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Clinical relevance of balance between type 1 and type 2 immune responses of lymphocyte subpopulations in aplastic anaemia patients
Author(s) -
Giannakoulas Nikolaos C.,
Karakantza Marina,
Theodorou Georgios L.,
Pagoni Maria,
Galanopoulos Athanasios,
Kakagianni Theodora,
KouraklisSymeonidis Alexandra,
Matsouka Panagiota,
Maniatis Alice,
Zoumbos Nicholas C.
Publication year - 2004
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.2003.04729.x
Subject(s) - cd8 , immunology , immune system , cytotoxic t cell , haematopoiesis , pathogenesis , interferon , biology , medicine , stem cell , in vitro , microbiology and biotechnology , biochemistry
Summary Immune dysfunction, which leads to the suppression of haemopoiesis by cytokines that are secreted by activated T lymphocytes, is considered to play a key role in the pathogenesis of acquired aplastic anaemia (AAA). We investigated the intracytoplasmic expression of type‐1 [interferon γ (IFN‐ γ ), interleukin (IL)‐2] and type‐2 (IL‐4, IL‐10) cytokines in CD4+ and CD8+ T cells before and after in vitro activation in 16 patients with AAA and 17 normal controls. Untreated or refractory patients had a significantly higher proportion of unstimulated CD4+ and CD8+ T cells that produced IFN‐ γ and IL‐2 whereas the IL‐4 and IL‐10 producing T cells did not differ from that of controls, resulting in a shift of IFN‐ γ /IL‐4 ratio towards a type‐1 response. Patients in remission had also increased proportion of IFN‐ γ ‐producing unstimulated CD4+ and CD8+ cells, with a parallel rise of IL‐4‐ and IL‐10‐producing cells and normal IFN‐ γ /IL‐4 ratio. These data indicate that, in newly diagnosed and refractory patients with AAA, CD4+ cells are polarized towards a type‐1 response that in turn leads to activation of cytotoxic CD8+ cells and finally to haemopoietic stem cell destruction. The type‐1 response persists in patients in remission although this effect is compensated by the increase of IL‐4 and IL‐10 production.