Presence of cutaneous interferon-a producing cells in patients with systemic lupus erythematosus

Author:

Blomberg S1,Eloranta M L,Cederblad B2,Nordlind K3,Alm G L2,Rönnblom L4

Affiliation:

1. Section of Rheumatology, Department of Medical Sciences, Uppsala University, Uppsala, Sweden; Immunology (V), Biomedical Centre, Box 588, 751 23 Uppsala, Sweden

2. Section of Immunology, Department of Veterinary Microbiology, SLU, Uppsala, Sweden

3. Section of Dermatology and Venereology, Department of Medical Sciences, Uppsala University, Sweden; Unit of Dermatology and Venereology, Department of Medicine, Karolinska Hospital, Stockholm, Sweden

4. Section of Rheumatology, Department of Medical Sciences, Uppsala University, Uppsala, Sweden

Abstract

Systemic lupus erythematosus (SLE) patients have increased levels of interferon-alfa (IFN-a) in the circulation but a reduced number of functionally intact natural IFN-a producing cells (IPC) in peripheral blood. In search for tissue localisation of activated IPC, we investigated skin biopsies from SLE patients for the occurrence of such cells. Eleven SLE patients with inflammatory skin lesions and six healthy controls were biopsied. An immunohistochemical technique (IH) and in situ hybridisation (ISH) were used to detect intracellular IFN-a protein and IFN-a mRNA, respectively. In all 11 biopsies from SLE lesions, a high number of IPC were detected by IH. In the nonlesional SLE biopsies we could also demonstrate IPC in 10=11 patients. In 6=11 SLE patients, IFN- a mRNA containing cells could be detected in the specimens. A low number of IPC were detected in 1=6 healthy controls by IH, but no ISH positive cells were seen. Our results demonstrate that SLE patients have active IPC in both dermal lesions and in noninflammatory skin. A recruitment of IPC from blood to peripheral tissues may explain the low number of circulating natural IPC in SLE patients. Because the type I IFN system is involved in the SLE disease process, these results are of interest for the understanding of the pathogenesis in SLE.

Publisher

SAGE Publications

Subject

Rheumatology

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