Murine T cell Ia antigens: specificity Iat.46 maps in I-J to I-E chromosomal segment of H-2 complex.

Hayes, Colleen E.; Maier, John Michael

doi:10.1073/pnas.77.11.6783

Cited by 3 publications

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References 37 publications

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“…Anti-Thy-l.2 serum was made according to Reifand Allen (8). Goat antimouse immunoglobulin was produced in our laboratory (9). Culture supernatant containing anti-I-J k monoclonal antibody WF8.C 12.8 was kindly provided by Dr. C. Waltenbaugh (Northwestern University Medical School, Chicago, IL).…”

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confidence: 99%

T cell surface I-J glycoprotein. Concerted action of chromosome-4 and -17 genes forms an epitope dependent on alpha-D-mannosyl residues.

Klyczek¹,

Cantor²,

Hayes³

1984

The Journal of Experimental Medicine

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Two genes acting in concert control murine T cell I-Jk expression. We determined I-Jk expression with I-Jk--specific monoclonal antibodies WF8 .C12.8 and five others produced in our laboratory in a cytotoxicity assay. Previous experiments established that an H-2k gene and a chromosome 4 gene, Jt , regulate I-Jk expression. We show here that B10. HTT and B10.S( 9R ) do not differ at the H-2k locus required for I-Jk expression. Rather B10. HTT , like B10.A(3R), lacks some important non--H-2 gene (possibly Jt ). The intra--H-2k I-J--controlling locus maps to the right of the I-A subregion. The I-Jk determinant involves a carbohydrate structure associated with protein; inhibiting either protein synthesis or glycosylation prevents T cell I-Jk reexpression after proteolytic removal. Treatment with alpha-mannosidase destroys I-Jk determinants, implicating terminal alpha-D-mannosyl residues in the I-Jk epitope. Models for H-2 and Jt control of I-J expression are discussed.

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T cell surface I-J glycoprotein. Concerted action of chromosome-4 and -17 genes forms an epitope dependent on alpha-D-mannosyl residues.

Klyczek¹,

Cantor²,

Hayes³

1984

The Journal of Experimental Medicine

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“…Several laboratories using diverse experimental systems agreed completely with the I-J gene placement. Mouse strains with different H-2 gene complexes exhibited apparently allelic I-J polymorphisms (Murphy 1981, Dorf & Benacerraf 1984, Hayes & Maier 1980. When distinct regulatory T cells within a strain displayed unique I-J epitopes, an I-J multigene family was postulated .…”

Section: I-region Dna and Mrnamentioning

confidence: 99%

The I‐J Glycoprotein: Genetic Control, Biochemistry, and Function

Hayes

Klyczek

1985

Immunological Reviews

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The I-J molecule is a mannosylated protein expressed early in T cell ontogeny in partially shielded form, later fully exposed on an activated T cell subset. Others determined a 25-30,000 molecular weight for cellular (Kumagai et al. 1984) and secreted forms (Taniguchi et al. 1984). Both the cell membrane and secreted types seem to govern genetically-restricted interactions completing suppressor cell circuits. The soluble I-J polypeptide has no antigen-binding site, but associates with an antigen-binding chain via disulfide bonding (Taniguchi et al. 1984, Lei et al. 1983). Similarly, evidence suggests that cellular I-J molecules are part of or proximal to T cell antigen receptor complexes (Fig. 4). At least two genes control T cell I-Jk expression, one apparently in I-E, another on chromosome 4. Undiscovered loci may also participate. Since I-J+ T cells do not transcribe I-region DNA, the I-E gene must be an untranscribed regulatory element in T cells or a protein translated in the host environment. If in the host environment, it probably does not function enzymatically to form T cell I-J epitopes; removed from the host, T cells biosynthesize complete I-J determinants. Host I-E gene products may regulate I-J expression in an early T cell maturation step. For example, the E alpha E beta proteins of thymic macrophages and epithelial cells may drive the expansion of T cells with E alpha E beta-complementary receptors encoded by I-J genes outside H-2. Genetic control of this self receptor would then apparently map to the selective ligand gene, I-E, as well as the I-J structural gene elsewhere (Klyczek et al. 1984b). This attractive theory, proposed in its original form by Jerne (1971) and later by Schrader (1979), has received significant support. Definitive proof must await further experimentation.

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Murine T cell-specific Ia antigens: monoclonal antibodies define an I-A-encoded T lymphocyte structure.

Hayes¹,

Hullett²

1982

Proc. Natl. Acad. Sci. U.S.A.

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T lymphocytes express a unique I-A subregioncontrolled surface molecule that is not expressed on B lymphocytes. We produced antisera and monoclonal antibodies recognizing this structure. Exhaustive B cell adsorption of (A.TH x BIO.HTT)Fj antiserum, produced against activated A.TL T cells, left antibodies that bind an I-Ak specificity on some B10.A(4R) T lymphocytes (11 ± 2%, mean ± SEM). Similarly, exhaustive B cell adsorption of (A/J x BIO.MBR)F1 antiserum, produced against activated BIO.A(5R) cells, left antibodies specific for an I-A determinanton B10.A(5R) Tcells (17 ± 2%). We fused A.TL-immune (ATH x BIO.HTT)F1 splenocytes with NS-1 myeloma cells and identified antibody-producing hybrid cells by a fluorescent enzyme-linked immunosorbent microassay described herein. Eight monoclonal antibodies were selected; these lyse 7-26% of peripheral T cells from I-Ak strains. Thymocytes and bone marrow cells do not express the I-Ak T cell determinant. Exhaustive B cell adsorption did not remove I-Ak T cell-specific monoclonal antibodies.

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Murine T cell Ia antigens: specificity Iat.46 maps in I-J to I-E chromosomal segment of H-2 complex.

Abstract: ABSTRACT

Cited by 3 publications

References 37 publications

T cell surface I-J glycoprotein. Concerted action of chromosome-4 and -17 genes forms an epitope dependent on alpha-D-mannosyl residues.

T cell surface I-J glycoprotein. Concerted action of chromosome-4 and -17 genes forms an epitope dependent on alpha-D-mannosyl residues.

The I‐J Glycoprotein: Genetic Control, Biochemistry, and Function

Murine T cell-specific Ia antigens: monoclonal antibodies define an I-A-encoded T lymphocyte structure.

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