Nonspecific suppressor T cells cause decreased mixed lymphocyte culture reactivity in bone marrow transplant patients.

Harada, Masatake; Ueda, Mikio; Nakao, Shinsuke; Kondo, Kenta; Odaka, K; Shiobara, Shintaro; Matsue, Keiko; Mori, Takesada; Matsuda, Tamotsu

doi:10.4049/jimmunol.137.2.428

Cited by 15 publications

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Defective interleukin 2 receptor expression is associated with the T cell disfunction subsequent to bone marrow transplantation

et al. 1987

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In the present work we have used monoclonal antibodies (mAb) as probes to attempt a dissection of the mechanisms underlying the immunodeficiency subsequent to bone marrow transplantation (BMT). To this end we have studied 19 allogeneic BMT recipients, analyzing the proliferative response of peripheral blood mononuclear cells (PBMC) after activation with either phytohemagglutinin (PHA), anti-CD3 or anti-CD2 mAb. All patients presented normal proportions of CD2+ and CD3+ lymphocytes, as assessed by flow cytometry. Our results indicated that in most cases both CD2 and CD3-mediated activation pathways were inefficient to trigger normal T cell proliferation. The addition of exogenous interleukin 2 (IL2) did not restore in most cases the proliferative response, pointing out that additional defects contribute to the hyporesponsiveness. This was more evident in the group of patients studied during the first 6 months. To further dissect the T cell defect we analyzed the effect of a phorbol ester (phorbol myristate acetate, PMA), which activates protein kinase C, on the anti-CD3-induced response. Our data showed that PMA synergized with anti-CD3 similarly to exogenous IL2, and restored the proliferative response only in certain cases. The expression of IL2 receptors (CD25) as assessed by cytofluorimetry, after either PHA or anti-CD3 and PMA stimulation, was shown to be depressed, and the addition of IL2 did not restore it. Finally, we observed that the early increase of intracytoplasmic Ca2+ after anti-CD3 stimulation was comparable to that detected in normal PBMC. Altogether these results indicate that a diminished CD25 expression is associated with the T cell defect, and cannot apparently be attributed to an inability of the CD3 molecule to transduce early activation signals thus suggesting that either protein kinase C itself or an as yet undefined metabolic step preceding IL2 receptor expression is abnormal in variable proportions of T cells after BMT, and constitutes another manifestation of this complex immunodeficiency.

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Defective interleukin 2 receptor expression is associated with the T cell disfunction subsequent to bone marrow transplantation

et al. 1987

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Recapitulation of immune ontogeny: A vital component for the success of bone marrow transplantation

Lum¹

1990

Cancer Treatment and Research

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Relation of suppressor activity to lymphocyte subsets, in vitro IL-2R expression, and biopsy results in cardiac transplant patients

Völker¹,

Geörger

Leusch

et al. 1992

Transplant International Official Journal of the European Society for Organ Transplantation

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Nonspecific suppressor T cells cause decreased mixed lymphocyte culture reactivity in bone marrow transplant patients.

Cited by 15 publications

References 0 publications

Defective interleukin 2 receptor expression is associated with the T cell disfunction subsequent to bone marrow transplantation

Defective interleukin 2 receptor expression is associated with the T cell disfunction subsequent to bone marrow transplantation

Recapitulation of immune ontogeny: A vital component for the success of bone marrow transplantation

Relation of suppressor activity to lymphocyte subsets, in vitro IL-2R expression, and biopsy results in cardiac transplant patients

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