       Document 0798
 DOCN  M95A0798
 TI    Maturation and migration of cutaneous dendritic cells.
 DT    9510
 AU    Steinman R; Hoffman L; Pope M; Laboratory of Cellular Physiology and
       Immunology, Rockefeller; University, New York, NY 10021, USA.
 SO    J Invest Dermatol. 1995 Jul;105(1 Suppl):2S-7S. Unique Identifier :
       AIDSLINE MED/95341043
 AB    Dendritic cells have been isolated from the epidermis, dermis, and
       lymphatics of skin. Cells from each cutaneous compartment can exhibit
       the distinct morphology, surface phenotype, and strong
       T-cell-stimulating activity of dendritic cells that are isolated from
       other organs. Of importance are the mechanisms by which the maturation
       and movement of dendritic cells are regulated within intact tissues.
       Epidermal dendritic cells turn over slowly in the steady state. Stimuli,
       including contact allergens and transplantation, perhaps by inducing a
       release of cytokines such as granulocyte macrophage-colony-stimulating
       factor, mobilize these dendritic cells into the dermis and lymph. This
       migration is accompanied by the maturation of dendritic cell functions;
       e.g., antigen-presenting major histocompatibility complex molecules and
       B7 costimulators increase markedly. On the other hand, there is a
       sizable, steady-state flux of dendritic cells in afferent lymph draining
       the skin, which suggests a constant traffic through the dermis that is
       independent of sessile epidermal dendritic cells. When explants of skin
       are placed in organ culture, dendritic cells emigrate into the medium
       for 1-3 d. The dendritic cells are mature and can bind tightly to small
       memory T cells that also migrate in these cultures. The emigrated
       mixtures of dendritic cells and T cells should be useful in the study of
       many clinical states. This is illustrated by recent experiments showing
       that migratory skin cells are readily infected with human
       immunodeficiency virus (HIV)-1. A strong productive infection takes
       place in the absence of exogenous cytokines, foreign sera, or mitogens
       or antigens. The dendritic cell-T-cell conjugates are the essential site
       for infection. This cellular milieu may model events during the sexual
       transmission of HIV-1, where relevant mucosal surfaces are covered by
       skin-like epithelia. The capture of CD4+ memory T cells by dendritic
       cells may explain the chronic drain of immune memory in HIV infection.
 DE    Animal  Cell Aging  Cell Movement  Dendritic Cells/*PHYSIOLOGY
       Homeostasis  Human  HIV Infections/PHYSIOPATHOLOGY  HIV-1/PHYSIOLOGY
       Immunologic Memory  Skin/*CYTOLOGY/PHYSIOPATHOLOGY/VIROLOGY  Skin
       Transplantation  Support, Non-U.S. Gov't  Support, U.S. Gov't, P.H.S.
       T-Lymphocytes/PHYSIOLOGY  JOURNAL ARTICLE  REVIEW  REVIEW, TUTORIAL

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

