Fine Specificity and Idiotype Diversity of the Murine Anti-Hla-A2, A28 Monoclonal Antibodies Cr11–351 and Ks1

Tsujisaki, Masayuki; Sakaguchi, Kohsaku; Igarashi, Muneo; Richiardi, P.; Perosa, Federico; Ferrone, Soldano

doi:10.1097/00007890-198803000-00026

Cited by 44 publications

(15 citation statements)

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“…With the exception of HLA-DR, most surface markers tested demonstrated a trend to downregulation in rVV-infected compared with noninfected DC independent of their status of maturation (Figure 2a) three consecutive experiments we also tested the effect of rVV infection on HLA-A*0201 expression using the HLA-A2-specific mAb KS-1. 26 Surface expression of HLA-A*0201 was significantly downregulated by rVV infection and equally affected iDC and mDC (Figure 2 b and c). In addition, overnight treatment with IFN-a (1000 IU/ml) did not restore the expression of HLA-A*0201 by either DC population (data not shown).…”

Section: Effect Of Rvv-gp100 Infection On the Phenotype Of Idc And MDCmentioning

confidence: 90%

“…The antibodies used were anti-CD80-FITC, anti-CD83-FITC, anti-CD86-FITC, anti-HLA-DR-FITC, KS-1 (anti-HLA-A2), and HMB (anti-gp100). Except for KS-1 26 and HMB45 (Enzo Diagnostics, Farmingdale, NJ, USA), all antibodies were purchased from Becton Dickinson. For analysis of gp100 expression, cells were fixed in acetone for 5 min and then washed prior to staining.…”

Section: Facs Analysis Of Maturation State and Gp100 Expression Of DCmentioning

confidence: 99%

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Biased epitope selection by recombinant vaccinia-virus (rVV)-infected mature or immature dendritic cells

et al. 2003

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Section: Effect Of Rvv-gp100 Infection On the Phenotype Of Idc And MDCmentioning

confidence: 90%

Section: Facs Analysis Of Maturation State and Gp100 Expression Of DCmentioning

confidence: 99%

Biased epitope selection by recombinant vaccinia-virus (rVV)-infected mature or immature dendritic cells

et al. 2003

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“…The mouse mAbs W6/32, which recognize ␤ 2 m-associated HLA-A, -B, -C, -E, and -G H chains (9, 10); mAb LGIII-147.4.1, which recognizes ␤ 2 massociated HLA-A H chains, excluding -A23, -A24, -A25, -A32 (11); mAb B1.23.1, which recognizes ␤ 2 m-free and -associated HLA-B and -C H chains (12); anti-HLA-A2, -A24, -A28 mAb CR11-351 (13,14); anti-HLA-A2, -A28 mAb KS-1 (14); anti-HLA-B7, -B27, -Bw42, -Bw54, -Bw55, -Bw56, -Bw67, -Bw73 mAb KS-4 (15); mAb HCA-2, which recognizes ␤ 2 m-free HLA-A (excluding -A24), -B7301, and -G H chains (16,17); mAb HC-10, which recognizes ␤ 2 m-free HLA-A3, -A10, -A28, -A29, -A30, -A31, -A32, -A33, -B (excluding -B5702, -B5804, and -B73) H chain (16 -18) …”

Section: Mabs and Polyclonal Absmentioning

confidence: 99%

Immune Selection of Hot-Spot β2-Microglobulin Gene Mutations, HLA-A2 Allospecificity Loss, and Antigen-Processing Machinery Component Down-Regulation in Melanoma Cells Derived from Recurrent Metastases following Immunotherapy

Chang

Campoli

Restifo

et al. 2005

The Journal of Immunology

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Scanty information is available about the mechanisms underlying HLA class I Ag abnormalities in malignant cells exposed to strong T cell-mediated selective pressure. In this study, we have characterized the molecular defects underlying HLA class I Ag loss in five melanoma cell lines derived from recurrent metastases following initial clinical responses to T cell-based immunotherapy. Point mutations in the translation initiation codon (ATG→ATA) and in codon 31 (TCA→TGA) of the β2-microglobulin (β2m) gene were identified in the melanoma cell lines 1074MEL and 1174MEL, respectively. A hot-spot CT dinucleotide deletion within codon 13–15 was found in the melanoma cell lines 1106MEL, 1180MEL, and 1259MEL. Reconstitution of β2m expression restored HLA class I Ag expression in the five melanoma cell lines; however, the HLA-A and HLA-B,-C gene products were differentially expressed by 1074MEL, 1106MEL, and 1259MEL cells. In addition, in 1259MEL cells, the Ag-processing machinery components calnexin, calreticulin, and low m.w. polypeptide 10 are down-regulated, and HLA-A2 Ags are selectively lost because of a single cytosine deletion in the HLA-A2 gene exon 4. Our results in conjunction with those in the literature suggest the emergence of a preferential β2m gene mutation in melanoma cells following strong T cell-mediated immune selection. Furthermore, the presence of multiple HLA class I Ag defects within a tumor cell population may reflect the accumulation of multiple escape mechanisms developed by melanoma cells to avoid distinct sequential T cell-mediated selective events.

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“…Cytospins and frozen sections were fixed in acetone for 10 min, then rinsed in PBS and blocked in 3-5% goat serum in PBS for 20 min. The following primary mAbs were used: HMB-45 for assessment of gp100/ Pmel-17 expression (Biogenex, San Ramon, CA), M2-7C10 for the assessment of MART-1/MelanA expression (6,25), and KS-1 for the assessment of HLA-A2 Ag expression (26). Primary Ab was applied for 2 h at room temperature.…”

Section: Immunohistochemistry (Ihc)mentioning

confidence: 99%

Short-Term Kinetics of Tumor Antigen Expression in Response to Vaccination

Ohnmacht¹,

Wang²,

Mocellin

et al. 2001

The Journal of Immunology

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The melanoma patient’s immune response to tumor has been extensively studied. Yet, the frequently observed coexistence of tumor-associated Ag (TAA)-specific T cells with their target cells in vivo remains unexplained. Loss of TAA expression might contribute to this paradox. We studied TAA expression in metastases by obtaining fine-needle aspirations from 52 tumor lesions in 30 patients with melanoma before and soon after immunotherapy. Limitations due to low amounts of starting material were overcome with a high fidelity antisense RNA amplification method. TAA expression was measured by quantitative real-time PCR of anti-sense RNA. Decrease in gp100/Pmel-17 TAA preceded tumor disappearance in several instances and could be best explained by immune selection because most patients had received gp100/Pmel-17-specific vaccination. Conversely, immune selection was absent in nonregressing lesions. These observations suggest that vaccination, when successful, triggers a broad inflammatory reaction that can lead to tumor destruction despite immune selection. Additionally, lack of clinical response might be attributed to lack of this initiating event rather than immune escape. This study provides an insight into the natural history of tumors and defines a strategy for the characterization of gene expression in tumors during therapy.

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Fine Specificity and Idiotype Diversity of the Murine Anti-Hla-A2, A28 Monoclonal Antibodies Cr11–351 and Ks1

Cited by 44 publications

References 0 publications

Biased epitope selection by recombinant vaccinia-virus (rVV)-infected mature or immature dendritic cells

Biased epitope selection by recombinant vaccinia-virus (rVV)-infected mature or immature dendritic cells

Immune Selection of Hot-Spot β2-Microglobulin Gene Mutations, HLA-A2 Allospecificity Loss, and Antigen-Processing Machinery Component Down-Regulation in Melanoma Cells Derived from Recurrent Metastases following Immunotherapy

Short-Term Kinetics of Tumor Antigen Expression in Response to Vaccination

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