Unidirectional IgG allotype- and isotype-specific suppressor cells in congeneic mice

Kolb, Cornelia; DiPauli, R.; Weiler, Eberhardt

doi:10.1016/0008-8749(86)90242-x

Cited by 7 publications

(2 citation statements)

References 18 publications

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“…3. ,Enhancement of the anti-Igh-lb activity of normal T cells sure of (BALB/c x SJL)F1 to anti-Igh-lb antibodies (50% of individuals subjected to suppression at 45 weeks after birth [6]). As this work was being completed, an article was published [28] which reported that in all BALB/c x CB20 recipients of whole spleen cells from BALB/c mice pretreated with CB20 spleen cells two months before "the paternal allotype b was severely reduced in its expression.. .…”

Section: Igh-zbmentioning

confidence: 99%

Enhancement in Igh^a mouse strains of the “natural” suppressive activity of normal T splenocytes against the expression of Igh‐1b allotype. I. Molecular aspects of the chronic suppression obtained

Benaocb

Burdenave

1988

Eur J Immunol

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Several approaches have been used in our attempts to increase the "natural" ability of normal T splenocytes (Tn) from BALB/c or BC8 mice (both Igha) to induce, in F1 hybrids, a suppression of Igh-1b expression (IgG2a of b haplotype). These heterozygous F1 were produced by mating these Igha mice and their Ighb-congenic partners (CB20 and C57BL/6, respectively). The most powerful approaches were to sensitize the Igha mice by either autologous splenocytes coated with Igh-1b or B splenocytes from Ighb-congenic mice. In F1 having paternally inherited the b haplotype the sensitized T splenocytes (Ts) prepared from such mice are able to induce, like Tn, when injected at birth, a chronic suppression of Igh-1b expression. However, the suppression was established with a much higher efficiency: already at 6 weeks of age in 100% of the F1 treated with 1 x 10(7) Ts, vs. a final rate of 70% progressively reached only at 42 weeks of age in the F1 treated with 4 x 10(7) Tn. In F1 having maternally inherited Ighb the differences were even more pronounced than with 4 x 10(7) Tn, i.e. the suppression induction was almost totally ineffective, whereas with 2 x 10(7)-4 x 10(7) Ts, a rate of 100% treated F1 subjected to suppression was reached at 19 weeks of age. As the productions of IgM, IgD and IgA of the b haplotype were not affected by the suppression, the Ts are believed to act on the Igh-1b+ cells. Attempts were also made to induce allotypic suppression of other b allotypes by the use, as sensitizing cells, of myeloma cells carrying Igh-6b (IgM of b haplotype). We failed in revealing any sign of a T cell reactivity against Igh-6b similar to the reactivity against Igh-1b. The use of Igh-6b+ myeloma cells grown in an Ighb or in an Igha background allowed us to assume that the cells responsible for the sensitization are, in the Ighb B lymphocyte population, either the Igh-1b+ lymphocytes or the lymphocytes having passively adsorbed this allotype, or both.

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Section: Igh-zbmentioning

confidence: 99%

Enhancement in Igh^a mouse strains of the “natural” suppressive activity of normal T splenocytes against the expression of Igh‐1b allotype. I. Molecular aspects of the chronic suppression obtained

Benaocb

Burdenave

1988

Eur J Immunol

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“…While we were establishing our data, a report on allotypic suppression induced by total spleen cells neonatally injected in heterozygous mice was published (36) in which the authors state that "neonatal IgG2ab suppression was harder to achieve in homozygous CB20 mice, and titers scattered. However, at the age of 1 .5 yr, seven out of eight animals did not have detectable allotype b levels anymore.…”

Section: Discussionmentioning

confidence: 63%

Cellular induction of chronic allotype suppression of IgG2a in Ighb/b homozygous mice and its abrogation by in vivo treatment with anti-CD8 monoclonal antibody.

Benaroch

Georgatsou

Bordenave

1988

The Journal of Experimental Medicine

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We report here the successful induction of allotype suppression in homozygous Ighb/b mice (CB20 or C57BL/6) by neonatal injection of T splenocytes from Igha congenic sensitized mice (BALB/c or BC8, respectively). The sensitization of the T cell donors was achieved by two intravenous injections of B splenocytes from Ighb congenic mice. Treated homozygous Ighb/b mice developed, as of 16-24 wk of age, a chronic suppression of Igh-1b expression (IgG2a of Ighb haplotype). The other productions tested (IgM, IgD, and IgA) of Ighb haplotype were unaffected. In vivo treatment with cytotoxic anti-CD4 or anti-CD8 mAb of mice subjected to chronic Igh-1b suppression clearly showed that CD8+ lymphocytes (suppressor or cytotoxic cell) were essential for the maintenance of the suppression. The suppression was indeed abrogated after a 1-wk treatment with anti-CD8 mAb containing culture supernatant, whereas, the anti-CD4-treated mice continued to be subjected to suppression. This anti-CD8 in vivo treatment was shown to have no effect on thymus but to severely reduce the percentages of CD8+ cells in spleen and in peripheral blood without affecting the percentages of CD4+ cells, leading to a large and rapid Igh-1b expression (up to 0.5 mg per ml of serum, the day after the end of the treatment). This suppression abrogation, and thus the Igh-1b expression, was either transient or permanent. When it was transient, a second 1-wk treatment with anti-CD8 mAb containing culture supernatant induced once again a rapid and significant production of Igh-1b (up to 0.3 mg of Igh-1b per ml of serum).

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B cell dependence of the congeneic barrier towards idiotype‐carrying cells

1986

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Immune cells transferred into nonirradiated animals of the same genotype face a barrier which severely affects their capacity to function in the host. We studied this phenomenon in allotype-congeneic animals. When anti-dextran immune cells of the responder strain (BALB/c-Igha) are injected into an allotype-congeneic host (BALB-Ighb) the grafted cells are suppressed to give an idiotype-positive response. This congeneic barrier of thymus-independent immune cells is lost in mice carrying an X-linked B cell defect: when idiotype-positive immune cells from responder (CBA/N X BALB/c)F1 mice are transplanted into congeneic nonresponder animals (CBA/N X BALB-Ighb)F1, female recipients are nonpermissive towards grafted cells whereas B cell-defective male littermates allow donor cells to develop an idiotype-positive anti-dextran response. These results show that the congeneic barrier towards dextran-immune cells is related to the maturation stage of B cells in the recipient. Since B cell-defective (CBA/N X BALB/c)F1 animals do not display an anti-idiotypic response in contrast to intact littermates and because CB16-KN mice are nonpermissive towards CB8-K lymphocytes, differing in VH genes only, we suggest that the "isogeneic barrier" depends on a mechanism recognizing VH structures.

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Unidirectional IgG allotype- and isotype-specific suppressor cells in congeneic mice

Cited by 7 publications

References 18 publications

Enhancement in Igh^a mouse strains of the “natural” suppressive activity of normal T splenocytes against the expression of Igh‐1b allotype. I. Molecular aspects of the chronic suppression obtained

Enhancement in Igh^a mouse strains of the “natural” suppressive activity of normal T splenocytes against the expression of Igh‐1b allotype. I. Molecular aspects of the chronic suppression obtained

Cellular induction of chronic allotype suppression of IgG2a in Ighb/b homozygous mice and its abrogation by in vivo treatment with anti-CD8 monoclonal antibody.

B cell dependence of the congeneic barrier towards idiotype‐carrying cells

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Unidirectional IgG allotype- and isotype-specific suppressor cells in congeneic mice

Cited by 7 publications

References 18 publications

Enhancement in Igha mouse strains of the “natural” suppressive activity of normal T splenocytes against the expression of Igh‐1b allotype. I. Molecular aspects of the chronic suppression obtained

Enhancement in Igha mouse strains of the “natural” suppressive activity of normal T splenocytes against the expression of Igh‐1b allotype. I. Molecular aspects of the chronic suppression obtained

Cellular induction of chronic allotype suppression of IgG2a in Ighb/b homozygous mice and its abrogation by in vivo treatment with anti-CD8 monoclonal antibody.

B cell dependence of the congeneic barrier towards idiotype‐carrying cells

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Enhancement in Igh^a mouse strains of the “natural” suppressive activity of normal T splenocytes against the expression of Igh‐1b allotype. I. Molecular aspects of the chronic suppression obtained

Enhancement in Igh^a mouse strains of the “natural” suppressive activity of normal T splenocytes against the expression of Igh‐1b allotype. I. Molecular aspects of the chronic suppression obtained