Report of the second international soluble HLA (sHLA) workshop

Grumet, F. Carl; Buelow, Roland; Grosse‐Wilde, H.; Kubens, Britta S.; Garovoy, Marvin R.; Pouletty, Philippe

doi:10.1016/0198-8859(94)90062-0

Cited by 13 publications

(5 citation statements)

References 34 publications

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“…1,2 Beside being expressed on most nucleated cells, both b2-microglobulin associated and free HLA-I heavy chains have been detected in serum. [2][3][4][5] More recently, it has been shown that the serum level of these soluble molecules is significantly increased in patients with an activation of their immune system, such as during allograft rejection, autoimmune diseases or viral infections. 1,6 Because of the statistical significant association with clinical parameters, the amount of soluble human leukocyte antigens (sHLA)-I antigens has been proposed as a useful marker to predict the evolution of chronic viral infections and the clinical course of allografts.…”

Section: Introductionmentioning

confidence: 99%

In vivo apoptosis of CD8+ lymphocytes in acute myeloid leukemia patients: involvement of soluble HLA-I and Fas ligand

et al. 2006

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In this study, we show that high serum levels of soluble human leukocyte antigens (HLA) class I molecules (sHLA-I, range: 0.7-1.7 lg/ml) and soluble Fas ligand (FasL, range: 0.4-1.9 ng/ml) are detected in patients with acute myeloid leukemia (AML) at diagnosis, compared with healthy donors (HD) (sHLA-I, range: 0.1-0.6 lg/ml; sFasL, range: 0.1-0.4 ng/ml). Patients' sera were able to induce transcription and secretion of FasL in CD8 þ T cells, followed by apoptosis in vitro; this apoptosis was inhibited by anti-HLA-I-specific monoclonal antibodies, suggesting that sHLA-I is responsible for cell death. These findings closely relate to the in vivo upregulation of FasL transcription observed in peripheral blood (PB) lymphocytes from AML patients; in the same cells, mRNA for the antiapoptotic proteins Bcl-2 and Bcl-x L was downregulated. Interestingly, caspase-8 and caspase-3, both downstream mediators of death receptorinduced apoptosis, were activated in CD8 þ cells of AML patients; one-third of these cells were already apoptotic in vivo, at variance with lymphocytes of HD. These data strongly suggest that in AML, increased levels of sHLA-I molecules may contribute to the elimination of potentially anti-tumor effector cells through a FasL/Fas interaction.

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Section: Introductionmentioning

confidence: 99%

In vivo apoptosis of CD8+ lymphocytes in acute myeloid leukemia patients: involvement of soluble HLA-I and Fas ligand

et al. 2006

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“…Surface expression of HLA class I molecules on neurons has recently been demonstrated along with its differential regulation by electric membrane activity, IFN-gamma and tumor necrosis factor (TNF)-alpha (Neumann et al, 1995(Neumann et al, , 1997. These antigenically reactive molecules are known to occur naturally in body fluids in soluble form (sHLA), with different sizes: the 44 -45 kDa shed from cells as intact membrane antigen, the 39 kDa secreted molecule lacking the transmembrane domain because of alternative splicing, and the 36 -37 kDa determinant resulting from the proteolytic digestion of the 39 and 44 -45 kDa forms (Grumet et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

“…While increased sHLA-I levels have been detected in different conditions associated with T cell activation, including viral infections, chronic renal diseases and post renal status, liver and bone marrow transplant (Grumet et al, 1994), lower amounts of sHLA-I have been observed in solid tumors (Mc Donald and Adamashvili, 1998), suggesting a possible role of these antigenic structures in tolerance induction (Zavazava et al, 1991) and, more recently, in apoptosis (Zavazava and Kronke, 1996). Furthermore, cells expressing HLA class I antigens have been identified in active inflammatory CNS lesions of MS patients (Traugott, 1987).…”

Section: Introductionmentioning

confidence: 99%

Clinical and MRI disease activity in multiple sclerosis are associated with reciprocal fluctuations in serum and cerebrospinal fluid levels of soluble HLA class I molecules

Fainardi

Granieri

Tola

et al. 2002

Journal of Neuroimmunology

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“…They are produced by shedding or proteolysis or by alternative splicing, which creates isoforms that lack the transmembrane domain [29][30][31]. Furthermore, it has been shown that the presence of soluble HLA-class I molecules differs not only in respect of particular alleles [32,33], but also in that its concentration varies in females over the course of the menstrual cycle [34], in several disorders, after vaccinations of elderly persons and after transplantations (for a review see [35,36]). A concentration range of sHLA-class I molecules between 0.14 and 3.37 gg/ml has been determined [24].…”

Section: Discussionmentioning

confidence: 99%

HLA-B27 determination using serological methods. A comparison of enzyme immunoassay and a microlymphocytotoxic test with flow cytometry and a molecular biological assay

Dunky

Neumüller²,

Hübner³

et al. 1996

Rheumatol Int

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Typing for HLA-B27 is routinely performed in patients with seronegative spondarthritides. Besides the microlymphocytotoxic test (MLCT), other serological techniques have been developed such as enzyme immunoassays (EIA) using serum or plasma as a source for the determination of soluble HLA-B27 (sHLA-B27) and flow cytometric (FC) methods. The aim of the present study was to check the accuracy and reliability of the EIA for sHLA-B27 in comparison to the MLCT using antibodies against HLA-B27 and cross-reacting specificities (CRS), as well as an FC method and a molecular biological method. Any discrepant results should be typed with the MLCT using a complete panel of anti-HLA-class I antibodies, with FC and with a molecular biological technique. The EIA should also be repeated in those patients, using serum and plasma from a new venipuncture. In 81 patients with rheumatic disorders, the EIA and the MLCT using antibodies against HLA-B27 and CRS were performed. Based on the MLCT with a complete panel of anti-HLA-class I antibodies as a standard, discrepant test results were obtained for 9 out of 81 patients with the MLCT using antibodies against HLA-B27 and CRS and with the EIA. The following wrong results occurred: in the MLCT with anti-HLA-B27 and CRS, there were two false-negative results; in the EIA there were four false-negative and one false-positive results; one sample was undeterminable. In comparison with the MLCT, including the complete panel of HLA-class I antibodies, as well as with a molecular biological technique, typing with FC showed a complete concordance. Our investigations demonstrated that for routine typing for HLA-B27 the MLCT cannot be replaced by EIA because of a significant number of mistypings. The MLCT performed only with antibodies against HLA-B27 and CRS may also lead to typing errors. No errors were detected using flow cytometry. If only serological methods can be performed in a laboratory a combination of flow cytometry and MLCT could therefore enhance the safety of HLA-B27 typing.

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Report of the second international soluble HLA (sHLA) workshop

Cited by 13 publications

References 34 publications

In vivo apoptosis of CD8+ lymphocytes in acute myeloid leukemia patients: involvement of soluble HLA-I and Fas ligand

In vivo apoptosis of CD8+ lymphocytes in acute myeloid leukemia patients: involvement of soluble HLA-I and Fas ligand

Clinical and MRI disease activity in multiple sclerosis are associated with reciprocal fluctuations in serum and cerebrospinal fluid levels of soluble HLA class I molecules

HLA-B27 determination using serological methods. A comparison of enzyme immunoassay and a microlymphocytotoxic test with flow cytometry and a molecular biological assay

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