Bioengineered soluble HLA-B7

Hiraki, Debra D.; See-Tho, K.; Filvaroff, Ellen; Krishnaswamy, Shalini; Bello, W. De; Taidi-Laskowski, Behnaz; Grumet, F. Carl

doi:10.1016/0198-8859(94)90074-4

Cited by 22 publications

(5 citation statements)

References 49 publications

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“…Roth and coworkers [28] have shown in a mouse system that inhibition of NK killing by soluble forms of Kd occurs when mAb against the a 3 domain was present in the preincubation medium, leading to MHC class I dimer formation. In some experiment, we observed a similar phenomenon without any previous antibody-mediated sHLA class I dimerization due to the presence of sHLA aggregates already present in our concentrated class I supernatants [6]. However, when we pretreated the effectors with sHLA dimerized by W6-32 mAb we observed an enhanced inhibition (Fig.…”

Section: Discussionsupporting

confidence: 66%

“…Supernatants used in our study included: U-200, containing sHLA-A1 and B52; C-2200, containing A3, 23 and B50, 55; and S-4300, containing A24, B27, 44. As sHLA-B7 we used a supernatant containing a bioengineered soluble HLA-B7 (T.sB7) lacking the transmembrane and cytoplasmic domains [6]. Alternatively, the sHLA molecules of the allele products HLA-A2, B7 and HLA-A2, B5 were obtained from the HLA class I protein shedding of J Y and T2lTAP1+2 cell lines, respectively.…”

Section: Shla Supernatant Preparationmentioning

confidence: 99%

“…Molecular forms identified so far include a 44-kDa variant that results from a shedding process and which bears extracellular domains, the transmembrane segment and the cytoplasmic tail, and a secreted 39-kDa variant lacking the transmembrane domain due to deletion of exon 5 based on alternative RNA splicing. Moreover, a 120-kDa form, comprising soluble MHC class I dimers, has been recently described [3][4][5][6]. A similar molecular form was described for the HLA class I expressed on the cell membrane of human B lymphoma cells [7].…”

Section: Introductionmentioning

confidence: 99%

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Natural killer clones recognize specific soluble HLA class I molecules

Carbone

Terrazzano

Colonna³

et al. 1996

Eur J Immunol

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Enhancement of major histocompatibility complex (MHC) class I expression leads to protection from natural killer (NK) cell recognition in several systems. MHC class I gene products are released from the cell surface and can be found in sera as soluble forms. To investigate the possible immunoregulatory role of soluble HLA (sHLA) in NK cell-target recognition, several sHLA antigens were studied for their ability to induce NK cell cytotoxicity modulation. NK cell-target recognition was inhibited by the addition of sHLA during the cytotoxicity assay. Our results indicate that sHLA molecules can down-regulate NK killing at the effector level. Moreover, different NK clones are able to specifically recognize different sHLA antigens. Kp43 molecules seem to be involved in the NK recognition of sHLA-B7.

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Section: Discussionsupporting

confidence: 66%

Section: Shla Supernatant Preparationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Natural killer clones recognize specific soluble HLA class I molecules

Carbone

Terrazzano

Colonna³

et al. 1996

Eur J Immunol

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“…The purification of the soluble HLA class I-B7 antigen was performed by affinity column in accordance with a report by Hiraki et al [11]. C1R-neo-B7, which has been genetically engineered to secrete a soluble HLA-B7 antigen, was kindly provided by Prof. Carl Grumet of Stanford University, USA.…”

Section: Purification Of the Soluble Hla Class I Antigenmentioning

confidence: 99%

“…It caused no apoptosis in MKN45 cells. It has been reported that the 39 kDa form of sHLA-I did not have a transmembrane region [11]. Peptide 3 was produced for the investigation of whether nos.…”

Section: Inhibition Of Peritoneal Dissemination By Shla-i In Nude Micementioning

confidence: 99%

Peptides Derived from a Soluble Molecule of the Human Leukocyte Antigen (HLA) Class I Cause Apoptosis in Gastric Cancer Cell Lines

et al. 2008

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We have reported that the levels of the soluble molecule of the human leukocyte antigen class I (sHLA-I) in patients with advanced gastric cancer were significantly lower than those in patients with cancer in the early stages. However, the effect of sHLA-I on gastric cancer cells has not been elucidated. Using human gastric cancer cell lines, MKN28, MKN45, and MKN74, we evaluated the effects of sHLA-I on cell growth, DNA synthesis, and apoptosis induction. Three types of synthesized peptides derived from HLA-I were also examined for their capacity to induce apoptosis. sHLA-I and a synthesized peptide, nos. 220-232 of the alpha3 domain of HLA-B7, caused cell growth inhibition by inducing apoptosis in human gastric cancer cells. This peptide also inhibited the in vivo growth of cancer dissemination caused by an intraperitoneal injection of MKN45 into severe combined immunodeficient mice. In conclusion, sHLA-I and the peptides derived from HLA-I cause apoptosis in human gastric cancer cell lines.

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Serum concentrations of soluble HLA-class I and CD8 forms in patients with viral hepatic disorders

Hagihara

Shimura²,

Takebe³

et al. 1997

J Gastroenterol

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Soluble HLA-class I and CD8 molecules were determined by sandwich ELISA in patients with viral-induced hepatic disorders. As a whole, the patients with hepatic disorders (acute hepatitis: AH; chronic hepatitis: CH; liver cirrhosis: LC; hepatocellular carcinoma: HCC) showed higher sHLA-class I and sCD8 levels than normal controls (P < 0.001). AH patients had the highest sHLA-class I levels (mean, 3513 +/- 2112 ng/ml), followed by CH (2896 +/- 1290 ng/ml), LC (2293 +/- 1266 ng/ml), and HCC (2221 +/- 1212 ng/ml) sCD8 levels wer highest in AH, followed by HCC, LC, and CH, in that order. Among histologically defined C virus-positive patients, sHLA-I levels were higher in those with chronic active hepatitis (CAH) 2A (3802 +/- 1124 ng/ml) than in those with chronic persistent hepatitis (CPH; 2200 +/- 711 ng/ml; P < 0.01), the levels then decreased as the disease progressed (CAH2B, 3564 +/- 1783 ng/ml, LC, 2376 +/- 1265 ng/ml). In contrast, sCD8 values showed little difference among the disorders. sHLA-class I levels showed a positive correlation with sCD8 values both in whole patients and in patients with AH (P < 0.01), but no correlation was shown, in any patients, with biochemical parameters such as GPT and GOT. These findings, taken together, suggest that hepatic destruction is not the only cause of sHLA-class I production, but that sHLA-class I levels, together with sCD8 levels, may reflect immunological activity in hepatic disorders.

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Bioengineered soluble HLA-B7

Cited by 22 publications

References 49 publications

Natural killer clones recognize specific soluble HLA class I molecules

Natural killer clones recognize specific soluble HLA class I molecules

Peptides Derived from a Soluble Molecule of the Human Leukocyte Antigen (HLA) Class I Cause Apoptosis in Gastric Cancer Cell Lines

Serum concentrations of soluble HLA-class I and CD8 forms in patients with viral hepatic disorders

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