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

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.

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.

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

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.

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.