Transferrin binding by mitogen-activated human peripheral blood lymphocytes

Galbraith, G.M.P.; Goust, Jean‐Michel; Mercurio, S.; Galbraith, Robert M.

doi:10.1016/0090-1229(80)90180-4

Cited by 42 publications

(22 citation statements)

References 14 publications

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“…TfR functions in iron transport, cellular growth, and T cell activation [3,4]. Therefore, TfR may be a novel therapeutic target for transplantation.…”

Section: Discussionmentioning

confidence: 99%

“…A dose-response study demonstrated that the immunosuppressive effect of anti-TfR mAb was due to alterations in immune function rather than toxicity of the mAb. TfR functions in T cell activation as well as in iron transport [1][2][3][4]. Nakamura et al demonstrated that iron availability had a strong effect on CD8 ϩ cytotoxicity [29].…”

Section: Discussionmentioning

confidence: 99%

“…Red blood cells were removed from the responder (CBA) and stimulator (C57BL/6J) cell populations by Tris-NH 4 Cl lysis. The CTL culture and assays were performed as previously described [26].…”

Section: Alloantigen-specific Ctlsmentioning

confidence: 99%

“…Red blood cells were removed by Tris-NH 4 Cl lysis. Responder CBA/J (7 ϫ 10 6 cells) were co-cultured with 6 ϫ 10 6 ␥-irradiated (1500 rads) C57BL/6 stimulators.…”

Section: Mixed Lymphocyte Reactionmentioning

confidence: 99%

“…TfR binds the major serum iron transporter protein, transferrin, and controls iron uptake by receptormediated endocytosis [1][2][3]. TfR is not only an iron transporter but is also involved in T cell activation [3,4]. However, the roles and mechanisms of TfR in T cell activation remain ill-defined.…”

Section: Introductionmentioning

confidence: 99%

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Transferrin receptor in T cell activation and transplantation

Bayer

Baliga

Woodward

1998

Journal of Leukocyte Biology

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Transferrin receptor (TfR) expression is up-regulated during T cell activation after the interaction of the T cell receptor with the antigenmajor histocompatibility complex and the expression of interleukin-2 (IL-2) receptor. We hypothesize that anti-TfR monoclonal antibody (mAb) will prolong allograft survival by altering T cell responses. In a murine heterotopic nonvascularized cardiac allograft model, CBA/J (H-2 k ) recipients were transplanted with neonatal C57BL/6 (H-2 b ) donor hearts. Anti-TfR or isotype-matched control mAbs (100 g) were administered at the time of transplantation and on the following day. Splenocytes from naive CBA/J mice were stimulated in vitro with C57BL/6 alloantigen. Anti-TfR mAb was administered at 5 g/mL during the initiation of culture. Cytotoxic T lymphocyte (CTL) and mixed lymphocyte responses (MLR) were performed to assess T cell function. After 24 h in culture, cells were harvested, RNA isolated, and semi-quantitative reverse transcriptase-polymerase chain reaction performed. Anti-TfR mAb prolonged allograft survival to 25.7 ؎ 0.9 days compared to the isotype control (10.7 ؎ 0.4 days, P F 0.01, Wilcoxon rank sum). Anti-TfR mAb completely abrogated the CTL response and suppressed the MLR by 70-86% compared to the isotype controls. Anti-TfR mAb suppressed IL-2, interferon-␥ (IFN-␥), IL-10, and IL-12 p40 mRNA expression, but had no effect on IL-4, IL-12 p35, and IL-15 mRNA expression. In conclusion, anti-TfR mAb prolongs allograft survival, suppresses T cell function, and alters IL-2, IL-10, IL-12 p40, and IFN-␥ mRNA expression. These data suggest that the downregulation in IL-12 mRNA by anti-TfR mAb may prevent the development of T helper cells, thereby promoting graft survival and altering cell-mediated immune responses. The partial effect by anti-TfR mAb on cytokine mRNA expression may be due to other contributing factors such as costimulation.

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“…TfR functions in iron transport, cellular growth, and T cell activation [3,4]. Therefore, TfR may be a novel therapeutic target for transplantation.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Alloantigen-specific Ctlsmentioning

confidence: 99%

“…Red blood cells were removed by Tris-NH 4 Cl lysis. Responder CBA/J (7 ϫ 10 6 cells) were co-cultured with 6 ϫ 10 6 ␥-irradiated (1500 rads) C57BL/6 stimulators.…”

Section: Mixed Lymphocyte Reactionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Transferrin receptor in T cell activation and transplantation

Bayer

Baliga

Woodward

1998

Journal of Leukocyte Biology

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Effects of anti‐transferrin receptor antibodies on growth of normal and malignant myeloid cells

Taetle

Honeysett

Trowbridge

1983

Intl Journal of Cancer

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The effects of three monoclonal antibodies (B3/25, 43/31, and 42/6) reactive with human transferrin (Tf) receptors on growth of normal and malignant myeloid cells were examined using in vitro culture techniques. When added directly to cultures, all three antibodies caused dose-dependent inhibition of normal granulocyte/macrophage progenitor (CFU-GM) growth. Monoclonal antibody 42/6 was by far the most potent of the three, with an ID50 of less than 5 micrograms/ml. Identical effects were seen on CFU-GM from three patients with chronic myelogenous leukemia. Growth of colonies from two myeloid leukemia cells lines (KG-I, HL60) was also inhibited by all three antibodies, and these cells were generally more sensitive than normal CFU-GM. Blast colony-forming cells from three patients with acute non-lymphocytic leukemia were relatively resistant to the antibodies, and CFU-GM from a patient with myeloid metaplasia were resistant (ID50 greater than 50 micrograms/ml) to 42/6. In liquid culture, growth of the leukemic cell lines was inhibited by saturating concentrations of the three antibodies, although in both liquid and colony culture recovery was seen even after exposure to antibody for periods of up to 72 h. Analysis of the cell-cycle status of these cells showed that the antibodies did not cause accumulation of cells in any particular phase of the cell cycle. Addition to cultures of large quantities of human Tf failed to reverse the inhibitory effects of the antibodies. Competitive binding studies on the leukemia cell lines showed that only 42/6 inhibited binding of Tf to its receptor, although all three antibodies inhibited cell growth. Addition of Fe chelate (as ferric nitriloacetic acid, FeNTA) failed to reverse the inhibitory effects of the antibodies on CFU-GM and HL60 cells, but had variable effects on KG-I cell growth. FeNTA fully reversed inhibitory effects of 42/6 on KG-I cells. We conclude that monoclonal antibodies to Tf receptors can inhibit growth of both normal and malignant myeloid cells. Overall, no selectivity for malignant vs normal cells is apparent, although malignant cells from one individual were more sensitive to colony inhibition by 43/31 monoclonal antibody than normal CFU-GM.

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Transferrins

Brock¹

1985

Metalloproteins

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Transferrin binding by mitogen-activated human peripheral blood lymphocytes

Cited by 42 publications

References 14 publications

Transferrin receptor in T cell activation and transplantation

Transferrin receptor in T cell activation and transplantation

Effects of anti‐transferrin receptor antibodies on growth of normal and malignant myeloid cells

Transferrins

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