Autoreactive B-cell repertoire in mice with chronic graft versus host disease

Rolink, A G; Thalmann, Philipp; Berger, Cristoph; Radaszkiewicz, Thaddäus; Melchers, Fritz

doi:10.1016/0161-5890(88)90159-9

Cited by 12 publications

(18 citation statements)

References 19 publications

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“…This is confirmed by the presence of antierythrocyte autoantibodies [10] and increased IgG content in the peripheral blood of B6D2F1 mice with chronic GVHR [11].…”

Section: Resultssupporting

confidence: 66%

Combined disorders in erythro- and immunopoiesis in (C57Bl/6xDBA/2)F1 mice with immunodeficiency induced by graft-versus-host reaction and immunocomplex glomerulonephritis

2000

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“…This is confirmed by the presence of antierythrocyte autoantibodies [10] and increased IgG content in the peripheral blood of B6D2F1 mice with chronic GVHR [11].…”

Section: Resultssupporting

confidence: 66%

Combined disorders in erythro- and immunopoiesis in (C57Bl/6xDBA/2)F1 mice with immunodeficiency induced by graft-versus-host reaction and immunocomplex glomerulonephritis

2000

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“…The supernatants from the cultures were tested for the presence of Ig by enzyme-linked immuno-assay (ELISA) (Rolink et al, 1987). The cultures (10-24 wells per Ly clone) were incubated at 37°C for various periods (5, 6, 7, 8, 10, 15 and 20 days); the cultures incubated for a period > 8 days were fed at 4to 5-day intervals by replacing -0.5 ml of the medium with fresh culture medium.…”

Section: Antibodies (Mabs)mentioning

confidence: 99%

Ly1+ PRO-B lymphocyte clones. Phenotype, growth requirements and differentiation in vitro and in vivo.

Palacios¹,

Karasuyama²,

Rolink³

1987

The EMBO Journal

112

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Several clones obtained from the bone marrow of a BALB/c mouse were found to contain the heavy and light chain Ig genes in the germline configuration, to express Ly1 and to carry the B cell lineage markers B‐220, Lyb8 and BP‐1; these clones are Pgp‐1+, LFA‐1+, J11d+, Mac‐1+ and Thy1‐, Lyt2‐, L3T4‐, GM1.2‐ and Ia‐. Three clones analyzed in detail (Lyd9, LyH7 and Lyb9) have receptors for interleukin (IL) 2 and IL3 as assessed with the 7D4 and CC11 monoclonal antibodies respectively. They grow in rIL3 but not in rIL2 or rIL1; both rIL4 and rIL5 also promote their proliferation, albeit to a much lesser extent than rIL3. None of the interleukins tested alone or in various combinations promoted the clones to differentiate in vitro along the B cell pathway. Treatment with 5‐Azacytidine (5‐Aza) induced cell surface Ia expression but not rearrangement or expression of Ig genes. However, 5‐Aza‐treated Lyd9, LyH7 and Lyb9 cells co‐cultured with X‐ray irradiated accessory cells and LPS gave rise to Ly1+, IgM+ B lymphocytes (range 14‐51%) including mu + kappa + (78‐93%), and mu + lambda + (9‐25%) B lymphocytes. In vivo, the Lyd9, LyH7 and Lyb9 clones gave rise to IgM+ B lymphocytes (8.5‐17%) including mu + kappa +, and mu + lambda +, but not to Lyt2+ or L3T4+ T lymphocytes after 4‐6 weeks of transfer into Scid mice. Our results indicate that Ly1+ IgM+ cells comprise a subpopulation of B lymphocytes that is derived from IL3‐responsive Ly1+ PRO‐B lymphocytes.

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“…The unique response pattern -no detectable IgM, immediate IgG production -has, to our knowledge, so far only been observed in graft-versus-host reactions of parental CD4' T cells injected into F1 hosts which results in lupuslike symptoms of autoimmune disease with abundant autoantibody production of IgG isotypes [35]. There are interesting differences to experiments which report induction of tolerance in antibody responses by injection of B cells which might relate to the strength of T cell help which can be recruited in the host to the antigen.…”

Section: Discussionmentioning

confidence: 92%

Priming of helper T cell‐dependent antibody responses by hemagglutinin‐transgenic B cells

Kalberer¹,

Reininger²,

Melchers³

et al. 1997

Eur J Immunol

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Mice expressing the hemagglutinin (HA) gene of influenza virus PR8 (H1 subtype) under the control of kappa light chain promoter and enhancer have been generated. They express HA in and on B cells, and are tolerant to HA. In vitro, only lipopolysaccharide (LPS) blasts but not resting B cells of transgenic mice can stimulate HA-specific helper T cells of HA-specific alpha/beta T cell receptor (TCR)-transgenic mice. Transfer of HA-transgenic LPS blasts into syngeneic, non-transgenic recipients primes HA-specific antibody responses. Resting, small HA-transgenic B cells, which were purified by fluorescence-activated cell sorting, prime lower antibody responses. Host B cells produce the HA-specific antibody response. The donor HA-transgenic B cells need to express major histocompatibility complex (MHC) class II molecules and need to be alive to induce the antibody response in the host. Most notably, the host antibody response never produces detectable levels of IgM, but only of switched IgG isotypes. Neither resting nor activated HA-transgenic B cells induce tolerance in antibody responses. These results suggest that HA-transgenic B cells, presenting both the intact antigen on the cell surface and peptides of the antigen on MHC class II, are effective inducers of helper T cell responses, and as judged by the Ig-isotype response pattern, which is mainly IgG1, of Th2 type.

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Autoreactive B-cell repertoire in mice with chronic graft versus host disease

Cited by 12 publications

References 19 publications

Combined disorders in erythro- and immunopoiesis in (C57Bl/6xDBA/2)F1 mice with immunodeficiency induced by graft-versus-host reaction and immunocomplex glomerulonephritis

Combined disorders in erythro- and immunopoiesis in (C57Bl/6xDBA/2)F1 mice with immunodeficiency induced by graft-versus-host reaction and immunocomplex glomerulonephritis

Ly1+ PRO-B lymphocyte clones. Phenotype, growth requirements and differentiation in vitro and in vivo.

Priming of helper T cell‐dependent antibody responses by hemagglutinin‐transgenic B cells

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