Regulation of immune responses by I-J gene products. I. Production and characterization of anti-I-J monoclonal antibodies.

Waltenbaugh, Carl

doi:10.1084/jem.154.5.1570

Cited by 67 publications

(38 citation statements)

References 26 publications

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“…variety of antigenic systems have been shown to involve T cells that bear determinants encoded by the I-J subregion of the H-2 gene complex (16,(23)(24)(25)(26). The I-J phenotype of pork insulin-specific suppressor cells was evaluated next.…”

Section: Requirement For I-j + Cells For Suppression Suppressor Pathmentioning

confidence: 99%

Regulatory mechanisms in immune responses to heterologous insulins. II. Suppressor T cell activation associated with nonresponsiveness in H-2b mice.

Jensen¹,

Pierce²,

Kapp³

1984

The Journal of Experimental Medicine

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Murine antibody responses to insulins are controlled by MHC-linked Ir genes. Although mice of the H-2b haplotype do not make antibody in response to pork insulin, we demonstrate in this communication that immunization with pork insulin stimulates radioresistant, Lyt-1+2- helper T cells that are capable of stimulating secondary antibody responses to pork insulin in vitro, but that this activity is masked by radiosensitive, Lyt-1-2+, I-J+ suppressor T cells. The suppressor T cells, present after immunization with pork insulin but not beef insulin, suppress the secondary response to pork but not beef insulin. The amino acid sequences of pork and beef insulins differ only at the A-chain loop; thus, pork insulin-specific suppressor T cells appear to recognize the A-chain loop determinant of pork insulin. The amino acid sequences of mouse and pork insulin are identical in the A-chain loop, which suggests that these suppressor T cells may be self-reactive. If this interpretation is correct, these suppressor T cells could be involved in the maintenance of self-tolerance to insulin. Nevertheless, these data clearly demonstrate that genetically determined nonresponsiveness in H-2b mice is conferred by activation of dominant, insulin-specific suppressor T cells (Ts), rather than by a defect in the stimulation of insulin-specific helper T cells (Th).

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Section: Requirement For I-j + Cells For Suppression Suppressor Pathmentioning

confidence: 99%

Regulatory mechanisms in immune responses to heterologous insulins. II. Suppressor T cell activation associated with nonresponsiveness in H-2b mice.

Jensen¹,

Pierce²,

Kapp³

1984

The Journal of Experimental Medicine

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“…Kanno and coworkers isolated monoclonal, I-J-specific antibodies that bind to a T cell hybridoma (27). Waltenbaugh used a functional assay to isolate monoclonal antibodies specific for I-J determinants (28 (38)(39)(40). Perhaps more than one immunoregulatory mechanism may be ascribed to Ir genes.…”

Section: Resultsmentioning

confidence: 99%

“…A second family of I-region gene products, Tat molecules, occurs on some T lymphocytes and regulatory T cell products (19)(20)(21)(22)(23) but not on B lymphocytes or B cell products (20,(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35). Tat determinants are observed primarily in studies ofregulatory T lymphocyte function (19)(20)(21)(22)(23)26).…”

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confidence: 99%

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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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“…(3R) (anti-I-J b) were produced by immunization with spleen and lymph node cells, as described elsewhere (19). Monoclonal anti-I-J antibodies, WF8.C2.4 (anti-I-jk), WF8.D2.3 (ant-I-jk), and WF9.40.5 (anti-I-J b) were characterized previously (20,21). Both monoclonal antiThy-l.1 and Thy-l.2 antibodies were purchased from New England Nuclear, Boston, MA.…”

Section: Methodsmentioning

confidence: 99%

The role of I-J and Igh determinants on F1-derived suppressor factor in controlling restriction specificity.

Minami

Aoki

Honji

et al. 1983

The Journal of Experimental Medicine

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In the 4-hydroxy-3-nitrophenyl acetyl (NP) contact sensitivity system, the activity of third-order suppressor cells and their factors is restricted by H-2(I-J) and Igh linked genes. The present report analyzes the specificity of NP-specific Ts3 cells and factors derived from H-2 and Igh heterozygous (B6 X C3H)F1 mice. Two approaches were used. First, heterogeneous populations of F1 Ts3 cells were activated in vitro and then assayed in Ts3-depleted recipients which carried different combinations of H-2 and Igh alleles. The second approach was to hybridize the Ts3 cells and analyze the specificity of the F1-derived TsF3. The combined data demonstrated four functionally distinct populations of Ts3 cells. The activity of each population was restricted by a particular combination of H-2 and Igh haplotypes. Thus, Ts3 cells derived from F1 donors can demonstrate an apparent scrambling of H-2 and Igh restriction specificities. There was functional allelic exclusion of the H-2(I-J) and Igh determinants expressed on (B6 X C3H)F1 hybridoma-derived TsF3. Thus, TsF3 from each cloned hybridoma line expressed only one set of I-J and Igh determinants. Furthermore, there was a complete correlation between the I-J and Igh linked determinants expressed on TsF3 and the restriction specificity. In view of the recent findings on the molecular biology of the I-J region, an alternative interpretation of the role of I-J determinants on suppressor cells and factors is offered.

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Regulation of immune responses by I-J gene products. I. Production and characterization of anti-I-J monoclonal antibodies.

Cited by 67 publications

References 26 publications

Regulatory mechanisms in immune responses to heterologous insulins. II. Suppressor T cell activation associated with nonresponsiveness in H-2b mice.

Regulatory mechanisms in immune responses to heterologous insulins. II. Suppressor T cell activation associated with nonresponsiveness in H-2b mice.

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

The role of I-J and Igh determinants on F1-derived suppressor factor in controlling restriction specificity.

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