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>Eosinophilia VI, spontaneous synthesis of chemokinetic, chemotactic, complement receptor‐inducing activities for eosinophils by bronchial T lymphocytes of asthmatic‐bronchitic patients
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Eosinophilia VI, spontaneous synthesis of chemokinetic, chemotactic, complement receptor‐inducing activities for eosinophils by bronchial T lymphocytes of asthmatic‐bronchitic patients
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机译：Eosinophilia VI, spontaneous synthesis of chemokinetic, chemotactic, complement receptor‐inducing activities for eosinophils by bronchial T lymphocytes of asthmatic‐bronchitic patients
SummaryT lymphocytes were separated from the bronchial mucus of five patients with extrinsic asthma and chronic mild bronchitis and who had numerous eosinophils in the bronchial mucus but no significant blood eosinophilia. The bronchial lymphocytes spontaneously, that is without treatment with antigens or mitogens, released into serum‐free synthetic medium one or more substances in the molecular weight range of 30 000 to 60 000 daltons. These substances when tested on eosinophils of normal persons stimulated random movement (chemokinesis), attracted them (chemotaxis), enhanced their chemotactic response to activated complement, and increased the expression of C4 and C3b receptors. Chemokinetic and chemotactic activity for neutropils was weak. No eosinophil‐stimulating activity was found in cultures of bronchial lymphocytes treated with puromycin to inhibit synthesis. The blood lymphocytes did not spontaneously synthesize the substance(s).It is not known if the several eosinophil‐stimulating activities are due to one or more substance(s), but the nature of the eosinophil responses, molecular weight and other features, indicate similarities with the ‘eosinophil stimulation promoter‐chemotactic’ factor reported to be released from mouse or human lymphocytes treated with antigen.Eosinophil stimulation resulting in increased expression of specific receptors, and potential for non‐specific adherence, by trapping or arresting randomly migrating cells, is believed to mediate accumulation of cells in an affected organ. Prolonged synthesis of such products, as from activated lymphocytes in the lung, could account for much of the local
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