The molecular basis of T helper cell function—I. Allotype- and MHC-linked determinants on antigen-specific, H-2-restricted T cell lines, hybridomas and lymphomas

Rubin, Bent; Suzan, M; Maier, Tom; Lonai, Peter

doi:10.1016/0161-5890(84)90148-2

Cited by 4 publications

(2 citation statements)

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“…The antibody stains epitopes indicative of embryonic liver (alpha-fetoprotein [RAFP, Chemicon (Mujoo et al, 1983)]). Lastly, the cultures were also stained for rat-specific major histocompatibility complex-I [RMHC-I, Chemicon (Rubin et al, 1984;Prabhala and Wira, 1995)], which is characteristic of differentiated rat cells.…”

Section: ])mentioning

confidence: 99%

Clonogenic analysis reveals reserve stem cells in postnatal mammals: I. Pluripotent mesenchymal stem cells

et al. 2001

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Clonal populations of lineage-uncommitted pluripotent mesenchymal stem cells have been identified in prenatal avians and rodents. These cells reside in the connective tissue matrices of many organs and tissues. They demonstrate extended capabilities for selfrenewal and the ability to differentiate into multiple separate tissues within the mesodermal germ line. This study was designed to determine whether such cells are present in the connective tissues of postnatal mammals. This report describes a cell clone derived by isolation from postnatal rat connective tissues, cryopreservation, extended propagation, and serial dilution clonogenic analysis. In the undifferentiated state, this clone demonstrates a high nuclear-to-cytoplasmic ratio and extended capacity for self-renewal. Subsequent morphological, histochemical, and immunochemical analysis after the induction of differentiation revealed phenotypic markers characteristic of multiple cell types of mesodermal origin, such as skeletal muscle, smooth muscle, fat cells, cartilage, and bone. These results indicate that this clone consists of pluripotent mesenchymal stem cells. This report demonstrates that clonal populations of reserve stem cells are present in mammals after birth. Potential roles for such cells in the maintenance, repair, and regeneration of mesodermal tissues are discussed.

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Section: ])mentioning

confidence: 99%

Clonogenic analysis reveals reserve stem cells in postnatal mammals: I. Pluripotent mesenchymal stem cells

et al. 2001

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“…The LPF was produced by an FCS-specific, /-y4''-restricted T-cell line and clones derived from it (Table III), All isolated clones were FCS-specific and 7-/1''-restricted (Table I), but they varied in their cross-reactivity towards CBA spleen cells and their production of T-LPF and B-LPF (Tables I and III), A very interesting finding was that line 12 cell growth stimulated by I-A'' gene-bearing stimulator cells was completely inhibited by anti-I-A'' MAb (Ox3) but not by anti-I-A'' MAb (Ox6); in contrast, line 12 cell growth stimulated by CBA spleen cells was inhibited by anti-I-A" MAb (0x6) but not by anti-Z-yl'' MAb (0x3) (Table II), These data suggest that anti-I-A'' MAb block I-A'' gene products on the stimulator cells rather than intrinsic line 12 T-cell I-A'' (biosyntheticallylabelled line 12 T-cell la molecules react with Ox3 and not with 0x6: [37] and that I-A'' gene products are involved in the cross-reactive CBA membrane antigens. At present, we do not know what else is necessary for the creation of the CBA spleen cell antigenie determinant(s) that cross-react with the FCS/I-A'' complex seen by certain line 12 T-cell clones.…”

Section: Discussionmentioning

confidence: 82%

On the Molecular Basis of T Helper Cell Function

et al. 1984

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The differentiation of Ig+ B cells into plaque-forming cells is dependent on antigen and factors produced by T cells and/or macrophages. We describe here the production of T-cell factors termed lymphocyte promotor factors (LPF). A foetal calf serum-specific T-cell line and its clones synthesize LPF, which is defined as factors that polyclonally stimulate normal spenic T cells to differentiate into cytotoxic T lymphocytes (T-LPF) and normal splenic B cells to differentiate into plaque-forming cells into (PFC) (B-LPF) in the apparent absence of specific antigen. The proliferation of and the B-LPF production of all T-cell clones tested were foetal calf serum-specific and I-Ab-restricted. Some of these clones produced only T-LPF, some clones produced only B-LPF, and some clones produced both T-LPF and B-LPF. B-LPF stimulate the polyclonal differentiation of Ig+ B cells into PFC without the apparent need for helper T cells, is different from T-LPF, and induces almost exclusively IgM PFC. The B-LPF described in the present paper are compared with previously described T-cell factors, which stimulate antigen-specific B-cell responses or bystander B-cell responses. The conclusion is that B-LPF are probably different from B-cell growth factors, T-cell replacing factors, allogeneic effector factors, and interleukin 2.

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