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Lymphokine Production in Ty Lymphoproliferative Disorders
Author(s) -
RAMBALDI A.,
ROSSI V.,
ALLAVENA P.,
INTRONA M.,
LANDOLFO S.,
BASSAN R.,
BARBUI T.,
MANTOVANI A.
Publication year - 1986
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1986.tb01956.x
Subject(s) - phytohaemagglutinin , lymphokine , autocrine signalling , lymphocytosis , immunology , stimulation , biology , lymphoproliferative response , interleukin 2 , monoclonal antibody , lymphocyte , antibody , interferon , cytokine , receptor , endocrinology , immune system , in vitro , biochemistry , peripheral blood mononuclear cell
We have studied five patients with chronic lymphoeytosis consisting of large granular lymphocytes (LGL). The increased numbers of LGL in these patients had little or no natural killer activity, mediated antibody‐dependent cellular cytotoxicity, and were induced to kill tumour lines after culture for 3 days with interleukin 2 (IL‐2). Patients' LGL showed considerable reactivity with HNK‐1 and AB8.28 monoclonal antibodies (MoAb), whereas positivity for OKM1 and N901 was found m only two subjects, and only one patient reacted with B73.1. No appreciable reactivity has been found with anti‐Tac MoAb in the four patients tested. In the absence of stimulation, the patients’ LGL produced no IL‐2 and only minimal amounts of IL‐1 and interferon (IFN). On stimulation with lipopolysaccharides (for IL‐1) or phytohaemag‐glutinin A (PHA) (for IL‐2 and IFN), they produced IL‐1 and IFN in amounts similar to those produced by normal lymphocytes, but only modest levels of IL‐2. These results indicated that proliferating LGL, like normal LGL, have a secretory capacity. The lack of constitutive lymphokine production, the lack of Tac receptor expression, and the defect in IL‐2 production after PHA stimulation do not support the hypothesis of an autocrine proliferation sustained by a known growth factor.