Tissue expression

TfR-specific mAbs react with many cell types. Although it was originally thought that the TfR was a marker for proliferating cells because most express it, some resting cells can also express the TfR. Indeed, its expression is rather related to the intracellular iron levels, and it is because iron is essential for the activity of ribonucleotide reductase, which is required for DNA synthesis, that the TfR plays an important regulatory role in cell proliferation.

The TfR is broadly expressed in cells of hematopoietic origin (Table 1). In lymphoid tissues, it is present on germinal center cells and macrophages. Resting peripheral blood lymphocytes and monocytes do not express it, but its expression is induced upon activation.

During ontogeny, the TfR is expressed in the populations of cell precursors which are more actively proliferating and is downregulated as cells differentiate to a resting state. Thus, during T cell maturation, the TfR is only expressed in large-sized immature CD4"CD8-CD3-, CD4"CD8+CD3- and CD4+CD8+CD3" thymocytes of fetal as well as of

Table 1 TfR cell surface expression on nontransformed cells newborn and adult mice, and is subsequently gradually downregulated in the CD4+CD8+CD3" population. Similarly, the TfR is also downregulated during granulocyte maturation.

Because the TfR is expressed by proliferating cells, it is not, therefore, surprising that it is broadly expressed on carcinomas and sarcomas of different origin as well as on hematopoietic cell tumors. Nevertheless, TfR expression does not seem to correlate with malignant phenotype because it is found, for instance, in low- as well as in high-grade lymphomas, although they may express qualitatively different TfR proteins. Thus, the epitope recognized by mAb Trump is expressed in high-grade but not in low-grade lymphomas.

TfR expression in rapidly proliferating cells makes it a possible target for antitumor therapy. For instance, it has been shown that treatment of bone marrow cells with an anti-TfR/toxin complex kills committed progenitors to CFU-GM and BFU-F1 bur spares immature noncycling, TfR-negative progenitors. Such treatment has been proposed as a purging method for bone marrow autotransplants in leukemic patients.

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