Cross‐blocking studies with monoclonal antibodies against I‐A molecules of haplotypes b, d and k

Koch, Norbert; Hämmerling, Günter J.; Tada, Nobuhiko; Kimura, Shoji; Hämmerling, Ulrich

doi:10.1002/eji.1830121103

Cited by 81 publications

(33 citation statements)

References 40 publications

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“…anti-H-2D b (K7-65, mIgG2a) [28], anti-I-A d (K24-199, mIgG2a), and anti-I-A b (K25-137, mIgG2A) [29] were kindly provided by G. Hämmerling, Department of Immunogenetics, German Cancer Research Center. Rat IgG and culture supernatant-derived mAb were purified by passage over Protein A-or Protein G-Sepharose [30,31].…”

Section: Antibodiesmentioning

confidence: 99%

Treatment of mice with anti-CD44 after allogeneic bone marrow cell transplantation is lethal

Zöller

Föhr

Herrmann

1998

Journal of Leukocyte Biology

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Because CD44 is known to be of functional importance in hematopoiesis, we were interested in whether anti-CD44 would interfere with syngeneic or allogeneic bone marrow cell engraftment. Syngeneic and allogeneic grafts were accepted by over 80% of mice. In both the syngeneic and the allogeneic host, homing, repopulation, and regain of immunoreactivity was delayed by anti-CD44 treatment. But in the syngeneic host the overall survival rate was unaltered. Instead, less than 25% of anti-CD44-treated, allogeneically reconstituted mice survived by recovery of the host's hematopoietic system, i.e. graft acceptance was close to 0%. The mice died between 4 and 15 days after engraftment and showed severe alterations of the gut. The high death rate of the allogeneically reconstituted mice was specific for anti-CD44 treatment. It did not depend on an ADCC mechanism, could not be abrogated by depletion of T cells, and was only mitigated by depletion of NK cells. According to the histological appearance of the gut, anti-CD44 strengthens a local (gut-associated) graft versus host reaction, which is not mediated by ␣␤ T cells and at least not exclusively by NK cells. Because gut death is one of the major reasons for failure in allogeneic bone marrow transplantation, the model of anti-CD44-induced lethality offers itself to clarify the underlying mechanism.

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Section: Antibodiesmentioning

confidence: 99%

Treatment of mice with anti-CD44 after allogeneic bone marrow cell transplantation is lethal

Zöller

Föhr

Herrmann

1998

Journal of Leukocyte Biology

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“…K24.199 (anti-I-Ad fJ.v) (17) and 13/4 (anti-I-Ed) (18) IgG2a monoclonal antibodies were purified from ascites fluid on staphylococcal protein A-Sepharose. Fluoresceinconjugated monoclonal anti-D3.137 (anti-I-Ad) (19) was kindly donated by M. H. Julius (Basel Institute for Immunology).…”

mentioning

confidence: 99%

B-lymphoma cells process and present their endogenous immunoglobulin to major histocompatibility complex-restricted T cells.

Weiß

Bogen

1989

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

199

137

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Antigen-presenting B-lymphoma cells were transfected with the gene encoding the immunoglobulin A2 light chain of MOPC315 cells (A2315). The A2 chain is expressed on the cell surface of the transfectants together with the endogenous heavy chain. (4) and that this recognition was under H-2-linked immune response (Ir) gene control (5). The hypothesis has been supported and extended by later work (6-8). Similar ideas have recently been proposed by others (9, 10), and MHC-restricted T cells specific for idiotypes (11,12) and allotypes (13) have been described. However, it is still unclear whether MHC-restricted T cells recognize processed forms of immunoglobulin exclusively and whether B cells can process their own immunoglobulin.To test this directly we have used recently established T-cell clones specific for an idiotope of A2315 in the context of the I-Ed MHC antigen (7,8). These clones, like the T cells studied in vivo before (4, 5), recognize an idiotypic determinant on A2315 around amino acid positions 94, 95, and 96 (7, 8

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“…Transfected cells were screened by Western blotting with In-1, specific for the cytosolic domain of Ii [23]. Antisera 657 and 658 were generated by immunizing rabbits with a synthetic peptide corresponding to amino acids 1-29 of the murine Ii cytosolic domain using published protocols [24].…”

Section: Cell Lines and Antibodiesmentioning

confidence: 99%

The chondroitin sulfate form of invariant chain trimerizes with conventional invariant chain and these complexes are rapidly transported from thetrans-Golgi network to the cell surface

Arneson

Miller

2007

Biochemical Journal

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Targeting of MHCII-invariant chain complexes from the transGolgi network to endosomes is mediated by two di-leucinebased signals present in the cytosolic domain of invariant chain. Generation of this endosomal targeting signal is also dependent on multimerization of the invariant chain cytosolic domain sequences, mediated through assembly of invariant chain into homotrimers. A small subset of invariant chain is modified by the addition of chondroitin sulfate and is expressed on the cell surface in association with MHCII. In the present study, we have followed the biosynthetic pathway and route of intracellular transport of this proteoglycan form of invariant chain. We found that the efficiency of chondroitin sulfate modification can be increased by altering the invariant chain amino acid sequence around Ser-201 to the xylosylation consensus sequence. Our results also indicate that, following sulfation, the proteoglycan form is transported rapidly from the trans-Golgi network to the cell surface and is degraded following internalization into an endocytic compartment. Invariant chain-chondroitin sulfate is present in invariant chain trimers that also include conventional non-proteoglycan forms of invariant chain. These data indicate that invariant chain-chondroitin sulfate-containing complexes are transported rapidly from the trans-Golgi network to the cell surface in spite of the presence of an intact endosomal localization signal. Furthermore, these results suggest that invariant chainchondroitin sulfate may play an important role in the generation of cell-surface pools of invariant chain that can serve as receptors for CD44 and macrophage migration inhibitory factor.

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Cross‐blocking studies with monoclonal antibodies against I‐A molecules of haplotypes b, d and k

Cited by 81 publications

References 40 publications

Treatment of mice with anti-CD44 after allogeneic bone marrow cell transplantation is lethal

Treatment of mice with anti-CD44 after allogeneic bone marrow cell transplantation is lethal

B-lymphoma cells process and present their endogenous immunoglobulin to major histocompatibility complex-restricted T cells.

The chondroitin sulfate form of invariant chain trimerizes with conventional invariant chain and these complexes are rapidly transported from thetrans-Golgi network to the cell surface

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