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. 2009 Dec;34(8):910-4.
doi: 10.1111/j.1365-2230.2009.03297.x. Epub 2009 May 18.

Identification of granzyme B-expressing CD-8-positive T cells in lymphocytic inflammatory infiltrate in cutaneous lupus erythematosus and in dermatomyositis

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Identification of granzyme B-expressing CD-8-positive T cells in lymphocytic inflammatory infiltrate in cutaneous lupus erythematosus and in dermatomyositis

M Grassi et al. Clin Exp Dermatol. 2009 Dec.

Abstract

Background: Lupus erythematosus (LE) and dermatomyositis (DM) are interface dermatitis, histologically characterized by formation of colloid bodies and a CD4+ CD8+ lymphocyte infiltrate. Colloid bodies are examples of intraepidermal apoptosis. Granzyme (Gr)B, synthesized by activated cytotoxic lymphocytes, is a serine protease able to prime apoptosis. GrB+ lymphocytes have been previously found in infiltrates in skin lesions from other types of interface dermatitis.

Aim: To evaluate, on histological skin specimens from patients with LE and DM, GrB expression as a mediator of keratinocyte apoptosis in lymphocyte infiltrate.

Methods: In total, 22 patients with cutaneous LE [9 with discoid lupus erythematosus (DLE), 9 with subacute lupus erythematosus (SCLE) and 4 with systemic lupus erythematosus (SLE)] and 20 patients with DM were studied. Skin specimens underwent immunohistochemical staining with antibodies to CD3, CD4, CD8 and GrB.

Results: Immunohistochemical study with GrB was positive in 17 of the 22 patients with LE but only 2 of the 20 patients with DM. In LE, in systemic and subacute forms of LE, the median obtained was < 10 (+) whereas in the chronic forms, the median was 10-50% (++). Patients with DM were negative for GrB.

Conclusions: In LE, a correlation between GrB+ lymphocyte and the presence of DLE form was found, but in DM, GrB is poorly expressed. GrB labels a subpopulation of effector cells involved in ongoing cytotoxic action and should be considered as a specific marker showing the extent of the direct local cytotoxic damage. GrB could play a role in the induction of skin apoptosis mechanisms in LE.

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