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Use of an autologous reaction in vitro to assess contributions of T and B lymphocytes to immune hyperreactivity of atopics
Author(s) -
DUKECOHAN J. S.,
HIRT RALY,
ROTTEM M.,
BENZVI A.,
RUBINOW A.,
NAOR D.
Publication year - 1989
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.1989.tb02359.x
Subject(s) - pokeweed mitogen , stimulation , immunology , medicine , in vitro , priming (agriculture) , immune system , mixed lymphocyte reaction , lymphoblast , peripheral blood mononuclear cell , t cell , chemistry , biology , cell culture , biochemistry , botany , germination , genetics
Summary The in‐vitro proliferative reaction of peripheral blood lymphocytes (measured by [ 3 H]thymidine incorporation) to autologous pokeweed mitogen (PWM)‐induced lymphoblasts (PWM‐lymphoblast‐stimulated autologous mixed leucocyte reaction, PWM.AMLR) was used as a measure of immune hyperreactivity for comparison of atopic with non‐atopic individuals. Accordingly, 10/24 non‐atopics responded in the PWM.AMLR, and 19/19 atopics reacting to inhaled allergens responded. Autologous stimulation was associated with release of mitogenic factors from the PWM‐activated stimulating cells (2/15 non‐atopics, 9/15 atopics). For non‐atopics, stimulation delivered by staphylococcus A (SAC)‐activated cells was similar to that delivered by PWM‐induced cells, while in atopics, the SAC.AMLR was never more than 50% of the PWM.AMLR, indicating a possible T cell component. Separation by panning of the stimulation cells into lymphocyte subsets supported the notion that stimulation involved a cooperation between B and T4 + T cells. It is proposed that a positive PWM.AMLR is dependent upon an initial B cell activation followed by the PWM stimulus dependent upon a previous T cell activation, where atopics have more lymphocytes in an activated state than healthy non‐atopics. Such a baseline priming may contribute to an innate sensitivity of atopics to environmental allergens.