Lymphocytic Exocytosis Research Articles

Keratinocytes in lesional skin of atopic eczema bear HLA-DR, CD1a and IgE molecules

Apparently normal, and lesional skin from patients with atopic eczema were investigated immunohistochemically with anti-HLA-DR, -CD1a and -IgE antisera. A CD1a+ intercellular pattern was observed in uninvolved skin in the majority of the patients whereas an HLA-DR+/CD1a+ network, mostly localized in basal and supra-basal areas, was shown in lesional skin of virtually all of them. Moreover, an HLA-DR+/CD1a+IgE+ intercellular pattern was observed in some of the patients only and was predominantly localized in those areas characterized by lymphocyte exocytosis, spongiosis or vesicle formation. Whether keratinocytes are able to synthesize CD1a antigen and Fc epsilon R or if these molecules are only produced and shed by CD1a+/IgE+ epidermal dendritic cells remains unclear.

Cyclosporine-induced cell-mediated injury of the thymic medullary epithelium.

Cyclosporine (CsA) can induce prolonged tolerance to alloantigens, but it requires an intact thymus. In normal rats, CsA causes a rapid but reversible ablation of the thymic medulla with an associated loss of the Hassall's corpuscles and apparent maturation arrest of the thymocytes. We have tested the hypothesis that CsA induces a cell-mediated lysis of the medullary epithelium. Normal rats were treated with CsA (15 mg/kg) or vehicle. The thymocytes were then adoptively transferred into syngeneic target rats, purged of thymocytes by recent total-body irradiation. After 4-48 hr, the target animals were sacrificed. The target thymi showed increased lymphocytic exocytosis of the Hassall's corpuscles with OX-8+ (CD8+) T lymphocytes (OX-19+, OX-44+) and associated epithelial cell injury. Compared to recipients of control thymocytes, ultrastructural evaluation showed broad-based and point contact between lymphocytes and adjacent medullary epithelium with increased epithelial cell injury. The results support a cell-mediated injury to the Hassall's corpuscles in CsA-treated animals.

Necrotizing lymphocytic folliculitis: The early lesion of acne necrotica (varioliformis)

Skin biopsy specimens from four patients who had recurrent bouts of lesions conforming to the clinical description of acne necrotica were studied. The pathologic findings were dominated by lymphocytic inflammation around centrally placed follicles evolving to follicular necrosis that extended to the perifollicular epidermis and dermis. Early lesions showed the development of multiple individual necrotic keratinocytes within the follicular sheath and adjacent epidermis with lymphocytic exocytosis. Later lesions showed more intense necrosis and scale crust obscuring the central target but were still dominated by a peripheral lymphocytic infiltrate. The early pathologic findings of acne necrotica (varioliformis) are represented by a necrotizing lymphocytic folliculitis and differ from the pattern seen in association with nonspecific excoriations, acute bacterial folliculitis, classic comedogenic acne, or acnitis.

HLA-DR antigen expression on the keratinocyte surface in dermatoses characterized by lymphocytic exocytosis (e.g. pityriasis rosea).

We have investigated the immunoperoxidase staining pattern of the epidermis in several dermatoses characterized by exocytosis of mononuclear cells into the epidermis. We found that HLA-DR antigens showed an intercellular distribution in localized areas of the epidermis in nine of ten cases of pityriasis rosea, and in all four cases of spontaneously regressing flat warts, two cases of pityriasis lichenoides chronica, two of Schamberg's disease, and one case of lichen striatus. Lichen planus and mycosis fungoides cases were used as positive controls. OKT6 antigen was recognized only on the dendritic cells of the epidermis in all these cases. Judging from the distribution of Langerhans cells, the epidermal intercellular HLA-DR antigen seems to be expressed on the keratinocytes in such diseases, and this feature was confirmed by immunoelectron microscopy. These findings support the hypothesis that the expression of HLA-DR antigen on keratinocytes in these dermatoses is linked to cellular immune reactions involving the epidermis.

Delayed and persistent cutaneous reactions to coelenterates

Three patients are described who developed firm, persistent papules and plaques at sites of previous contact with two species of coelenterates. Histologically, a predominantly mononuclear inflammatory cell infiltrate located primarily in the reticular dermis was observed with destruction of hair follicle epithelium and arrectores pilorum. Epidermal changes included focal spongiosis and exocytosis of lymphocytes. The eruptions subsided no sooner than 7 weeks from time of onset. It is hypothesized that this cutaneous reaction represents a persistent delayed hypersensitivity response to an antigenic component of the coelenterate nematocyst.

Inflammatory Seborrheic Keratoses with Mononuclear Cell Infiltration

Inflammation in inflammatory seborrheic keratoses was found to be composed of mononuclear cells, particularly lymphocytes. Accumulations of mononuclear cells in the papillary and subpapillary dermis frequently showed no tendency to infiltrate the epithelium. However, dramatic interaction of the seborrheic keratosis and the inflammatory process also was common. The lymphocytic exocytosis into the epithelium followed two basic patterns: eczematous, characterized by intercellular and intracellular edema, microvesicle formation, and epithelial necrosis; and lichenoid, in which a bandlike infiltrate attacked the dermoepidermal junction and hyaline bodies occurred in the infiltrated epithelium and in the dermis. Epithelial changes consisted of necrosis of epithelial cells and related parakeratosis; squamous eddies were occasionally found. Inflammatory cell infiltration in seborrheic keratoses possibly represents a process other than irritation, and we propose that mononuclear cell infiltration in seborrheic keratoses may be related to an involutionary process.