Syngeneic antiidiotypic monoclonal antibodies to the murine anti-HLA-DR,DP monoclonal antibody CR11-462

Perosa, Federico; Ferrone, Soldano

doi:10.1016/0198-8859(88)90061-4

Cited by 14 publications

(7 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The frequency we have obtained is markedly higher than that we have obtained using splenocytes from BALB/c mice immunized with MAbs to monomorphic determinants of HLA-DR and DP antigens (18), to polymorphic determinants of HLA-DQ antigens, to monomorphic and polymorphic determinants of HLA Class I antigens (Ferrone, S., unpublished observations) and to monomorphic determinants of human high molecular weight-melanoma associated antigen (Kusama, M., T. Kageshita, Z. J. Chen, and S. Ferrone. 1989.…”

Section: Methodscontrasting

confidence: 38%

“…The murine antiidiotypic MAb F3-C25 and F3-B6 to idiotopes within (or closely related to) and outside the antigen combining site, respectively, of the syngeneic anti HLA-DR,DP MAb CR1 1-462 (18) and the murine antiidiotypic MAb T1O-440 to an idiotope within (or closely related to) the antigen combining site of the syngeneic anti-HLA-A2,A28 MAb CR1 1-351 (Ferrone, S., unpublished observations) have been prepared and characterized following procedures similar to the ones we have used in this investigation.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Murine antiidiotypic monoclonal antibodies that bear the internal image of HLA-DR allospecificities.

Perosa

Ferrone²

1989

J. Clin. Invest.

View full text Add to dashboard Cite

Hybridization of murine myeloma cells P3-X63-Ag8.653 with splenocytes from a BALB/c mouse immunized with the syngeneic anti HLA-DR1,4,w6,w8,w9 MAb AC1.59 resulted in the development of 108 hybridomas secreting antiidiotypic antibodies. 100 of them inhibited the binding of MAb AC1.59 to target cells. Detailed analysis of the antiidiotypic MAb F5-444, F5-830, F5-963, F5-1126, F5-1336, and F5-1419 showed that all of them recognize idiotopes within or spatially close to the antigen combining site of MAb AC1.59. In crossblocking experiments, the six antiidiotypic MAbs crossblocked each other. It is likely that the six MAbs recognize spatially close, but not identical idiotopes because they elicited antiantiidiotypic antibodies of different or similar, but not identical specificity and differ in their ability to elicit anti-HLA class II antibodies. The latter, which were found only in sera from BALB/c mice immunized with antiidiotypic MAb F5444 and F5-830, mimic the specificity of MAb AC1.59 and express the idiotope defined by the immunizing antiidiotypic MAb. These results indicate that the MAb F5A444 and F5-830 are antiidiotypes,6 and the remaining four are antiidiotypes -y.

show abstract

Section: Methodscontrasting

confidence: 38%

Section: Methodsmentioning

confidence: 99%

Murine antiidiotypic monoclonal antibodies that bear the internal image of HLA-DR allospecificities.

Perosa

Ferrone²

1989

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…In this regard, Lehmann et al (51) demonstrated that the TAs recognized by the CTLs isolated from recurrent melanoma metastases were different from those recognized by the CTLs isolated from autologous primary lesions. In addition, some of us (14) have shown a shifting of CTL specificity from HLA-A2-MART-1 [27][28][29][30][31][32][33][34][35] complexes to HLA-A2-Tyr 369 -377 complexes in two sequential melanoma metastases with distinct HLA class I abnormalities caused by a mutant ␤ 2 m protein (32). These results are consistent with the possibility that the specificity of a patient's immune response can change in response to changes in the expression of targets by melanoma cells, which have developed immunoescape mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…All of the abovementioned mouse mAb are IgG1 except mAb W6/32 and HC-10, which are both IgG 2a . The anti-idiotypic mAb MK2-23, IgG 1 (28) and F3-C25, IgG 2a (29), which were both used as isotype-matched irrelevant controls, were developed and characterized as described. Actin-specific mAb was from EMD Millipore (Billerica, MA).…”

Section: Methodsmentioning

confidence: 99%

Multiple Structural and Epigenetic Defects in the Human Leukocyte Antigen Class I Antigen Presentation Pathway in a Recurrent Metastatic Melanoma Following Immunotherapy

Chang

Pirozzi²,

Wen

et al. 2015

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

Background: Understanding the mechanism of tumor immune resistance can help design effective cancer immunotherapy. Results: A novel tapasin mutation, haplotype loss, and HLA epigenetic repression were identified and characterized in a single tumor population. Conclusion:The first evidence for combined HLA genetic and epigenetic defects in malignant cells was presented. Significance: Combinatorial immunotherapy harnessing T cell responses and DNA demethylation may counteract tumor immune resistance.

show abstract

“…The mAb 225.28 recognizing CSPG4 and the anti-idiotypic mAb F3-C25 recognizing an idiotope in the antigen combining site of the HLA class II antigen-specific mAb CR11-462 were developed and characterized as described [25,26]. The mAbs were purified from mouse ascitic fluid by sequential ammonium sulfate and caprylic acid precipitation [27].…”

Section: Monoclonal Antibodiesmentioning

confidence: 99%

The CSPG4-specific monoclonal antibody enhances and prolongs the effects of the BRAF inhibitor in melanoma cells

Favoino

Wang

et al. 2011

Immunol Res

View full text Add to dashboard Cite

PLX4032 is a BRAF-selective inhibitor shown to be efficacious in the treatment of melanomas presenting with the BRAF(V600E) mutation. However, favorable responses to treatment are short-lived, and complete remission is rarely observed. Therefore, it is important to identify novel therapies designed to enhance treatment responses and to increase the longevity of initial response to BRAF inhibitors. To this end, we characterized the effects of the 225.28 chondroitin sulfate proteoglycan 4 (CSPG4)-specific monoclonal antibody (mAb) capable of blocking multiple signaling pathways important to cell growth, migration, and survival. Addition of 225.28 to the treatment regimen enhanced the in vitro response magnitude and the duration efficacy of PLX4032 in treating CSPG4(+), BRAF(V600E) melanoma cells (melanoma(BRAF(V600E)/CSPG4+) cells). Data presented in this report demonstrated that (1) treatments comprised of PLX4032 and mAb 225.28 were more effective at inhibiting melanoma(BRAF(V600E)/CSPG4+) cell growth than either agent alone, (2) mAb 225.28 prevented/delayed the development of resistance in melanoma(BRAF(V600E)/CSPG4+) cells to PLX4032, and (3) the mechanism of action of the combination therapy caused a down-regulation in multiple signaling pathways. This study provides a foundation for future investigations designed to improve BRAF inhibitor effectiveness in vitro and in vivo for treating melanoma(BRAF(V600E)/CSPG4+) cells in combination with a CSPG4-specific mAb.

show abstract

Syngeneic antiidiotypic monoclonal antibodies to the murine anti-HLA-DR,DP monoclonal antibody CR11-462

Cited by 14 publications

References 31 publications

Murine antiidiotypic monoclonal antibodies that bear the internal image of HLA-DR allospecificities.

Murine antiidiotypic monoclonal antibodies that bear the internal image of HLA-DR allospecificities.

Multiple Structural and Epigenetic Defects in the Human Leukocyte Antigen Class I Antigen Presentation Pathway in a Recurrent Metastatic Melanoma Following Immunotherapy

The CSPG4-specific monoclonal antibody enhances and prolongs the effects of the BRAF inhibitor in melanoma cells

Contact Info

Product

Resources

About