HB. An immunofluorescence study of lichen planus. Br J Dermatol 1974;90:365-71.  Back to cited text no. 2  [PUBMED]  
3.Abell E, Presberry DG, Marks R, Ramnarain D. The diagnostic significance of immunoglobulin and fibrin deposition in lichen planus. Br J Dermatol 1975;93:17-24.  Back to cited text no. 3    
4.Olsen RG, Du Plessis DP, Barron C, Schulz EJ, Villet W. Lichen Planus dermopathy: Demonstration of Lichen Planus specific antigen in affected patients. J Clin Lab Immunol 1983;10: 103-6.  Back to cited text no. 4    
5.Olsen RG, Du Plessis DP, Schultz EJ, Camisa C. Indirect immunofluorescence microscopy of lichen planus. Br J Dermatol 1984;110:9-15.  Back to cited text no. 5    
6.Lee CW, Yoon JY. Lichen planus specific antigen and antibodies in a patient with generalized lichen planus. J Korean Med Sci 1987;2:259-62.  Back to cited text no. 6  [PUBMED]  
7.Bhan AK, Harrist TJ, Murphy GR, Mihm MC Jr. T cell subsets and Langerhans cells in lichen planus: In situ characterization using monoclonal antibodies. Br J Dermatol 1981;105:617-22.  Back to cited text no. 7    
8.Daoud MS, Pittelkow MR. Lichen Planus. In : Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, editors. Fitzpatrick's Dermatology in general medicine. 6th ed. Mc Graw- Hill Publication: New York; 2003. p. 463-77.  Back to cited text no. 8    
9.Camisa C, Neff, Rosanna C, Bennet JL. Bullous lichen planus: Diagnosis by indirect immunofluorescence and treatment with dapsone. J Am Acad Dermatol 1986;15:464-9.  Back to cited text no. 9    
10.Camisa C, Neff JC, Olsen RG. Use of indirect immunofluorescence in the lupus erythematosus/lichen planus overlap syndrome: An additional diagnostic clue. J Am Acad Dermatol 1984;11: 1050-9.  Back to cited text no. 10  [PUBMED]  


[Figure - 1]


[Table - 1], [Table - 2]

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