Lymphocytes recognize human vascular endothelial and dermal fibroblast Ia antigens induced by recombinant immune interferon. 1983

J S Pober, and T Collins, and M A Gimbrone, and R S Cotran, and J D Gitlin, and W Fiers, and C Clayberger, and A M Krensky, and S J Burakoff, and C S Reiss

T-lymphocyte-mediated responses to the cellular components of blood vessels are important in rejection of allografts. The induction of cytolytic T lymphocytes (CTLs) depends on recognition of foreign class II major histocompatibility complex antigens (human HLA-DR, DC/DS, SB and others, collectively referred to as Ia) on the target cells whereas killing by CTLs usually depends on recognition of foreign class I antigens (HLA-A, B), although some alloreactive CTLs recognize foreign Ia instead of HLA-A, B (refs 5-8). The expression of Ia antigens has traditionally been regarded as restricted to immunological cell types, and the presence of class II antigen-bearing 'passenger' leukocytes in rodent organ grafts appears necessary for graft rejection. Recently, Ia antigens have been observed by immunofluorescence microscopy on human renal and dermal capillary endothelium. We have previously shown that human umbilical vein endothelial (HUVE) cells in standard culture conditions do not bear Ia antigens, but may be induced to do so by products of lectin- or alloantigen-activated T lymphocytes. Furthermore, we found that recombinant immune interferon (IFN-gamma), free of other lymphokines, is a potent inducer of Ia expression in HUVE cells. Here we report that IFN-gamma also induces Ia expression on human foreskin capillary endothelial (HFCE) cells, HUVE cells transformed by Simian virus 40 viral DNA (SV-HUVE cells) and human dermal fibroblast (HDF) cells in culture. Further, we present evidence that Ia present on HUVE cells and HDF cells can be functionally recognized by human T cells, resulting in a two-way interaction between T cells and mesenchymal cells that may be important in allograft rejection.

UI MeSH Term Description Entries
D007231 Infant, Newborn An infant during the first 28 days after birth. Neonate,Newborns,Infants, Newborn,Neonates,Newborn,Newborn Infant,Newborn Infants
D007371 Interferon-gamma The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES. Interferon Type II,Interferon, Immune,gamma-Interferon,Interferon, gamma,Type II Interferon,Immune Interferon,Interferon, Type II
D008214 Lymphocytes White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS. Lymphoid Cells,Cell, Lymphoid,Cells, Lymphoid,Lymphocyte,Lymphoid Cell
D002478 Cells, Cultured Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others. Cultured Cells,Cell, Cultured,Cultured Cell
D003001 Cloning, Molecular The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells. Molecular Cloning
D004727 Endothelium A layer of epithelium that lines the heart, blood vessels (ENDOTHELIUM, VASCULAR), lymph vessels (ENDOTHELIUM, LYMPHATIC), and the serous cavities of the body. Endotheliums
D005347 Fibroblasts Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. Fibroblast
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000949 Histocompatibility Antigens Class II Large, transmembrane, non-covalently linked glycoproteins (alpha and beta). Both chains can be polymorphic although there is more structural variation in the beta chains. The class II antigens in humans are called HLA-D ANTIGENS and are coded by a gene on chromosome 6. In mice, two genes named IA and IE on chromosome 17 code for the H-2 antigens. The antigens are found on B-lymphocytes, macrophages, epidermal cells, and sperm and are thought to mediate the competence of and cellular cooperation in the immune response. The term IA antigens used to refer only to the proteins encoded by the IA genes in the mouse, but is now used as a generic term for any class II histocompatibility antigen. Antigens, Immune Response,Class II Antigens,Class II Histocompatibility Antigen,Class II Major Histocompatibility Antigen,Ia Antigens,Ia-Like Antigen,Ia-Like Antigens,Immune Response Antigens,Immune-Associated Antigens,Immune-Response-Associated Antigens,MHC Class II Molecule,MHC II Peptide,Class II Antigen,Class II Histocompatibility Antigens,Class II MHC Proteins,Class II Major Histocompatibility Antigens,Class II Major Histocompatibility Molecules,I-A Antigen,I-A-Antigen,IA Antigen,MHC Class II Molecules,MHC II Peptides,MHC-II Molecules,Antigen, Class II,Antigen, I-A,Antigen, IA,Antigen, Ia-Like,Antigens, Class II,Antigens, Ia,Antigens, Ia-Like,Antigens, Immune-Associated,Antigens, Immune-Response-Associated,I A Antigen,II Peptide, MHC,Ia Like Antigen,Ia Like Antigens,Immune Associated Antigens,Immune Response Associated Antigens,MHC II Molecules,Molecules, MHC-II,Peptide, MHC II,Peptides, MHC II
D012867 Skin The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.

Related Publications

J S Pober, and T Collins, and M A Gimbrone, and R S Cotran, and J D Gitlin, and W Fiers, and C Clayberger, and A M Krensky, and S J Burakoff, and C S Reiss
February 1987, Journal of cellular physiology,
J S Pober, and T Collins, and M A Gimbrone, and R S Cotran, and J D Gitlin, and W Fiers, and C Clayberger, and A M Krensky, and S J Burakoff, and C S Reiss
May 1987, Journal of immunology (Baltimore, Md. : 1950),
J S Pober, and T Collins, and M A Gimbrone, and R S Cotran, and J D Gitlin, and W Fiers, and C Clayberger, and A M Krensky, and S J Burakoff, and C S Reiss
March 1984, Journal of immunology (Baltimore, Md. : 1950),
J S Pober, and T Collins, and M A Gimbrone, and R S Cotran, and J D Gitlin, and W Fiers, and C Clayberger, and A M Krensky, and S J Burakoff, and C S Reiss
July 1984, The Journal of experimental medicine,
J S Pober, and T Collins, and M A Gimbrone, and R S Cotran, and J D Gitlin, and W Fiers, and C Clayberger, and A M Krensky, and S J Burakoff, and C S Reiss
October 1985, Journal of immunology (Baltimore, Md. : 1950),
J S Pober, and T Collins, and M A Gimbrone, and R S Cotran, and J D Gitlin, and W Fiers, and C Clayberger, and A M Krensky, and S J Burakoff, and C S Reiss
July 1983, Journal of immunology (Baltimore, Md. : 1950),
J S Pober, and T Collins, and M A Gimbrone, and R S Cotran, and J D Gitlin, and W Fiers, and C Clayberger, and A M Krensky, and S J Burakoff, and C S Reiss
April 1986, The American journal of pathology,
J S Pober, and T Collins, and M A Gimbrone, and R S Cotran, and J D Gitlin, and W Fiers, and C Clayberger, and A M Krensky, and S J Burakoff, and C S Reiss
October 2006, FEBS letters,
J S Pober, and T Collins, and M A Gimbrone, and R S Cotran, and J D Gitlin, and W Fiers, and C Clayberger, and A M Krensky, and S J Burakoff, and C S Reiss
September 1991, Journal of the National Cancer Institute,
J S Pober, and T Collins, and M A Gimbrone, and R S Cotran, and J D Gitlin, and W Fiers, and C Clayberger, and A M Krensky, and S J Burakoff, and C S Reiss
March 1981, Transplantation proceedings,
Copied contents to your clipboard!