Both dendritic cells and memory T lymphocytes emigrate from organ cultures of human skin and form distinctive dendritic-T-cell conjugates.

Prior studies of mouse skin in organ culture have shown that dendritic cells selectively emigrate from the explants over 1-3 d. This emigration may model the movements of dendritic cells that can occur in situ, as in transplantation and contact sensitivity. In this study, we cultured explants of normal human skin that had been removed with a dermatome. Dendritic cells with characteristic morphology and mixed leukocyte response-stimulatory activity emigrated. The dendritic cells had the expected phenotype, e.g., rich in major histocompatibility complex class II and accessory molecules such as B7-1, intercellular adhesion molecule-1, and leukocyte function-associated antigen-3. Small lymphocytes also were present in the emigrated populations and proved to be T cells exclusively, almost entirely of the TcR alpha beta and memory type (CD45RAweak, CD45RO LFA-3/CD58+), with a CD4:CD8 subset ratio of about 2:1. Some of the T cells were bound tightly to the dendritic cells. These conjugates did not dissociate after exposure to trypsin or to calcium- and magnesium-free medium, or during cytofluorography. This made it possible to sort distinct populations of single dendritic cells, single T cells, and conjugates of the two cell types. Conjugates would continue to form from mixtures of separated dendritic cells and T cells in culture. Therefore, cutaneous dendritic cells and memory T lymphocytes emigrate from human skin explants, and some of these cells form distinctive conjugates that we hypothesize contribute to immunologic recall reactions.

Conjugates of dendritic cells and memory T lymphocytes from skin facilitate productive infection with HIV-1.

Experimentally, a productive infection with HIV-1 requires that virus be administered to T cells that are activated by mitogens. We describe a productive milieu for HIV-1 within the confines of normal skin that does not require standard stimuli. The milieu consists of dendritic cells and T cells that emigrate from skin and produce distinctive stable, nonproliferating conjugates. These conjugates, upon exposure to each of seven different HIV-1 isolates, begin to release high levels of virus progeny within 4 days. Numerous infected syncytia, comprised of both dendritic and T cells, rapidly develop. We propose that conjugates of dendritic cells and T cells, as found in the external linings of organs involved in sexual transmission of HIV-1, represent an important site for the productive phase of HIV-1 infection. Because the affected T cells carry the memory phenotype, this site additionally provides a mechanism for the chronic depletion of CD4+ memory cells in HIV-1 disease.

Silicone migration to the pleural space associated with silicone-gel augmentation mammaplasty.

We present a case report of silicone particles found in the pleural fluid of a patient 20 years after bilateral augmentation mammaplasty with silicone-gel implants. The patient's history is notable for bilateral replacements of implants and multiple closed capsulotomies several years subsequent to the original augmentation procedure. A ruptured left implant was found in 1991 when she first experienced pain in the upper back. A left pleural effusion developed subsequently. Analysis of the pleural effusion fluid by scanning electron microscopy suggested the presence of silicone. All laboratory results were normal, and the effusion did not recur after thoracentesis. The patient has been under close follow-up, and further pulmonary complications or other symptoms have not developed. This case report demonstrates the potential for silicone migration to the pleura and the possibility of subsequent pulmonary complications, such as pleural effusion.

Autoimmune disease and silicone breast implants.

An association between crystalline silica and immune disease has long been recognized. However, despite ongoing case reports of systemic autoimmune disease in silicone implant recipients, the available data has not been sufficient to prove or disprove a causal relationship. Silicone has been shown to "bleed" from the implants and can migrate to distant sites. There is evidence of cellular and humoral immune responses to silicone in vivo, but the role of these responses in the development of connective tissue disorders has not been determined. Further studies are necessary to elucidate the role of silicone, if any, in the pathogenesis of autoimmune connective tissue disease. Meanwhile, the implant population needs to be closely monitored; their clinical management should be based on a case by case evaluation.