RsaI polymorphism of the human CD27 gene, a member of nerve growth factor receptor gene family.
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Biomedical subjects
Publications and source records attributed to I Rojo.
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CD27 mAb recognize a disulfide-linked homodimer of 55 kDa present in the majority of T cells and in a minor subpopulation of thymocytes. Although an increase of CD27 expression has been described in activated T cells, this Ag is poorly expressed in long term growing T cells. It has been also reported that CD27- becomes CD27+ upon activation. In the aim to better know the relationship between CD27 expression and the activation and maturation processes, the induction of this Ag in thymocytes was analyzed. The results obtained in this work show that: 1) CD27 is expressed only in thymocytes with high CD3 Ag density. 2) Its expression can be induced in low density CD3 CD4+ CD8+ cells by Con A and in low CD3 Ag density by PMA+ionomycin. 3) PMA alone or in combination with rIL-2 induces CD25 and CD71 expression but not CD27. 4) Unlike CD27, the Ag CD45RA, CD26, and CD76, which are present only in a minor thymocyte subpopulation, are not induced in double positive thymocytes. Because it has been reported that cyclosporin A interferes with thymocytes maturation and blocks the transition from double to single positive cells, its effect was measured on CD27 induction. Cyclosporin A did not inhibit CD25 expression induced by both Con A and PMA+ionomycin, but under these conditions it inhibited the induction of CD27. In this paper we discuss whether CD27 could be implicated in T cell maturation.
We have generated seven monoclonal antibodies (mAb) that recognize the T200 molecule. These mAb have been classified by competitive binding assay in flow cytometry into three groups each reacting with a different epitope of the T200 molecule: (a) 136-4B5, that shows a sialic acid nature, (b) 135-4H9, 135-4C5, 144-2, 155-2 and (c) 72-5D3, 124-2H12b. A heterogeneous effect was observed when they were tested on an anti-immunoglobulin-induced B cell proliferation. Whereas 72-5D3 and 135-4H9 mAb inhibited the proliferative response of B cells, 136-4B5 mAb greatly enhanced it, both effects being dose dependent. We can conclude that anti-CD45 mAb have a different and contrary functional behavior on anti-Ig-induced B cell proliferation, depending on the epitope recognized. The basis for such a difference could reside in the glucidic nature of the epitope recognized by the 136-4B5 mAb.
The induction of T cell mitogenesis through CD3 is a complex process that requires at least two signals. The first one can be provided by Sepharose-bound CD3. The second one is normally provided by monocytes. The signal provided by Sepharose-bound CD3 is unable by itself to induce mitogenesis in monocyte highly depleted cells (MHDC). We describe here that the monoclonal antibody (mAb) 72-5D3 belonging to CD45 (T200), which was not mitogenic by itself, could replace monocytes when MHDC were activated by Sepharose-bound CD3. That is to say, in the absence of monocytes, mAb 72-5D3 gave a second signal necessary for T cell proliferation. Using eleven anti-CD45 mAb from other investigators we show that this effect is not a peculiar characteristic of 72-5D3 mAb. The effect of the mAb 72-5D3 was only effective in CD4-positive cells and was not observed when MHDC were activated with either soluble CD3 or concanavalin A. As both phorbol myristate acetate and mAb 72-5D3 can replace monocytes, a comparative study of their effects was undertaken. Phorbol myristate acetate but not mAb 72-5D3 induced proliferation of MHDC when recombinant interleukin 2 (rIL2) was added. On the other hand mAb 72-5D3 induced IL2 production in MHDC activated by Sepharose-bound CD3 and increased the IL2 production in Sepharose-bound CD3-activated peripheral blood mononuclear cells. In conclusion, data presented in this report indicate that the T200 molecule could be involved in T cell proliferation by giving a signal that induces the production of IL2 and bypasses the necessity of monocytes.