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DOI 10.1164/ajrccm/141.4_pt_1.

Медицинская библиотека · The American review of respiratory disease · 1990

CD4 T-lymphocyte activation in acute severe asthma. Relationship to disease severity and atopic status.

Corrigan C J, Kay A B

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

Lymphocytes are prominent among the inflammatory cells infiltrating the asthmatic airways, and several studies have suggested that cell-mediated immunity may play a role in the pathogenesis of chronic asthma. We have measured (1) the expression of activation markers on the CD4+ and CD8+ T-lymphocyte phenotypic subsets in the peripheral blood of patients hospitalized with acute severe asthma ("status asthmaticus"), and (2) the serum concentrations of two proteins elaborated by activated T-lymphocytes (interferon-gamma and the soluble interleukin-2 receptor). The results were compared with those in control subjects (mild asthma, chronic obstructive airway disease, and normal). CD4+ lymphocytes from patients with acute severe asthma showed significant increases in the expression of three surface proteins associated with lymphocyte activation (interleukin-2 receptor [IL-2R], class II histocompatibility antigen [HLA-DR], and "very late activation" antigen [VLA-1]) as compared with those from normal control subjects. In contrast, CD8 cells were devoid of IL-2R and VLA-1, in both patients with acute severe asthma and control subjects, and the expression of HLA-DR on these cells was not increased above that of control subjects. The serum concentrations of interferon-gamma and soluble IL-2R were significantly elevated in patients with acute severe asthma as compared with all the control groups. Concentrations decreased as the patients improved clinically during the first 3-day period of hospital treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Для цитирования: Corrigan C J, Kay A B. CD4 T-lymphocyte activation in acute severe asthma. Relationship to disease severity and atopic status.. The American review of respiratory disease. 1990. DOI: 10.1164/ajrccm/141.4_pt_1..

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