Ir gene expression on T cells: Effect of a monoclonal antibody directed against I region‐controlled determinants on T cells

Yagi, Junji; Nonaka, Makoto; Ryo, Akihide; Tada, Tomio

doi:10.1002/eji.1830160506

Cited by 4 publications

(3 citation statements)

References 40 publications

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“…Anti-Iat have been shown to inhibit autologous and allogeneic mixed lymphocyte reaction by blocking the responder T cells but not stimulators (26) . The in vivo administration of an anti-Iatk was found (12) to be inhibitory for the H-2k-restricted helper T cell activity . We have recently observed that anti-Iatk are able to induce polyclonal proliferative response of a fraction of normal unprimed T cells of H-2k mice (Yagi, J ., Y. Asano, and T .…”

Section: Discussionmentioning

confidence: 99%

“…Monoclonal antibodies reactive with I region-controlled pol morphic determinants of H-2k haplotype that are uniquely expressed on T cells (anti-Iat ; 1 L9, 2L2, and 74L) are those described in previous papers (10)(11)(12) . 2 These anti-Iatk are the products of hybridomas derived from spleen cells of A .TH immune to A .TL lymphoid cells, and have been selected in the criteria that they can react with an augmenting T cell hybridoma (20) and some functional T cells but not with B cells and macrophages of H-2 k strains.…”

Section: Antibodiesmentioning

confidence: 99%

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Epitopes associated with the MHC restriction site of T cells. II. Somatic generation of Iat epitopes on T cells in radiation bone marrow chimeras.

Asano¹,

Tada²

1987

The Journal of Experimental Medicine

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We described in this paper systematic alterations in the expression of unique I region controlled epitopes on helper T cells (Th) in chimeras according to the changes in their H-2 restriction specificity. Taking advantage of the reactivity of monoclonal antibodies (anti-Iat) putatively specific for the epitopes indirectly controlled by I region and expressed in association with the Iak restriction site of Th, we examined the alterations of these epitopes on Th cells from various bone marrow chimeras. Iatk epitopes were physiologically expressed on Iak-restricted but not on Iab-restricted Th cells in (H-2k X H-2b)F1 mice. In the chimeric condition, the H-2k-restricted Th of B6----F1 chimera acquired the expression of Iatk even though B6 Th is unable to express Iatk when developed under the physiologic condition. Iatk are also found on Th of fully allogeneic chimera of B6----C3H, whereas Th cells of C3H----B6 completely lost the Iatk expression. These results indicate that Iat epitopes originally defined as unique I region-controlled determinants selectively expressed on T cells are not encoded by the I region genes but are associated with the T cell receptor that sees the self Ia. The epitopes undergo the adaptive alterations according to the acquisition of a new MHC restriction. This is the first example to demonstrate the epitope associated with T cell receptor which undergo the systematic adaptive differentiation.

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Section: Discussionmentioning

confidence: 99%

Section: Antibodiesmentioning

confidence: 99%

Epitopes associated with the MHC restriction site of T cells. II. Somatic generation of Iat epitopes on T cells in radiation bone marrow chimeras.

Asano¹,

Tada²

1987

The Journal of Experimental Medicine

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“…I-j is in many respects analogous to Iat, as it is expressed only on functional T cells (5). Although IJ was first demonstrated on Ts and TsF (1,2), it has been detected on a variety of T cell subsets including Th, Ts-inducer, and MLR responders (15,(28)(29)(30)(31) . It has recently been demonstrated that IJ can be adaptively expressed by T cells of different genotype that have developed in the radiation bone marrow chimera and in transgenic mice (29)(30)(31)(32).…”

Section: Discussionmentioning

confidence: 99%

Epitopes associated with MHC restriction site of T cells. III. I-J epitope on MHC-restricted T helper cells.

Asano

Nakayama

Kubo

et al. 1987

The Journal of Experimental Medicine

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I-J epitopes were found to be associated with the functional site of the class II MHC-restricted helper T (Th) cells: Virtually all of the H-2k-restricted Th cell function of H-2kxbF1 T cells was inhibited by the anti-I-Jk mAb, leaving the H-2b-restricted function unaffected. The I-Jk epitope was inducible in Th cells of different genotype origin according to the environmental class II antigens present in the early ontogeny of T cells. Although above results suggested that I-J is the structure reflecting the inducible MHC restriction specificity, further studies revealed some interesting controversies: First, the I-J phenotype did not always correlate with the class II restriction specificity, e.g., I-Ab-restricted Th from 5R was I-Jk-positive, whereas I-Ak-restricted Th of 4R was not. Second, there was no trans expression of parental I-J phenotypes and restriction specificities in F1 Th, e.g., the I-J phenotype was detected only on I-Ab-restricted Th of (4R X 5R)F1, whereas it was absent on I-Ak-restricted Th. This strict linkage between the restriction specificity and I-J phenotype was also found on Th cells developed in bone marrow chimera constructed with intra-H-2-recombinant mice. The expression of I-Jk was always associated with the restriction specificity of the relevant host. Thus, the restriction specificity of Th cells followed the host type, and the I-J expression on Th was exactly the same as that expressed by the host haplotype. These results indicate that I-J is an isomorphic structure adaptively expressed on Th cells that is involved in the unidirectional regulatory cell interactions, and that the polymorphism cannot be explained merely by the restriction specificity of the conventional T cell receptor heterodimer.

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Shared idiotopes between anti‐class II monoclonal antibodies and major histocompatibility complex recognition site of T cells

et al. 1987

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We have raised a number of monoclonal antibodies (mAb) against idiotopes (Id) on monoclonal anti-murine class II (anti-Ak or Ek) antibodies. Two anti-Id mAb among 31 were found to cross-react with some T cells but not with macrophages and B cells of H-2k animals. They were able to block syngeneic mixed lymphocyte reaction (SMLR) and antigen-induced major histocompatibility complex (MHC)-restricted T cell proliferation of H-2k but not of other haplotypes. These results indicated that antibodies were recognizing Id associated with the MHC restriction site of T cells. The injection of these anti-Id mAb into H-2k mice resulted in the stimulation of self-class II-reactive T cell clones as determined by SMLR. They were also able to stimulate in non-H-2k strains to prime H-2k alloreactive T cell clones. Some animals developed anti-class II (anti-Iak) antibodies by the injection of anti-Id. These results indicated that certain anti-Id (anti-anti-class II) antibodies cross-reacted with T cell receptors which carried class II restriction specificity and were involved in allorecognition. These antibodies were found to have an ability to alter the T cell repertoire in vivo by stimulating such MHC-restricted clones.

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Ir gene expression on T cells: Effect of a monoclonal antibody directed against I region‐controlled determinants on T cells

Cited by 4 publications

References 40 publications

Epitopes associated with the MHC restriction site of T cells. II. Somatic generation of Iat epitopes on T cells in radiation bone marrow chimeras.

Epitopes associated with the MHC restriction site of T cells. II. Somatic generation of Iat epitopes on T cells in radiation bone marrow chimeras.

Epitopes associated with MHC restriction site of T cells. III. I-J epitope on MHC-restricted T helper cells.

Shared idiotopes between anti‐class II monoclonal antibodies and major histocompatibility complex recognition site of T cells

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