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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Infection with human T-lymphotropic virus types I and II results in alterations of cellular receptors, including the up-modulation of T-cell counterreceptors CD40, CD54, and CD80 (B7-1).
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Infection with human T-lymphotropic virus types I and II results in alterations of cellular receptors, including the up-modulation of T-cell counterreceptors CD40, CD54, and CD80 (B7-1).

机译:感染人类I型和T型T淋巴细胞病毒会导致细胞受体改变,包括T细胞反受体CD40,CD54和CD80(B7-1)的上调。

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To examine the phenotypic alterations associated with human T-lymphotropic virus types I and II (HTLV-I and -II) infection, long-term cell lines (n = 12 HTLV-I cell lines; n = 11 HTLV-II cell lines; n = 6 virus-negative cell lines) were analyzed for the cell surface expression of various lineage markers (i.e., myeloid, progenitor, and leukocyte), integrin receptors, and receptor-counterreceptor (R-CR) pairs responsible for cellular activation. As expected, all cell lines expressed the markers characterizing the leukocyte lineage (CD43, CD44, and CD53). Of the progenitor-myeloid markers examined (CD9, CD13, CD33, CD34, and CD63), only the percent expression of CD9 was significantly increased on HTLV-I and -II-infected cell lines as compared with that on virus-negative cell lines. Analysis of the beta 1 integrin subfamily (CD29, CD49b, CD49d, CD49e, and CD49f) showed no significant change, except that CD49e was significantly decreased on the HTLV-infected cell lines. For the beta 2 integrin subfamily, the cell surface density was increased for CD18 and CD11a, while the CD11c molecule was expressed exclusively on the HTLV-I- and HTLV-II-infected cell lines. Analysis of several R-CR pairs (CD2-CD58, CD45RO-CD22, CD5-CD72, CD11a-CD54, gp39-CD40, and CD28-CD80) demonstrated that comparable levels of expression of the Rs (CD2, CD45RO, CD5, and CD28) and of some of the CRs (CD58, CD22, and CD72) were in all cell lines; however, CD54, CD40, and CD80 were expressed constitutively on the HTLV-I- and HTLV-II-infected cell lines. Functionally, the expression of these R-CR pairs did not appear to affect the autologous proliferation since monoclonal antibodies to these R-CR pairs were not able to inhibit proliferation of the infected cell lines. Taken together, our results indicate that HTLV-I and -II can modulate the expression of several T-cell activation molecules and CRs normally expressed on alternate cell types.
机译:为了检查与人I型和II型T淋巴细胞病毒(HTLV-I和-II)感染相关的表型改变,需要长期的细胞系(n = 12 HTLV-I细胞系; n = 11 HTLV-II细胞系; n = 11)。分析n = 6病毒阴性细胞系的各种谱系标记(即,髓样,祖细胞和白细胞),整联蛋白受体和受体-反受体(R-CR)对在细胞表面的表达。如预期的那样,所有细胞系均表达表征白细胞谱系的标记(CD43,CD44和CD53)。在所检查的祖骨髓标记(CD9,CD13,CD33,CD34和CD63)中,与病毒阴性细胞系相比,在HTLV-1和-II感染的细胞系中CD9的表达百分比仅显着增加。对β1整联蛋白亚家族(CD29,CD49b,CD49d,CD49e和CD49f)的分析显示无显着变化,除了在HTLV感染的细胞系中CD49e显着减少。对于β2整联蛋白亚家族,CD18和CD11a的细胞表面密度增加,而CD11c分子仅在HTLV-I和HTLV-II感染的细胞系中表达。对几个R-CR对(CD2-CD58,CD45RO-CD22,CD5-CD72,CD11a-CD54,gp39-CD40和CD28-CD80)的分析表明,Rs的表达水平相当(CD2,CD45RO,CD5和CD28)和某些CR(CD58,CD22和CD72)都存在于所有细胞系中。但是,CD54,CD40和CD80在HTLV-I和HTLV-II感染的细胞系中组成性表达。从功能上讲,这些R-CR对的表达似乎不影响自体增殖,因为针对这些R-CR对的单克隆抗体无法抑制被感染细胞系的增殖。两者合计,我们的结果表明HTLV-I和-II可调节几种T细胞活化分子和通常在其他细胞类型上表达的CR的表达。

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