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Year : 1995  |  Volume : 61  |  Issue : 1  |  Page : 21-25

Paucity of immune complexes in skin lesions of lichen planus

Correspondence Address:
Sandipan Dhar

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Source of Support: None, Conflict of Interest: None

PMID: 20952866

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The significance of deposition of immunoglobulin and/or complements at the dermoepidermal junction (DEJ) and civatte bodies in skin lesions of 15 histopathologically confirmed cases of lichen planus (LP) was evaluated. Civatte boides were seen in 6 (40%) patients while in 9 (60%) these were absent. IgM, IgG, IgA and C3 were seen within civatte bodies in 6, 3, 2 and 3 specimens respectively in various combinations. LP lesions of a shorter duration (one year or less) had civatte bodies while these were absent in those with disease of a longer duration (more than 1 year). Immune complex deposition was seen in only 2 patients. It is concluded that civatte bodies are of diagnostic importance in lichen planus lesions of a short duration only and immune complexes do not seem to play a significant role in its pathogenesis.

Keywords: Lichen planus, Civatte body, Immune complex, Complement, Dermoepidermal junction

How to cite this article:
Dhar S, Dawn G, Se. Paucity of immune complexes in skin lesions of lichen planus. Indian J Dermatol Venereol Leprol 1995;61:21-5

How to cite this URL:
Dhar S, Dawn G, Se. Paucity of immune complexes in skin lesions of lichen planus. Indian J Dermatol Venereol Leprol [serial online] 1995 [cited 2019 Nov 22];61:21-5. Available from: http://www.ijdvl.com/text.asp?1995/61/1/21/4119

  Introduction Top

Although there are various hypotheses regarding aetiopathogenesis of lichen planus (LP), the exact pathogenesis is still elusive. Its association with lupus erythematosus,[1] myasthenia gravis,[2] bullous pemphigoid[3] and hypogammaglobulinaemia,[4] points towards an underlying immunopathogenetic mechanism. Several studies[5],[6] have shown deposition of immunoglobulins IgM, IgG, IgA and complements within globular masses known as civatte/colloid bodies at the dermoepidermal junction (DEJ) and in upper dermis on direct immunofluorescence (DIF) testing. However, unlike other conditions viz. lupus erythematosus, eczema, dermatitis herpetiformis and erythema multiforme,[6] the pathogenic significance of immunglobulins is questionable in lichen planus. Nevertheless, a uniform and large number of colloid bodies at the DEJ is usually considered diagnostic of LP. Although the type of immunoglobulin deposition and complement activation (classical or alternate pathway) depends on the stage of LP,[5] its correlation with the age of LP lesions has not been established. In the present study an attempt was made to find a correlation between the duration of LP lesions and immunoglobulin and/or complement deposition at the DEJ and presence of civatte bodies.

  Patients and Methods Top

Fifteen clinically diagnosed and histopathologically confirmed cases of LP were selected for the study. In each patient, a detailed history was taken regarding the duration of LP, degree of itching and treatment taken with duration. A thorough clinical examination emphasizing the type and distribution of LP lesions and presence of mucosal lesions was noted. Involvement of nails and hairs, if any, was also recorded. The specimen obtained for histopathological examination was washed several times in phosphate buffer saline (PBS) and 5 micron thick sections were cut in a cryostat. Four sections from each cases were stained with IgG, IgA, IgM and C3 antibodies labelled with fluorescein isothiocyanate using direct immunofluorescence assay. Careful evaluation of deposits was done in relation to blood vessels, dermoepidermal junction (DEJ) and civatte bodies. Briefly the conjugates were diluted 1:16 in PBS and 10 μl layered on the sections and slides, incubated at 37C in a humid chamber. After several gentle washings with PBS, the slides were mounted in glycerine PBS mixture and viewed in a Zeiss 16 research microscope fitted with HBO 50 U.V. lamp.

  Results Top

Of 15 patients, 13 (86.7%) were females and 2 (13.3%) males, female to male ratio being 6.5:1. Their ages ranged from 29 to 45 years (mean 37 years). The duration of LP ranged from 3 months to 2 years (mean 19.2 months). Ten patients had classical LP, 3 had classical LP with LP hypertrophicus (LPH) and 2 eruptive LP. Distribution of lesions has been shown in [Table - 1]. While generalized involvement was seen in 7(46.7%) patients, 5(33.3%), 2(13.3%) and 1(6.7%) patients had isolated involvement of legs, trunk and forearm respectively. Four (26.7%) patients had involvement of oral mocosa(e). Eleven (73.3%) patients received topical corticosteroids, 2(13.3%) systemic corticosteroids, one each (6.7%) a combination of dapsone, systemic corticosteroid and topical corticosteroids [Table - 1].

Various types of civatte bodies found depending upon the types of immunoglobulins and complements are shown in [Table - 2]. Of 15 biopsy specimens, in 6(40%) civatte bodies were seen while in 9(60%) civatte bodies were conspicuous by their absence. Civatte bodies were present in LP lesions of shorter duration (one year or less) and absent in those of longer duration (more than 1 year). Civatte bodies with IgG, IgM, IgA and C3, IgG, IgM and C3, Igm and C3 were seen in one patient each, while civatte bodies with IgA and IgM and only IgM were found in 2 and 1 patients respectively. In 1 patient (No. 15) the biopsy specimen revealed faint IgM deposition at the dermoepidermal junction (DEJ). In another patients (No. 8) there was heavy deposition of IgM around dermal capillaries.

  Discussion Top

Immunopathological changes in LP follow a sequence of events, the formation of civatte bodies probably being the earliest of such events.[5] The concomitant presence of Clq, C3, C4 fragments and C5 in or around colloid or civatte bodies indicate the activation of complement cascade via the classical pathway and the presence of immunoglobulins indicate their probable role in the activation process.[5]

The cellular events follow immune complex deposition and polymorphonuclear leucocytes accumulate in early lesions of LP.[5] The presence of fibrin in the upper dermis further contributes to this phenomenon by attracting leucocytes.[7] Later on lymphocyte chemotaxis produces a band like infiltrate at the DEJ classical of LP.[8]

In the present study civatte bodies containing Igs and complement deposition occurred in LP lesions of shorter duration (1 year or less), while in all the lesions of more than 1 year old these were absent. We also found IgM civatte bodies in maximum number of cases as observed by other. [5, 6] However, immune complexes were conspicuous by their absence except in skin lesions of 2 patients (patient no. 8 and 15).

Several studies on serum immunoglobulins in patients with LP have shown deficiency of various immunoglobulins particularly IgM and IgA in patients with active and settled LP.[9][10][11] On the contrary, Mahood[12] observed an increase in the levels of circulating IgG, IgA and IgM after resolution of LP lesions. The cause and effect relationship of humoral imune deficiency and LP lesions is yet to be established. Some authors[9] feel that the patients with LP have an immunological deficiency and are susceptible to unknown viral agent which may be released when the unaffected skin is subjected to damage.[13] While others believe that the deficiency of circulating IgM and IgA is because of their deposition in the skin.[11] The observation of circulation immunoglobulin deficiency is patients with active and settled lesions of LP[9],[10] and its increase after resolution of LP lesions[12] further supports this hypothesis. Therefore, "immunoglobulin shift" from circulation to tissue and vice versa probably contributes to the pathogenesis of LP. To prove this hypothesis, a sequential estimation of immunoglobulins is mandatory to reveal that immunoglobulin levels are in fact changing. No antibody estimation was done in this study. However, this hypothesis is fraught with difficulty in explaining the changes in civatte bodies. Because with sequential lowering of immunoglobulins, civatte bodies should increase, but they featured just the opposite in our cases [Figure - 1],[Figure - 2],[Figure - 3]. We presume that these mummified civatte bodies with immunoglobulins are eventually being absorbed and phagocytosed. It is therefore concluded that although civatte bodies are characteristic of LP, they may be absent in lesions of long duration. Immune complexes were also found only in two cases. Therefore, immune complexes probably do not play a significant role in the pathogenesis of lichen planus. However, a larger study incorporating more numbers of patients is warranted to evaluate the role of immune complexes in the pathogenesis of lichen planus.

  References Top

1.Roare RW, Nesbitt LT, Reed FJ. Unusual variant of LE or LP. Arch Dermatol 1977;113:741-8.  Back to cited text no. 1    
2.Aronson JK, Soltani K, Paik Kl. Trial of lichen planus, myasthenia gravis and thymoma. Arch Dermatol 1978;114:225-8.  Back to cited text no. 2    
3.Stingle G, Holubar K. Co-existance of lichen planus and bullous pemphigoid. Br J Dermatol 1975;93:313-20.  Back to cited text no. 3    
4.Mann RJ, Wallington TB, Warin RP. Lichen planus with late onset hypogammaglobulinemia. Br J Dermatol 1982;106:357-60.  Back to cited text no. 4  [PUBMED]  
5.Faille-Kuyper EHB, Faille HB. An immunofluorescence study of lichen planus. Br J Dermatol 1974;90:365-71.  Back to cited text no. 5    
6.Abell E, Presbury DGC, Marks R, Ramarain D. The diagnositc significance of immunoglobulin and fibrin deposition in lichen planus. Br J Dermatol 1975;93:17-24.  Back to cited text no. 6    
7.Barnhart ML. Role of blood coagulation in acute inflammation. Biochemical Pharmacology 1968; (Suppl) 205:19-23.  Back to cited text no. 7    
8.Black MM. The pathogenesis of lichen planus. Br J Dermatol 1972;86:302-6.  Back to cited text no. 8  [PUBMED]  
9.Shankar L. Deficiency of circulating IgA and IgM in adult patients with lichen planus. Br J Dermatol 1975;93:25-7.  Back to cited text no. 9    
10.Jack WK, Greenword BM. Serum immunoglobulin in Nigerian patients with lichen planus. Clin Exp Dermatol 1978;3:83-6.  Back to cited text no. 10    
11.Nigam PK, Singh G, Sharma L, Khurana SK. Humoral immunodeficiency in lichen planus. Ind J Dermatol Venereol Leprol 1988;54:244-6.  Back to cited text no. 11    
12.Mahood JM. Serum immunoglobulins in lichen planus. Br J Dermatol 1981;104,207-8.  Back to cited text no. 12    
13.Stankler L, Ewen SWB. The effects of experimental skin damage in patients with lichen planus. Br J Dermatol 1974;90:25-9.  Back to cited text no. 13    


[Figure - 1], [Figure - 2], [Figure - 3]


[Table - 1], [Table - 2]

This article has been cited by
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Westbrook, R., Riley, S.
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