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Immune response-associated (Ia) antigens are important as molecules in antigen recognition by T cells. Keratinocytes can express La antigens in many inflammatory dermatoses and by action of gamma interferon (IEN-γ). A keratinocyte cell line, Pam 212 cells, expressed Ia antigens at maintaining culture. They also expressed Ia antigens under the influence of IFN-γ. Liposomes carrying molecules from trinitrophenylated-Pam cells did not stimulate lymphnode cells (LCs) of contact sensitivity; however, liposomes carrying a large amount of those molecules stimulated LCs. This stimulation was attributable to contaminated Ia antigens in those molecules. Liposomes with a small amount of those molecules or trinitrophenylated-proteins from Pam cells were prepared. Into them were inserted Ia antigen-rich proteins from Pam cells, spleen cells, IFN-γ-treated Pam cells, or epidermal cells containing Langerhans cells. Thus prepared liposomes stimulated the LCs significantly. The Ia antigens obtained from IFN-γ--treated Pam cells worked as well as Ia antigens from epidermal cells that contained Langerhans cells as the molecule of antigen presentation in contact sensitivity. [ABSTRACT FROM AUTHOR]

Liposomes carrying molecules from trinitrophenylated epidermal cells (TNP-EC) liposomes stimulated the hapten-specific proliferation of lymphocytes in vitro in our previous study. In order to analyze the role of TNP- EC liposomes in vivo, they were injected into naive mice. TNP-EC liposomes induced contact sensitivity effectively when injected either s.c. or i.p. Contact sensitivity induced by TNP-EC liposomes was a long-lived T cell-mediated reaction. A s.c. injection of liposomes with molecules from TNP-Ia antigen-depleted epidermal cells [TNP-EC (Ia-) liposomes] failed to induce contact sensitivity and developed unresponsiveness. This unresponsiveness was transferred by T cells, i.e., suppressor T cells. Therefore, it is suggested that Ia antigens in epidermal cells play a critical role for induction and suppression of contact sensitivity. [ABSTRACT FROM AUTHOR]

Liposomes containing the extract of trinitrophenylated (TNP) epidermal cells stimulated lymph node cells from TNCB-sensitized mice effectively. Optimal stimulation was achieved by the liposome containing 0.06 μg of the extract of TNP epidermal cells/μg of phospholipid at a concentration of 20 μg phospholipid/ml. The response was hapten-specific and macrophage-dependent. UV irradiation of the epidermal cells abolished their ability to stimulate the lymph node cells. Furthermore, the liposomes containing the extract of TNP epidermal cells treated with anti-Ia and complement failed to stimulate the lymph node cells. The liposomes recovered their reactivity when nonhaptenated Ia antigen-rich epidermal extract was added. Taken together, it is likely that haptenated molecules and Ia antigen on the liposome stimulated T-lymphocytes in the presence of macrophages. [ABSTRACT FROM AUTHOR]

In order to demonstrate an epidermal influence on blood vessels various tissues from neonatal hamsters, enclosed by Millipore filters, were transplanted into hamster cheek pouch chambers. Epidermis, buccal membrane and lung induced new vessel growth, while heart muscle, dermis and other tissues did not. The new capillaries grew as loops over the Millipore filter to surround the epidermal transplant but never to cover it. They anastomosed with each other and formed a network: similar to that seen in normal human skin. Only incomplete capillary growth was noted around the lung transplant. New capillary growth was prominent at the vascular membrane side around buccal membrane. At least three kinds of epidermal influence on blood vessels were suggested by this experiment: a) stimulation of new vessel growth, b) scaffold formation for the capillaries to climb up over the Millipore filter, and c) barrier formation to prevent vessel invasion into the epidermis. [ABSTRACT FROM AUTHOR]