Acute lethal graft-versus-host reaction induced by major histocompatibility complex class II-reactive T helper cell clones.

Lehmann, Paul; Schumm, G; Moon, Dain; Hurtenbach, Ursula; Falcioni, Fiorenza; Müller, Sören; Nagy, Z A

doi:10.1084/jem.171.5.1485

Cited by 32 publications

(18 citation statements)

References 26 publications

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“…On day 15 the lines were readjusted to 2 x 10 s ceUs/ml and were restimulated with irradiated, syngeneic, human APC (PBMC, 2 x 106/ml), CD3 mAb (1/zg/ml), and rlL-2 (10 ng/ml) in 24-well plates in 2 ml DMEM-FCS medium per well. Thereafter, the cells were fed weekly with fresh DMEM-FCS medium containing rib2 (10 ng/ml) and restimulated with syngeneic, human APC and Ag (CD3 mAb) once a month according to the protocol previously described (19).…”

Section: T Cell Proliferation Assay With Cells Freshly Prepared From mentioning

confidence: 99%

Human mature T cells that are anergic in vivo prevail in SCID mice reconstituted with human peripheral blood.

Tary‐Lehmann

Saxon

1992

The Journal of Experimental Medicine

157

106

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SummaryIn these studies we have characterized the human cells that repopulate severe combined immunodeficient (SCID) mice after injection of adult peripheral blood or cord blood (hu-PBD SCID mice). In all organs of the chimeras, and at any time point tested, single-positive (CD4 + or CD8 +) T cells that expressed the or//3 T cell receptor (TCR) prevailed. All T cells were CD45RO * and the majority were also HLA-DR § . Thus, the human T cells in the chimeras exhibited the phenotype of mature, memory cells that showed signs of recent activation. Cell cycle studies revealed a mitotically active human T cell population in the murine host. However, when freshly isolated from the chimeras, the human T cells were refractory to stimulation by anti-CD3 antibody but proliferated in response to exogenous interleukin 2. Chimera-derived human T cell lines retained this state of unresponsiveness to TCR-triggered proliferation for 4-6 wk in vitro. Subsequently, the T cell lines developed responses to anti-CD3 stimulation and 9 of 11 of the lines also proliferated in response to splenic stimulator cells of SCID mice. These data demonstrate that the human T cells are in a state of reversible anergy in the murine host and that xenoreactivity might play a critical role in hu-PBL-SCID mice. Mechanisms that may determine repopulation of SCID mice with human peripheral blood mononuclear cells are discussed.

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Section: T Cell Proliferation Assay With Cells Freshly Prepared From mentioning

confidence: 99%

Human mature T cells that are anergic in vivo prevail in SCID mice reconstituted with human peripheral blood.

Tary‐Lehmann

Saxon

1992

The Journal of Experimental Medicine

157

106

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“…49,50 However, these cells engage in recirculation after 5-7 days. 51,52 This might be the reason why we did not detect ex vivo CD8 ϩ T cells that would produce increased levels of PFN. The PFN-producing cells that can be detected in the blood might have encountered antigen more than 5 days before testing, but still in the recent past.…”

Section: Fig 3 Hiv Peptides Induced Pfn Secretion In Pbmcs and Cd8 mentioning

confidence: 66%

Dissociated Production of Perforin, Granzyme B, and IFN-γ by HIV-Specific CD8⁺Cells in HIV Infection

Küerten

Nowacki

Kleen

et al. 2008

AIDS Research and Human Retroviruses

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CD8(+) T cells play a crucial role in the control of viral infections such as HIV. The functional characterization of HIV-specific CD8(+) T cells has so far been largely restricted to studies of IFN-gamma. The TCR-triggered release of the effector molecules perforin (PFN) and granzyme B (GzB), however, is thought to be a central pathway for the destruction of virus-infected target cells by CD8(+) effector T cells. Here we would like to address two major findings. On the one hand we propose that ex vivo measurements of PFN and GzB secretion via ELISPOT may permit the distinction between in vivo resting versus activated CD8(+) memory T cells in healthy and HIV-infected individuals. Therefore, extending the present standard of IFN-gamma measurements to the analysis of PFN and GzB release in functional T cell assays will provide new insights into CD8(+) effector T cell functions. It should enable the evaluation of therapeutic vaccination efficacy by its ability to reactivate and convert IFN-gamma-positive, but GzB- and PFN-negative memory CD8(+) T cells into PFN/GzB-secreting effector cells. On the other hand, we report on a frequent ex vivo dissociation of the HIV peptide-induced secretion of PFN and GzB in chronic HIV infection underlining CD8(+) effector T cell diversity in this disease--an aspect that also has to be accounted for in immune monitoring approaches.

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“…To induce acute lethal GVHD in unirradiated recipients, certain strain combinations of MHC class I + IT-disparity and relatively large numbers (108) of donor cells are required (Rolink et al, 1983). Recently, Lehmann et al (1990) demonstrated that alloreactive T cell clones can induce acute lethal GVHD in unirradiated recipients with single MHC disparity after i.v. injection of 5 x 106-107 cells.…”

Section: Discussionmentioning

confidence: 99%

Induction of cutaneousgraft-versus-hostdisease by local injection of unprimed T cells

Kawai

Matsumoto

Watanabe

et al. 1991

Clinical and Experimental Immunology

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SUMMARYThe skin is a major target organ in human graft-versus-host disease (GVHD) after bone-marrow transplantation. GVHD can be induced in mice by i.v. injection of T cells into unirradiated semiallogeneic or lethally irradiated allogeneic recipients. However, in the murine systemic GVHD model, cutaneous lesions occur only in lethally irradiated recipients. Since lethal irradiation itself might induce the epidermal cell damage, several investigators have employed another murine model of cutaneous GVHD, in which cutaneous lesions were induced by intradermal injection of alloreactive T cell clones. Using this system, it has been reported that both MHC class I-and IIreactive T cell clones can induce cutaneous GVHD in non-irradiated or sublethally irradiated recipients. However, it has remained unknown whether or not freshly prepared T cells are able to induce cutaneous GVHD after local injection into non-irradiated recipients. We show that unprimed T cells can induce cutaneous GVHD after local injection into unirradiated MHC class II-or I + IIdisparate recipients. In contrast to alloreactive T cell clones, unprimed T cells could elicit only mild cutaneous lesions in MHC class I-disparate recipients. Since sublethal irradiation of MHC class Idisparate recipients did not result in the manifestation of cutaneous lesions after injection of unprimed T cells, host anti-donor responses by radiosensitive cells could not be responsible for this phenomenon. This experimental system provides a useful model for analysis of the regulation mechanisms in the induction of GVHD by unprimed T cells.

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Acute lethal graft-versus-host reaction induced by major histocompatibility complex class II-reactive T helper cell clones.

Cited by 32 publications

References 26 publications

Human mature T cells that are anergic in vivo prevail in SCID mice reconstituted with human peripheral blood.

Human mature T cells that are anergic in vivo prevail in SCID mice reconstituted with human peripheral blood.

Dissociated Production of Perforin, Granzyme B, and IFN-γ by HIV-Specific CD8⁺Cells in HIV Infection

Induction of cutaneousgraft-versus-hostdisease by local injection of unprimed T cells

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Acute lethal graft-versus-host reaction induced by major histocompatibility complex class II-reactive T helper cell clones.

Cited by 32 publications

References 26 publications

Human mature T cells that are anergic in vivo prevail in SCID mice reconstituted with human peripheral blood.

Human mature T cells that are anergic in vivo prevail in SCID mice reconstituted with human peripheral blood.

Dissociated Production of Perforin, Granzyme B, and IFN-γ by HIV-Specific CD8+Cells in HIV Infection

Induction of cutaneousgraft-versus-hostdisease by local injection of unprimed T cells

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Dissociated Production of Perforin, Granzyme B, and IFN-γ by HIV-Specific CD8⁺Cells in HIV Infection