Downregulation of class II molecules on epidermal Langerhans cells in Lyme borreliosis
β Scribed by M. Silberer; F. Koszik; G. Stingl; E. Aberer
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- English
- Weight
- 487 KB
- Volume
- 143
- Category
- Article
- ISSN
- 0007-0963
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β¦ Synopsis
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.
π SIMILAR VOLUMES
Retroviral antibody capable of binding to the major histocompatibility complex (MHC) Class II molecule has been documented in human immunode"ciency virus-1 (HIV-1)-infected patients. Interactions between the MHC Class II receptor and the T-cell receptor (TCR) are central to the immune response. Impo