Expression of different CD8 isoforms on distinct human lymphocyte subpopulations

Moebius, Ulrich; Kober, Gabriela; Griscelli, Anne Lise; Hercend, Thierry; Meuer, Stefan

doi:10.1002/eji.1830210803

Cited by 149 publications

(107 citation statements)

References 44 publications

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“…6A, virtually all CD3 ϩ CD8 ϩ CD5 ϩ and CD3 ϩ CD8 ϩ CD5 Ϫ lymphocytes stained with an anti-CD8␣ mAb, whereas an anti-CD8 mAb recognizing a CD8 epitope generated by coupling of the ␣-and ␤-chains recognized all CD3 ϩ CD8 ϩ CD5 ϩ cells, but only a fraction of CD3 ϩ CD8 ϩ CD5 Ϫ lymphocytes. As a consequence, we could conclude that a significantly higher ( p Ͻ 0.01) proportion of CD3 ϩ CD8 ϩ CD5 Ϫ cells expressed the ␣␣ form of the CD8 molecule compared with the CD5 ϩ counterpart, which, as expected (38,43,44), mostly expressed the ␣␤ variant of this coreceptor (Fig. 6B).…”

Section: Phenotypic Characterization Of Cd3supporting

confidence: 62%

“…This finding is somewhat surprising and may help in explaining some experimental and/or clinical observations. The ␣␣ form of CD8 is mostly expressed on NK cells (43,62) and is usually associated with a poor proliferative response to mitogenic stimulation and preferential display of non-MHC-restricted cytotoxic activity (43,63). Indeed, in several repeated attempts we never succeeded in stabilizing in vitro long term CD3 ϩ CD8 ϩ CD5 Ϫ lines or clones; the inability of these cells to undergo substantial in vitro expansion was apparently not due to the production of immunomodulatory cytokines, such as TGF-␤ (data not shown).…”

Section: Discussionmentioning

confidence: 99%

“…It is known that the CD8 Ag may be expressed on the cell surface in two molecular forms, as a homodimer composed of two ␣-chains or as a heterodimer composed of an ␣-and a ␤-chain (43,44); the CD8␣␤-expressing population is much more represented in the circulation (38,43,44). To evaluate the expression of these two CD8 forms at the surface of CD3 ϩ CD8 ϩ CD5 Ϫ lymphocytes and in view of the absence of an anti-CD8 mAb specifically directed against the CD8␤ chain, we were forced to calculate the proportion of CD8␣␣-expressing cells as the difference between the figures obtained with two mAb recognizing different epitopes of the CD8 molecule.…”

Section: Phenotypic Characterization Of Cd3mentioning

confidence: 99%

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CD8+αβ+ T Cells That Lack Surface CD5 Antigen Expression Are a Major Lymphotactin (XCL1) Source in Peripheral Blood Lymphocytes

Stievano

Tosello

Marcato

et al. 2003

The Journal of Immunology

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To better characterize the cellular source of lymphotactin (XCL1), we compared XCL1 expression in different lymphocyte subsets by real-time PCR. XCL1 was constitutively expressed in both PBMC and CD4+ cells, but its expression was almost 2 log higher in CD8+ cells. In vitro activation was associated with a substantial increase in XCL1 expression in both PBMC and CD8+ cells, but not in CD4+ lymphocytes. The preferential expression of XCL1 in CD8+ cells was confirmed by measuring XCL1 production in culture supernatants, and a good correlation was found between figures obtained by real-time PCR and XCL1 contents. XCL1 expression was mostly confined to a CD3+CD8+ subset not expressing CD5, where XCL1 expression equaled that shown by γδ+ T cells. Compared with the CD5+ counterpart, CD3+CD8+CD5− cells, which did not express CD5 following in vitro activation, showed preferential expression of the αα form of CD8 and a lower expression of molecules associated with a noncommitted/naive phenotype, such as CD62L. CD3+CD8+CD5− cells also expressed higher levels of the XCL1 receptor; in addition, although not differing from CD3+CD8+CD5+ cells in terms of the expression of most α- and β-chemokines, they showed higher expression of CCL3/macrophage inflammatory protein-1α. These data show that TCR αβ-expressing lymphocytes that lack CD5 expression are a major XCL1 source, and that the contribution to its synthesis by different TCR αβ-expressing T cell subsets, namely CD4+ lymphocytes, is negligible. In addition, they point to the CD3+CD8+CD5− population as a particular T cell subset within the CD8+ compartment, whose functional properties deserve further attention.

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Section: Phenotypic Characterization Of Cd3supporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Section: Phenotypic Characterization Of Cd3mentioning

confidence: 99%

See 1 more Smart Citation

CD8+αβ+ T Cells That Lack Surface CD5 Antigen Expression Are a Major Lymphotactin (XCL1) Source in Peripheral Blood Lymphocytes

Stievano

Tosello

Marcato

et al. 2003

The Journal of Immunology

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“…[29][30][31][32][33][34][35][36] In the case of melanoma lines, B7 expression appeared to be necessary to induce allogeneic responses; whereas this was not found to be the case here with the RCC-26 renal carcinoma line. Although it has been found that CTL responses directed against tumorassociated antigens could be induced following stimulation with B7-modified melanoma lines, the priming procedures utilized purified CD8 T cells and culture conditions that did not support the development of alloresponses; 32,33 thus, the influence of dominating allospecific CTL on development of tumor-specific CTL could not be assessed in these studies.…”

Section: Discussionmentioning

confidence: 58%

Expression of B7.1 (CD80) in a renal cell carcinoma line allows expansion of tumor-associated cytotoxic T lymphocytes in the presence of an alloresponse

et al. 2000

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We have selected a well-characterized human renal cell carcinoma (RCC) line as the basis for development of a genetically engineered tumor cell vaccine to be applied in an allogeneic setting. This cell line was genetically modified by retroviral transduction to express B7.1 costimulatory molecules. The unmodified tumor cells and B7.1-expressing tumor cells were compared for their ability to induce tumorassociated responses in allogeneic peripheral blood mononuclear cells (PBMC) of two normal control donors having single MHC class I allele matches with the tumor cells. PBMC primed using B7.1-modified tumor cells showed a preponderance of CD3 + CD8 + cytotoxic T lymphocytes (CTL)

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“…CD8 proteins are encoded by two genes, CD8a and CD8b, and expressed on the cell surface as homodimeric CD8aa and heterodimeric CD8ab [16]. Although both CD8aa and CD8ab bind to the classic MHCI molecules and function as coreceptors to enhance recognition of peptide antigens by TCR, CD8ab is apparently more efficient than CD8aa [17][18][19].…”

Section: Introductionmentioning

confidence: 99%

An active CD8α/pMHCI interaction is required for CD8 single positive thymocyte differentiation

et al. 2010

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Recognition of viral antigenic peptides bound to major histocompatibility complex class I molecules (MHCI) by TCR is critical for initiating the responses of CD8 1 T cells that ultimately lead to elimination of virus-infected cells. This antigen recognition is enhanced by the CD8 coreceptor through its interaction with the peptide-MHCI complexes (pMHCI). Mouse CD8ab can form two different complexes with pMHCI via either the CD8a-or CD8b-dominated interaction. To understand the functional significance of these complexes in vivo, we generated Tg mice carrying a variant CD8ab (CD8a m3 b) capable of forming only the CD8b-dominated CD8ab/pMHCI complex. These mice show sub-optimal thymic differentiation with reduced populations of CD8 1 single-positive thymocytes. Tg CD8 1 T cells exhibit a compromised developmental capacity when competing with CD8 1 T cells from B6 mice in mixed bone marrow chimera experiments. However, once these CD8 1 T cells have emigrated to the peripheral lymphoid organs, they exhibit normal effector function against viral infection. Our observations indicate that, in addition to the CD8 activity conferred by CD8b-dominated CD8ab/pMHCI complexes, full thymocyte differentiation requires additional coreceptor activities conferred by CD8aa and/or CD8ab with CD8a-dominated CD8/pMHCI complexes.Key words: CD8/pMHCI interaction . Coreceptor functions . T-cell differentiation .Viral infection . Tg mice Supporting Information available online IntroductionThe recognition of peptide antigen loaded on the major histocompatibility complex I (pMHCI) displayed on APC by the TCR is greatly enhanced by the simultaneous engagement of pMHCI with CD8 proteins on class I restricted CD8 1 T lymphocytes [1][2][3]. Such enhancement of antigen recognition is critical not only for triggering the activation of CD8 1 T cells but also for the differentiation of CD8 1 T cells in thymus [4][5][6][7][8][9][10]. Development of CD8 1 T cells in thymus starts with the differentiation of CD4 À CD8 À double negative (DN) precursor T cells into CD4 1 CD8 1 double positive (DP) cells, then into CD4 1 CD8b lo transition cells, and finally maturation into CD8 1 single positive (SP) cells [11][12][13][14]. After emigration into periphery, these CD8 1 T cells, in response to viral infection, can be activated by viral antigens and expanded as effector cytotoxic T lymphocytes, 836which are capable of eliminating the virus-infected cells [15]. The roles played by the interactions between CD8 proteins and MHCI in thymic differentiation and effector functions are not all clear.CD8 proteins are encoded by two genes, CD8a and CD8b, and expressed on the cell surface as homodimeric CD8aa and heterodimeric CD8ab [16]. Although both CD8aa and CD8ab bind to the classic MHCI molecules and function as coreceptors to enhance recognition of peptide antigens by TCR, CD8ab is apparently more efficient than CD8aa [17][18][19]. Surface expression of CD8b requires its heterodimerization with CD8a [20] and, consequently, no cellsurface CD8b protein can be de...

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Expression of different CD8 isoforms on distinct human lymphocyte subpopulations

Cited by 149 publications

References 44 publications

CD8+αβ+ T Cells That Lack Surface CD5 Antigen Expression Are a Major Lymphotactin (XCL1) Source in Peripheral Blood Lymphocytes

CD8+αβ+ T Cells That Lack Surface CD5 Antigen Expression Are a Major Lymphotactin (XCL1) Source in Peripheral Blood Lymphocytes

Expression of B7.1 (CD80) in a renal cell carcinoma line allows expansion of tumor-associated cytotoxic T lymphocytes in the presence of an alloresponse

An active CD8α/pMHCI interaction is required for CD8 single positive thymocyte differentiation

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