Human gamma delta T-cell receptor-positive cell-mediated inhibition of
erythropoiesis in vitro in a patient with type I autoimmune polyglandular
syndrome and pure red blood cell aplasia [see comments]
T Hara, Y Mizuno, M Nagata, Y Okabe, S Taniguchi, M Harada, Y Niho, K Oshimi, S Ohga and Y Yoshikai
Department of Pediatrics, Faculty of Medicine, Kyushu University, Fukuoka,
Japan.
The gamma delta T-cell receptor-positive (gamma delta TCR+) lymphocytes
were markedly expanded up to 68% of peripheral blood lymphocytes in a case
with type I autoimmune polyglandular syndrome and pure red blood cell
aplasia (PRCA). The gamma delta TCR+ cells showed CD4 negative, 16% dim-CD8
positive and 10% to 46% human leukocyte antigen-D-related (HLA-DR)
positive, and exhibited no monoclonality as assessed by the patterns of TCR
gene rearrangements. Functional studies revealed that the proliferative
responses of the patient's peripheral blood mononuclear cells (PBMC) were
severely depressed to candida antigen, alloantigens, and autoantigens
(non-T cells). The gamma delta TCR+ cells had no suppressive effect on the
proliferative response of the alpha beta TCR+ cells to candida. The
patient's PBMC, isolated gamma delta TCR+ cells but not alpha beta TCR+
cells, exhibited non-major histocompatibility complex (MHC)-restricted
cytotoxicity. Furthermore, the patient's PBMC and isolated gamma delta TCR+
cells inhibited burst- forming units-erythroid (BFU-E), but not
colony-forming units/granulocyte-macrophage (CFU-GM). Supernatants derived
from the patient's T cells similarly inhibited BFU-E but not CFU-GM. The
clinical course of the patient also showed a close correlation between the
decreased number of total lymphocyte counts, especially HLA-DR + gamma
delta TCR+ cell counts, and recovery from PRCA. These observations suggest
that the gamma delta TCR+ cells might be functional in vivo and involved in
the pathogenesis of PRCA in this patient.
Volume 75,
Issue 4,
pp. 941-950,
02/15/1990
Copyright © 1990 by The American Society of Hematology
