A rat antibody against a structure functionally related to the mouse T-cell receptor/T3 complex

Tomonari, Kyuhei

doi:10.1007/bf00355379

Cited by 185 publications

(73 citation statements)

References 12 publications

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“…Graded numbers of splenocytes were activated with Concanavalin-A (5 g͞ml) or in anti-CD3-coated plates (coated with 5 g͞ml purified KT3 monoclonal antibody (19) The evaluation of cytokine mRNA in islets will be described in detail elsewhere (I.A., unpublished data). Briefly, islets were picked after collagenase digestion of the pancreas, and total RNA was extracted with guanidinium thiocyanate and used for cDNA synthesis.…”

Section: Methodsmentioning

confidence: 99%

Interferon-γ impacts at multiple points during the progression of autoimmune diabetes

Wang

André-Schmutz

González

et al. 1997

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

187

128

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The role of interferon-␥ in autoimmune diabetes was assessed by breeding a null mutation of the interferon-␥ receptor ␣ chain into the nonobese diabetic mouse strain, as well as into a simplified T cell receptor transgenic model of diabetes. In contrast to a previous report on abrogation of the interferon-␥ gene, mutation of the gene encoding its receptor led to drastic effects on disease in both mouse lines. Nonobese diabetic mice showed a marked inhibition of insulitis-both the kinetics and penetrance-and no signs of diabetes; the transgenic model exhibited near-normal insulitis, but this never evolved into diabetes, either spontaneously or after experimental provocation. This failure could not be explained by perturbations in the ratio of T helper cell phenotypes; rather, it ref lected a defect in antigen-presenting cells or in the islet ␤ cell targets.

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Section: Methodsmentioning

confidence: 99%

Interferon-γ impacts at multiple points during the progression of autoimmune diabetes

Wang

André-Schmutz

González

et al. 1997

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

187

128

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“…The main Abs used in this study were as follows: KT3 anti-CD3⑀ (25), YTS 191 anti-CD4 (26), 2.4G2 anti-CD16/32 (27), Pgp1 anti-CD44 (28), A1 anti-Ly49A (29), 5E6 anti-Ly49C (30), 4D11 anti-Ly49G (31), PK136 anti-NK1.1 (32), and 10A7 anti-10A7 (33), all kindly provided by the original investigators, with the exception of 2.4G2 which was obtained from the American Type Culture Collection (Manassas, VA …”

Section: Abs and Stainingmentioning

confidence: 99%

The Mouse Tumor Cell Lines EL4 and RMA Display Mosaic Expression of NK-Related and Certain Other Surface Molecules and Appear to Have a Common Origin

Gays

Unnikrishnan

Shrestha

et al. 2000

The Journal of Immunology

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As a potential means for facilitating studies of NK cell-related molecules, we examined the expression of these molecules on a range of mouse tumor cell lines. Of the lines we initially examined, only EL4 and RMA expressed such molecules, both lines expressing several members of the Ly49 and NKRP1 families. Unexpectedly, several of the NK-related molecules, together with certain other molecules including CD2, CD3, CD4, CD32, and CD44, were often expressed in a mosaic manner, even on freshly derived clones, indicating frequent switching in expression. In each case examined, switching was controlled at the mRNA level, with expression of CD3ζ determining expression of the entire CD3-TCR complex. Each of the variable molecules was expressed independently, with the exception that CD3 was restricted to cells that also expressed CD2. Treatment with drugs that affect DNA methylation and histone acetylation could augment the expression of at least some of the variable molecules. The striking phenotypic similarity between EL4 and RMA led us to examine the state of their TCRβ genes. Both lines had identical rearrangements on both chromosomes, indicating that RMA is in fact a subline of EL4. Overall, these findings suggest that EL4 is an NK-T cell tumor that may have retained a genetic mechanism that permits the variable expression of a restricted group of molecules involved in recognition and signaling.

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“…13 Serial sections were stained with various rat anti-mouse monoclonal antibodies: TIB122 (LCA (CD45)), 54 M1.42 (MHC class I), 55 FA/11 (macrophage-specific membrane protein macrosialin) 56 and KT3 (anti-mouse CD3). 57 All monoclonal antibodies were generously provided by the MRC Cellular Immunology Unit (Oxford, UK) and used as tissue culture supernatants. Control sections that omitted the primary antibody were consistently negative.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Local adenoviral expression of Fas ligand upregulates pro-inflammatory immune responses in the CNS

et al. 2004

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The central nervous system (CNS) is a site of relative immunological privilege; despite this it can be a target of the immune system under certain conditions. For example, adenoviral vectors elicit an immune response strong enough to result in antigen elimination, in immunologically primed animals. Fas ligand (FasL) contributes to the immune privilege of certain tissues by inducing apoptosis in activated T cells. We therefore investigated whether local overexpression of FasL could downregulate the immune response to adenovirus in the brain. Adenoviral vectors expressing FasL (AdFasL) and the reporter gene b-galactosidase (Adbgal) were co-injected into the striatum of naïve or immunologically primed mice. A co-injection of an adenovirus lacking a transgene (Ad0) and Adbgal acted as a control. At 2 weeks after inoculation, reporter protein expression was significantly reduced with the AdFasL:Adbgal combination compared with the Ad0:Adbgal controls. This was accompanied by a strong inflammatory cell infiltrate, local demyelination and upregulation of pro-inflammatory cytokine gene expression. These experiments demonstrate that FasL overexpression elicits a pro-inflammatory response in the CNS rather than immunosuppression. This was characterized by chronic inflammation and accelerated loss of transgene expression. Induction of such an unexpected pro-inflammatory response caused by introducing FasL may be a peculiarity of the relative immunoprivilege of the unique environment of the brain.

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A rat antibody against a structure functionally related to the mouse T-cell receptor/T3 complex

Cited by 185 publications

References 12 publications

Interferon-γ impacts at multiple points during the progression of autoimmune diabetes

Interferon-γ impacts at multiple points during the progression of autoimmune diabetes

The Mouse Tumor Cell Lines EL4 and RMA Display Mosaic Expression of NK-Related and Certain Other Surface Molecules and Appear to Have a Common Origin

Local adenoviral expression of Fas ligand upregulates pro-inflammatory immune responses in the CNS

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