Regulation of T-cell-mediated lympholysis by the murine major histocompatibility complex. II. Control of cytotoxic responses to trinitrophenyl-K and -D self products by H-2K- and H-2D-Region genes.

Levy, Robert B.; Shearer, Gene M.

doi:10.1084/jem.151.1.252

Cited by 13 publications

(2 citation statements)

References 18 publications

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“…H-2K is, therefore, an Ir gene and the H-2K glycoprotein is its molecular agent. Ir genes regulating the responses to trinitrophenylmodified cells (15) and to the Thy-1 alloantigen (16) have been mapped to the H-2K locus using H-2 recombinant mice. Our findings using the B6.H-2 ~ mutant mice strengthen the conclusion that an Ir regulatory function and a target cell H-2K syngeneic signal are pleiotropic effects coded for by a single H-2K structural gene expressed in both the target thyroid and the thymus.…”

Section: Discussionmentioning

confidence: 99%

H-2K mutation controls immune response phenotype of autoimmune thyroiditis. Critical expression of mutant gene product in both thymus and thyroid glands.

Maron¹,

Cohen²

1980

The Journal of Experimental Medicine

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Autoimmune thyroiditis (EAT) can be induced by immunizing mice against mouse thyroglobulin. A gene critical to the phenotypical expression of EAT was mapped to the H-2K locus by studying B6 mice and its mutant strain B6.H-2ba. To identify organs in which expression of the gene was decisive for the EAT phenotype, we transplanted thyroid or irradiated thymus glands into various strains of normal mice or thymusless nude mice. We found that the pathophysiology of EAT was controlled by the expression of specific H-2 genes in both the target thyroid gland and the thymus gland.

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Section: Discussionmentioning

confidence: 99%

H-2K mutation controls immune response phenotype of autoimmune thyroiditis. Critical expression of mutant gene product in both thymus and thyroid glands.

Maron¹,

Cohen²

1980

The Journal of Experimental Medicine

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“…Most hapten-(as well as virus) self CTL responses exhibit preferential recognition, that is, the predominant lytic activity is restricted by a single class I product (3,4,9,(13)(14)(15). Although a number of genetic and regulatory mechanisms have been proposed to account for this effect (3,5,(16)(17)(18), little biochemical evidence exists that can explain preferential recognition of certain class I molecules in conjunction with foreign antigens ( 19). H-2K k, in particular, is the major restricting element for several haptens and viruses including TNP (3, 4), FITC (9), Sendai, and influenza (16,20,21).…”

mentioning

confidence: 99%

Trinitrophenyl modification of H-2k and H-2b spleen cells results in enhanced serological detection of Kk-like determinants.

Levy¹,

Dower²,

Shearer³

et al. 1984

The Journal of Experimental Medicine

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Several anti-H-2Kk but not anti-H-2Dd monoclonal antibodies (mAb) exhibited enhanced binding to B10.A murine spleen cells after modification of the cells with trinitrobenzene sulfonate (TNBS). The number of antibody molecules bound to TNP-modified B10.A spleen cells increased by a factor of two or more. The same anti-2Kk mAb that exhibited enhanced binding to modified B10.A cells did not bind to unmodified C57BL/10 spleen cells, as expected, but did bind to TNP-modified C57BL/10 spleen cells. This TNP-dependent binding was not a result of cross-reactions with cell surface TNP groups nor with Fc receptors. TNP modification of a variant cell line that does not express class I H-2 products did not result in enhanced binding by these mAb. These findings can account for preferential recognition of TNP-Kk by B10.A and B10.BR CTL, and also for cross-reactive lysis by C57BL/10 CTL stimulated by C57BL/10-TNP against unmodified H-2Kk targets.

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Helper cell analysis in cytotoxic T lymphocyte responses I. Activation of specific and cross‐reactive helper effects in two hapten‐modified self responses

Levy¹,

Fujiwara²,

Shearer³

1980

Eur J Immunol

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C3H/HeN mice were immunized by skin painting with trinitrochlorobenzene or by inoculation of fluorescein isothiocyanate (FITC)-conjugated syngeneic cells. Approximately four weeks later, spleen cells were removed, irradiated, and cocultured with spleen cells from normal mice. These cultures were stimulated with syngeneic cells conjugated with different concentrations of trinitrobenzene sulfonate (TNP-self) or FITC (FITC-self). The results demonstrate (a) appreciable helper cell activity from TNP-self and FITC-self-primed mice, as determined by enhanced hapten-specific cytotoxic T lymphocyte (CTL) responses, (b) that FITC helper activity enhanced the FITC-self CTL more efficiently than the TNP-self CTL response, and vice versa, (c) an alloantigenic stimulating population failed to activate TNP-self helper activity and (d) that the helper activity was not exclusively specific, since FITC helpers did enhance the anti TNP CTL response, and TNP helpers could enhance the anti-FITC-self CTL response. The results of this study indicate that these cell-mediated lympholysis models permit an analysis of hapten specificity and cross-reactivity at the different levels of cellular interaction involved in the generation of an H-2-restricted CTL response.

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Regulation of T-cell-mediated lympholysis by the murine major histocompatibility complex. II. Control of cytotoxic responses to trinitrophenyl-K and -D self products by H-2K- and H-2D-Region genes.

Cited by 13 publications

References 18 publications

H-2K mutation controls immune response phenotype of autoimmune thyroiditis. Critical expression of mutant gene product in both thymus and thyroid glands.

H-2K mutation controls immune response phenotype of autoimmune thyroiditis. Critical expression of mutant gene product in both thymus and thyroid glands.

Trinitrophenyl modification of H-2k and H-2b spleen cells results in enhanced serological detection of Kk-like determinants.

Helper cell analysis in cytotoxic T lymphocyte responses I. Activation of specific and cross‐reactive helper effects in two hapten‐modified self responses

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