Normal T splenocytes are able to induce immunoglobulin allotypic suppression in F<sub>1</sub> hybrid mice

Benaroch, Philippe; Bordenave, Guy

doi:10.1002/eji.1830170203

Cited by 15 publications

(16 citation statements)

References 24 publications

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“…This system is based on the existence in untreated Igh" mice of a T cell activity specifically directed against the expression of IgG2ab [9]. This activity can be greatly enhanced in Igh" mice by their sensitization against this Ig allotype prior to adoptive transfer of their T splenocytes (Tsens) into histocompatible Igh& or Ighb newborns.…”

Section: Discussionmentioning

confidence: 99%

“…The procedures for sensitization and suppression induction have been described in detail elsewhere [23]. For the amplification of their normal anti-IgG2ab T cell activity, adult BC8 (Igh") mice received at a 15-day intervals i.v.…”

Section: Mouse Sensitization and Suppression Induction Protocolsmentioning

confidence: 99%

“…Indeed, Gens depleted in vitro of either CD4' or CD8+ T cells are unable to induce suppression, while a mixture of these two populations reestablishes the suppression induction capacity [ 11,121. We also showed that only CD8+ T cells constitute the suppression effectors [ 101.…”

Section: Introductionmentioning

confidence: 99%

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The T/B cell interaction involved in induction of the mouse IgG2a^h suppression is restricted by major histocompatibility complex class I, but not class II molecules

Majlessi

Bordenave

1997

Eur J Immunol

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To determine the major histocompatibility complex (MHC) restriction of the T/ B cell interaction involved in a negative regulation of Ig production, we used mouse model of T cell-induced IgG2ab suppression in vivo. Normal or specifically triggered T splenocytes from mice of the Igha haplotype, when neonatally transferred into histocompatible Igha/b heterozygotes, are able to induce a specific and total suppression of the IgG2ab allotype. Nevertheless, only transfer of IgG2ab-primed Igha T splenocytes induces this suppression in Ighb/b homozygous congenic mice in which the whole IgG2a isotype production is inhibited. This suppression is chronically maintained by CD8+ T cells, but can be experimentally reversed. We have established that the suppression induction required a CD4+CD8+ T cell cooperation and operated via the recognition by the involved TCR of C gamma 2ab-derived peptides presented by the target B cells in an MHC haplotype-restricted manner. Here, by using Ighb mice genetically deficient for MHC class I (beta 2-microglobulin%, or beta 2m%) or class II (I-A beta%) molecules, we demonstrate functionally that the suppression induction implicates an MHC class I-, but not class II-restricted interaction. Indeed, the anti-IgG2ab T cells transferred into Ighb H-2b I-A beta% mice carry out the suppression process normally, while in Ighb H-2b beta 2m% recipients, their suppression induction capacity is significantly inhibited. Moreover, the C gamma 2ab 103-118 peptide, identified as the sole C gamma 2ab-derived peptide able to amplify the anti-IgG2ab T cell reactivity in Igha H-2b mice, is also able to stabilize the H-2Db, but not the H-2Kb class I molecules at the surface of RMA-S (TAP2-, H-2b) cells. These results indicate that, despite the CD4+/CD8+ T cell cooperation during the induction phase of suppression only MHC class I molecule expression is required at the surface of IgG2ab+ B cells for suppression establishment.

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Section: Discussionmentioning

confidence: 99%

Section: Mouse Sensitization and Suppression Induction Protocolsmentioning

confidence: 99%

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The T/B cell interaction involved in induction of the mouse IgG2a^h suppression is restricted by major histocompatibility complex class I, but not class II molecules

Majlessi

Bordenave

1997

Eur J Immunol

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“…Thus, the Ag specificity of the Tcells was directly demonstrated only in one experimental system [47,48], and only preliminary data suggesting self MHC restriction have been published [47,48]. None of the reports defined a clonotypic Ag receptor as the Tcell recognition structure for Igh-lb; instead the possibility was raised that allotype suppression involved T cell FcyR [49].…”

Section: K Bartnes and K Hannestadmentioning

confidence: 99%

Igh‐1b‐specific CD4⁺CD8⁻ T cell clones of the T_h1 subset selectively suppress the Igh‐1b allotype in vivo

Bartnes

Hannestad

1991

Eur J Immunol

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The demonstration of major histocompatibility complex (MHC)-restricted T helper (Th) cells specific for peptides from the variable (V) regions of syngeneic immunoglobulin (Ig) (idiopeptides) opens the possibility that Th cells regulate B cell functions via idiopeptide-based cognate T-B interactions. As a model for such interactions we investigated the influence of Ig allotype-specific T cells on the differentiation of H-2-syngeneic B cells expressing that particular Ig allotype. We established a BALB/c (H-2d, Iga) CD4+CD8- T cell line and clones of the Th1 subset (interleukin 2+, interleukin 4-, interferon-gamma+, tumor necrosis factor-alpha+) that recognized Igh-1 (IgG2a) of the b allotype (Igh-1b) together with I-Ad. These T cells specifically suppressed surface Igh-1b+ B cells in vitro and in vivo. In 12 out of 15 6-week-old (BALB/c X B10.D2)F1 mice neonatally injected with Igh-1b-specific T cells, the serum Igh-1b concentrations were less than 5% of the levels in the controls. Thus, allotype suppression can be accomplished solely by adoptive transfer of Igh-1b-specific CD4+ T cells. The in vivo suppression was specific for Igh-1b+ B cells as the recipients' levels of Igh-1a and Igh-4b (IgG1b) were unaffected. The V beta 14-specific anti-T cell receptor (TcR) monoclonal antibody 14-2 inhibited activation of hybridomas derived from two of the clones. Collectively the data indicate that suppression resulted from cognate interactions between allopeptide-specific TcR alpha/beta+ T cells and normal unmanipulated B lymphocytes presenting their endogenous Igh-1b in association with MHC class II molecules. The data support the possibility that normal B cells can be suppressed by idiopeptide-specific T cells in vivo.

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“…T splenocytes from naive Igh a/a mice of diverse genetic backgrounds possess an intrinsic activity exclusively directed against the expression of IgG2a from the Igh b haplotype (12 (14) and suppression induction (15) phases, whereas only CD8 ϩ T cells are necessary to maintain suppression (16). The anti-IgG 2a b CD4 ϩ T cell help is thus indispensable to generate CD8 ϩ T suppression effectors.…”

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confidence: 99%

Role of CD40 in a T Cell-Mediated Negative Regulation of Ig Production

Majlessi

Bordenave

2001

The Journal of Immunology

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To investigate the possible role of CD40 in a negative regulation of Ig production, we used the mouse Ig allotype suppression model. T splenocytes from Igha/a mice are able in vivo to totally and chronically inhibit the production of IgG2ab (IgG2a from the Ighb haplotype). Accordingly, postnatal transfer of Igha/a T splenocytes into histocompatible Igha/b F1 or congenic Ighb/b mice leads to a characteristic IgG2ab suppression. The helper action of anti-IgG2ab CD4+ T cells is required for the recruitment of anti-IgG2ab CD8+ T suppression effectors. The latter use perforin (pore-forming protein, Pfp)- and/or Fas-dependent cytotoxic pathways to continuously eliminate B cells recently committed to IgG2ab production. In the present study we first showed that in vivo agonistic anti-CD40 mAb treatment of Igha/a mice, deprived of their CD4+ T cell compartment, could bypass the help of Ig allotype-specific CD4+ T cells and generate CD8+ T effector cells able to strongly inhibit IgG2ab production. This result demonstrates the usefulness of CD40 triggering in setting up an immune regulatory mechanism. Furthermore, with regard to the suppression-effector mechanism, we demonstrated that B cell CD40 expression was required for full suppression establishment via the Fas-dependent pathway. Indeed, Igha/a Pfp°/° T cells (using exclusively the Fas pathway) induced full IgG2ab suppression against Ighb/b CD40+/+ B cells, but only partial inhibition of IgG2ab production against Ighb/b CD40°/° B cells. This finding provides the first demonstration of direct involvement of B cell CD40 expression in in vivo negative control of an Ig production.

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Normal T splenocytes are able to induce immunoglobulin allotypic suppression in F₁ hybrid mice

Cited by 15 publications

References 24 publications

The T/B cell interaction involved in induction of the mouse IgG2a^h suppression is restricted by major histocompatibility complex class I, but not class II molecules

The T/B cell interaction involved in induction of the mouse IgG2a^h suppression is restricted by major histocompatibility complex class I, but not class II molecules

Igh‐1b‐specific CD4⁺CD8⁻ T cell clones of the T_h1 subset selectively suppress the Igh‐1b allotype in vivo

Role of CD40 in a T Cell-Mediated Negative Regulation of Ig Production

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Normal T splenocytes are able to induce immunoglobulin allotypic suppression in F1 hybrid mice

Cited by 15 publications

References 24 publications

The T/B cell interaction involved in induction of the mouse IgG2ah suppression is restricted by major histocompatibility complex class I, but not class II molecules

The T/B cell interaction involved in induction of the mouse IgG2ah suppression is restricted by major histocompatibility complex class I, but not class II molecules

Igh‐1b‐specific CD4+CD8− T cell clones of the Th1 subset selectively suppress the Igh‐1b allotype in vivo

Role of CD40 in a T Cell-Mediated Negative Regulation of Ig Production

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Normal T splenocytes are able to induce immunoglobulin allotypic suppression in F₁ hybrid mice

The T/B cell interaction involved in induction of the mouse IgG2a^h suppression is restricted by major histocompatibility complex class I, but not class II molecules

The T/B cell interaction involved in induction of the mouse IgG2a^h suppression is restricted by major histocompatibility complex class I, but not class II molecules

Igh‐1b‐specific CD4⁺CD8⁻ T cell clones of the T_h1 subset selectively suppress the Igh‐1b allotype in vivo