Downregulation of class II molecules on epidermal Langerhans cells in Lyme borreliosis.

BACKGROUND

Borrelia burgdorferi can be isolated from the skin of patients with acrodermatitis chronica atrophicans (ACA), a late-stage manifestation of Lyme borreliosis; despite a marked T-cell infiltrate in lesional skin and high antibody titres in patients' sera.

OBJECTIVES

To determine whether antigen-presenting Langerhans cells (LCs), which reportedly show signs of injury in erythema chronicum migrans (ECM), the early stage of disease, are altered in ACA.

PATIENTS/

METHODS

We studied the immunophenotype of cutaneous leucocytes on cryostat sections of lesional skin from both ECM and ACA patients.

RESULTS

The total number of CD1a+ cells evaluated by semiautomatic image analysis was lower in ECM (594 +/- 263 cells mm(-2) epidermis) than in ACA (835 +/- 317 cells mm(-2) epidermis). HLA-DR expression was remarkably downregulated on CD1a+ LCs to 29% in ECM and 18% in ACA, whereas in normal skin, most of the epidermal CD1a+ dendritic cells were HLA-DR+. The inflammatory infiltrate was mainly composed of CD68+ macrophages and CD45RO+ memory T cells, with a predominance of CD4+ helper T cells.

CONCLUSIONS

It is conceivable that the downregulation of major histocompatibility complex class II molecules on LC in both the early and late skin manifestations of Lyme borreliosis is indicative of a poorly effective anti-B. burgdorferi immune response and thus at least partly responsible for the insufficient elimination of this micro-organism from ACA skin.