TY - JOUR
T1 - Lymphocyte phenotype and lymphokines following anti‐thymocyte globulin therapy in patients with aplastic anaemia
AU - Platanias, Leonidas
AU - Gascon, Pedro
AU - Bielory, Leonard
AU - Griffith, Patricia
AU - Nienhuis, Arthur
AU - Young, Neal
PY - 1987/8
Y1 - 1987/8
N2 - Twenty‐two patients with adult onset aplastic anaemia were analysed before and after therapy with antithymocyte globulin (ATG). Lymphocyte phenotype, lymphokine levels or production, and haematopoietic progenitor cell number were measured 3 months after therapy: clinical response was determined 1 year post‐therapy. By flow cytometry there was a significant reduction in both the proportion and absolute number of peripheral blood lymphocytes expressing activation antigen Tac (IL‐2 receptor) and in the proportion of HLA‐DR+ lymphocytes. For T cells bearing HLA‐DR, there were proportional decreases in both activated helper and suppressor cells. There was no statistically significant difference pre‐ATG to post‐ATG in the absolute numbers of total, helper and suppressor lymphocytes. In all 10 haematologic responders the number of Tac bearing lymphocytes after ATG therapy was in the normal range, but half of 12 non‐responding patients continued to have abnormally elevated numbers of Tac+ T cells. The proportion of Tac+ cells were not related to transfusion history. γ‐interferon levels in serum by radioimmunoassay were elevated in almost half the aplastic patients; post‐ATG. γ‐interferon was detectable in only three patients. Haematologic response to ATG therapy was associated with increased numbers of haematopoietic progenitors post‐treatment, but pre‐treatment values were not predictive of a response. These results are consistent with a pathogenic role for activated T‐cells and their lymphokine products and suggest that the target of ATG therapy may be a Tac+ lymphocyte.
AB - Twenty‐two patients with adult onset aplastic anaemia were analysed before and after therapy with antithymocyte globulin (ATG). Lymphocyte phenotype, lymphokine levels or production, and haematopoietic progenitor cell number were measured 3 months after therapy: clinical response was determined 1 year post‐therapy. By flow cytometry there was a significant reduction in both the proportion and absolute number of peripheral blood lymphocytes expressing activation antigen Tac (IL‐2 receptor) and in the proportion of HLA‐DR+ lymphocytes. For T cells bearing HLA‐DR, there were proportional decreases in both activated helper and suppressor cells. There was no statistically significant difference pre‐ATG to post‐ATG in the absolute numbers of total, helper and suppressor lymphocytes. In all 10 haematologic responders the number of Tac bearing lymphocytes after ATG therapy was in the normal range, but half of 12 non‐responding patients continued to have abnormally elevated numbers of Tac+ T cells. The proportion of Tac+ cells were not related to transfusion history. γ‐interferon levels in serum by radioimmunoassay were elevated in almost half the aplastic patients; post‐ATG. γ‐interferon was detectable in only three patients. Haematologic response to ATG therapy was associated with increased numbers of haematopoietic progenitors post‐treatment, but pre‐treatment values were not predictive of a response. These results are consistent with a pathogenic role for activated T‐cells and their lymphokine products and suggest that the target of ATG therapy may be a Tac+ lymphocyte.
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U2 - 10.1111/j.1365-2141.1987.tb01324.x
DO - 10.1111/j.1365-2141.1987.tb01324.x
M3 - Article
C2 - 3117088
AN - SCOPUS:0023264940
SN - 0007-1048
VL - 66
SP - 437
EP - 443
JO - British Journal of Haematology
JF - British Journal of Haematology
IS - 4
ER -