Regulation of Fc receptor for IgE (CD23) and class II MHC antigen expression on Burkitt's lymphoma cell lines by human IL-4 and IFN-gamma. 1988

F Rousset, and R W Malefijt, and B Slierendregt, and J P Aubry, and J Y Bonnefoy, and T Defrance, and J Banchereau, and J E de Vries
UNICET, Laboratory for Immunological Research, Dardilly, France.

The effect of rIL-4 on the expression of low affinity receptor for the Fc part of IgE (Fc epsilon R2/CD23) and class II MHC antigens on Burkitt's lymphoma (BL) cell lines was investigated. Some of the BL lines contained low percentages of CD23 and HLA-DQ-positive cells, but virtually all cells expressed HLA-DR. IL-4 induced CD23 and class II MHC Ag expression on 7 of 9 BL. Optimal CD23 and class II MHC expression was observed after 48-72 h of incubation. Induction of CD23 and class II MHC Ag in the BL cell line BL2 by IL-4 was confirmed at the specific mRNA level. Significant activation of HLA-DQ mRNA was obtained after 6 h of incubation with IL-4 and gradually increased during prolonged incubation. Maximal induction of mRNA transcription occurred after 48 to 72 h. Optimal induction of HLA-DR and CD23 transcription in BL2 was also observed after 48 to 72 h. The induction of CD23 and class II MHC Ag seems to be specific for IL-4, because rIL-1, rIL-2, rIFN-gamma, recombinant granulocyte-macrophage-CSF, and a commercial source of low m.w. B cell growth factor were ineffective. In addition, the expression of class I MHC Ag, the transferrin receptor, CD38, CD25, CD10, CD20, and CD21 were not affected by IL-4. Interestingly, IFN-gamma and PGE2 suppressed the IL-4-induced membrane expression of CD23 and class II MHC Ag in a dose-dependent way. IFN-gamma also blocked IL-4-induced CD23 mRNA transcription in BL2 completely, whereas PGE2 (10(-7) M) was partially inhibitory. The induction of CD23 and class II MHC Ag by IL-4 required intact protein synthesis as shown by its inhibition by cycloheximide. These results indicate that the induction of CD23 and class II MHC Ag by IL-4 is regulated in a coordinated way.

UI MeSH Term Description Entries
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
D007378 Interleukins Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli. Interleukin
D011961 Receptors, Fc Molecules found on the surface of some, but not all, B-lymphocytes, T-lymphocytes, and macrophages, which recognize and combine with the Fc (crystallizable) portion of immunoglobulin molecules. Fc Receptors,Fc Receptor,Receptor, Fc
D011994 Recombinant Proteins Proteins prepared by recombinant DNA technology. Biosynthetic Protein,Biosynthetic Proteins,DNA Recombinant Proteins,Recombinant Protein,Proteins, Biosynthetic,Proteins, Recombinant DNA,DNA Proteins, Recombinant,Protein, Biosynthetic,Protein, Recombinant,Proteins, DNA Recombinant,Proteins, Recombinant,Recombinant DNA Proteins,Recombinant Proteins, DNA
D002051 Burkitt Lymphoma A form of undifferentiated malignant LYMPHOMA usually found in central Africa, but also reported in other parts of the world. It is commonly manifested as a large osteolytic lesion in the jaw or as an abdominal mass. B-cell antigens are expressed on the immature cells that make up the tumor in virtually all cases of Burkitt lymphoma. The Epstein-Barr virus (HERPESVIRUS 4, HUMAN) has been isolated from Burkitt lymphoma cases in Africa and it is implicated as the causative agent in these cases; however, most non-African cases are EBV-negative. African Lymphoma,Burkitt Cell Leukemia,Burkitt Tumor,Lymphoma, Burkitt,Burkitt Leukemia,Burkitt's Leukemia,Burkitt's Lymphoma,Burkitt's Tumor,Leukemia, Lymphoblastic, Burkitt-Type,Leukemia, Lymphocytic, L3,Lymphocytic Leukemia, L3,Burkitts Leukemia,Burkitts Lymphoma,Burkitts Tumor,L3 Lymphocytic Leukemia,L3 Lymphocytic Leukemias,Leukemia, Burkitt,Leukemia, Burkitt Cell,Leukemia, Burkitt's,Leukemia, L3 Lymphocytic,Lymphoma, African,Lymphoma, Burkitt's,Tumor, Burkitt,Tumor, Burkitt's
D005786 Gene Expression Regulation Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation. Gene Action Regulation,Regulation of Gene Expression,Expression Regulation, Gene,Regulation, Gene Action,Regulation, Gene Expression
D006681 HLA-D Antigens Human immune-response or Class II antigens found mainly, but not exclusively, on B-lymphocytes and produced from genes of the HLA-D locus. They are extremely polymorphic families of glycopeptides, each consisting of two chains, alpha and beta. This group of antigens includes the -DR, -DQ and -DP designations, of which HLA-DR is most studied; some of these glycoproteins are associated with certain diseases, possibly of immune etiology. Antigens, HLA-D,Class II Human Antigens,HLA-Dw Antigens,Human Class II Antigens,Ia-Like Antigens, Human,Immune Response-Associated Antigens, Human,Immune-Associated Antigens, Human,Immune-Response Antigens, Human,HLA-D,HLA-Dw,Immune Response Associated Antigens, Human,Antigens, HLA D,Antigens, HLA-Dw,Antigens, Human Ia-Like,Antigens, Human Immune-Associated,Antigens, Human Immune-Response,HLA D Antigens,HLA Dw Antigens,Human Ia-Like Antigens,Human Immune-Associated Antigens,Human Immune-Response Antigens,Ia Like Antigens, Human,Immune Associated Antigens, Human,Immune Response Antigens, Human
D006683 HLA-DQ Antigens A group of the D-related HLA antigens found to differ from the DR antigens in genetic locus and therefore inheritance. These antigens are polymorphic glycoproteins comprising alpha and beta chains and are found on lymphoid and other cells, often associated with certain diseases. HLA-DC Antigens,HLA-MB Antigens,HLA-DC,HLA-DQ,HLA-DS,HLA-DS Antigens,HLA-LB,HLA-LB Antigens,HLA-MB,Antigens, HLA-DC,Antigens, HLA-DQ,Antigens, HLA-DS,Antigens, HLA-LB,Antigens, HLA-MB,HLA DC Antigens,HLA DQ Antigens,HLA DS Antigens,HLA LB Antigens,HLA MB Antigens
D006684 HLA-DR Antigens A subclass of HLA-D antigens that consist of alpha and beta chains. The inheritance of HLA-DR antigens differs from that of the HLA-DQ ANTIGENS and HLA-DP ANTIGENS. HLA-DR,Antigens, HLA-DR,HLA DR Antigens
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man

Related Publications

F Rousset, and R W Malefijt, and B Slierendregt, and J P Aubry, and J Y Bonnefoy, and T Defrance, and J Banchereau, and J E de Vries
December 1989, Journal of immunology (Baltimore, Md. : 1950),
F Rousset, and R W Malefijt, and B Slierendregt, and J P Aubry, and J Y Bonnefoy, and T Defrance, and J Banchereau, and J E de Vries
February 1985, International journal of cancer,
F Rousset, and R W Malefijt, and B Slierendregt, and J P Aubry, and J Y Bonnefoy, and T Defrance, and J Banchereau, and J E de Vries
September 1991, Journal of immunology (Baltimore, Md. : 1950),
F Rousset, and R W Malefijt, and B Slierendregt, and J P Aubry, and J Y Bonnefoy, and T Defrance, and J Banchereau, and J E de Vries
May 1989, Immunology,
F Rousset, and R W Malefijt, and B Slierendregt, and J P Aubry, and J Y Bonnefoy, and T Defrance, and J Banchereau, and J E de Vries
March 1989, Journal of cellular biochemistry,
F Rousset, and R W Malefijt, and B Slierendregt, and J P Aubry, and J Y Bonnefoy, and T Defrance, and J Banchereau, and J E de Vries
May 1996, Cellular immunology,
F Rousset, and R W Malefijt, and B Slierendregt, and J P Aubry, and J Y Bonnefoy, and T Defrance, and J Banchereau, and J E de Vries
November 1988, Cell,
F Rousset, and R W Malefijt, and B Slierendregt, and J P Aubry, and J Y Bonnefoy, and T Defrance, and J Banchereau, and J E de Vries
January 1989, Journal of immunology (Baltimore, Md. : 1950),
F Rousset, and R W Malefijt, and B Slierendregt, and J P Aubry, and J Y Bonnefoy, and T Defrance, and J Banchereau, and J E de Vries
May 1989, Immunology,
F Rousset, and R W Malefijt, and B Slierendregt, and J P Aubry, and J Y Bonnefoy, and T Defrance, and J Banchereau, and J E de Vries
August 1990, Journal of immunology (Baltimore, Md. : 1950),
Copied contents to your clipboard!