T lymphocytes involved in inhibition of granulopoiesis in two neutropenic patients are of the cytotoxic/suppressor (T3+T8+) subset.

Bagby, Grover C.

doi:10.1172/jci110415

Cited by 52 publications

(20 citation statements)

References 17 publications

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“…In addition, normal Ty cells have been shown to suppress in vitro erythroid (6,36) and granulocyte (56) colony expression. These observations are strengthened by clinical examples, such as the one presented in this report, where anemia or neutropenia is correlated with in vitro inhibition of erythroid (7)(8)(9)(10) or myeloid (11,13) differentiation by such suppressor cells. These in vitro studies and clinical examples support the growing notion that a complex, genetically regulated network of T cells, some with a hybrid phenotype are involved in the regulation of hematopoietic differentiation.…”

Section: Discussionsupporting

confidence: 64%

“…Recent investigations have additionally suggested the existence of a second suppressive system exerted by T lymphocytes (5,6). The existence of such a system was initially suggested by clinical examples of anemia or granulocytopenia associated with an expansion of certain T lymphocyte populations (7)(8)(9)(10)(11)(12)(13). Furthermore, studies of normal cells have led to the suggestion that T lymphocyte-induced suppression of in vitro erythropoiesis may be genetically restricted (14).…”

Section: Introductionmentioning

confidence: 99%

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Evidence for genetic restriction in the suppression of erythropoiesis by a unique subset of T lymphocytes in man.

et al. 1983

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A B S T R A C T The suppression of erythropoiesis by lymphocytes from patients with a T cell lymphoproliferative syndrome and pure erythrocyte aplasia has been previously demonstrated. To study the nature of the suppressor cell and possible genetic restriction of this suppression, we investigated a patient with severe anemia, splenomegaly, lymphocytosis, and erythroid aplasia. A 3-mo course of low-dose daily oral cyclophosphamide achieved a complete remission for over 12 mo. The surface phenotype of his lymphocytes was analyzed by means of antibodies to lineage, differentiation, and activation-specific surface antigens. The cells expressed mature T cell antigens T3, T8, and Tll, while lacking Ti. Immature T cell, B cell, and the monocyte-specific antigen Mo2 were absent, while Mol, a monocyte-associated antigen not normally expressed on T cells, was present. T1O and Ia expressed as activation antigens were also present. The cells, cryopreserved at diagnosis, were thawed and co-cultured in plasma clot with patient remission marrow samples at T cell/bone marrow ratios of 1:1 and 2:1.There was nearly 90% suppression of erythroid colonyforming unit expression and 60% suppression of erythroid burst-forming unit expression at 2:1 T cell to bone marrow ratios and somewhat less suppression at 1:1. Granulocyte/macrophage progenitor expression was unaffected. Erythroid progenitor differentiation This work was presented in part at the 24th Annual Meeting of the American Society of Hematology, Washington, DC, 4-7 December 1982. Dr. Nadler was supported by a grant from the Medical Foundation of Boston.Received for publication 13 December 1982 and in revised form 20 April 1983. in the marrows of two HLA identical siblings was similarly suppressed. The cells were co-cultured with the marrows of nine nonrelated donors to investigate the potential genetic restriction of this suppression. Colony suppression equal to that observed in the marrow of the patient and his siblings was found in studies of two partially HLA identical individuals. No suppression was detected in marrow co-cultures of two entirely HLA dissimilar individuals. These results show that suppression of erythropoiesis by a unique subset of T8, Mol, Ia-positive lymphocytes isolated from a patient with lymphocytosis and erythrocyte aplasia is genetically restricted.

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Section: Discussionsupporting

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Evidence for genetic restriction in the suppression of erythropoiesis by a unique subset of T lymphocytes in man.

et al. 1983

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“…These patients may have had antibodies directed against sparsely distributed antigens, as has been found in the lack of complement fixation by anti-Rh IgG (35) or may possibly have had granulocyte-binding IgG of subclasses that do not react efficiently with Clq, such as IgG2 or IgG4 (36), both of which bind SPA (37). Alternatively, such patients may have pathophysiologically less important levels of antigranulocyte antibody and perhaps have suppressor T-cell mediated granulocytopenia (6).…”

Section: Discussionmentioning

confidence: 99%

“…Although cell-mediated immunity appears to be involved in some patients with autoimmune granulocytopenia (5,6), we and others have demonstrated that patients with Felty's syndrome (FS)' often have increased serum granulocyte-binding IgG (7)(8)(9)(10)(11). By analogy with immune hemolytic anemia and immune thrombocytopenia, one might expect some FS sera to bind complement to granulocytes.…”

Section: Introductionmentioning

confidence: 99%

Activation of human complement by immunoglobulin G antigranulocyte antibody.

Rustagi¹,

Currie²,

Logue³

1982

J. Clin. Invest.

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“…Re cently, evidence for an involvement of T lymphocytes in the pathogenesis of neutropenic syndromes of dif ferent etiology have been described [3][4][5]. Abnormali ties of T cell subsets have been reported in a few pa tients with cyclic neutropenia [6,7].…”

Section: Introductionmentioning

confidence: 99%