Increased expression of leukocyte function associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) by alveolar macrophages of patients with pulmonary sarcoidosis (Articolo in rivista)

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  • Increased expression of leukocyte function associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) by alveolar macrophages of patients with pulmonary sarcoidosis (Articolo in rivista) (literal)
Anno
  • 1991-01-01T00:00:00+01:00 (literal)
Alternative label
  • 1. Melis M, 1. Gjomarkaj M, 1. Pace E, 2. Malizia G, 2. Spatafora M (1991)
    Increased expression of leukocyte function associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) by alveolar macrophages of patients with pulmonary sarcoidosis
    in Chest (Amer. Coll. Chest Phys.); American College Of Chest Physicians, Northbrook (Stati Uniti d'America)
    (literal)
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  • 1. Melis M, 1. Gjomarkaj M, 1. Pace E, 2. Malizia G, 2. Spatafora M (literal)
Pagina inizio
  • 910 (literal)
Pagina fine
  • 916 (literal)
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  • 100 (literal)
Rivista
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  • 7 (literal)
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  • 4 (literal)
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  • PubMe (literal)
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  • 1. CNR, Ist. Fisiopatol. Respiratoria, Via Trabucco 180, 90146 Palermo, Italy 2. Ist. di Med. Generale e Pneumologia, Università degli Studi, Palermo, Italy (literal)
Titolo
  • Increased expression of leukocyte function associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) by alveolar macrophages of patients with pulmonary sarcoidosis (literal)
Abstract
  • Leukocyte function associated antigen-1 (LFA-1) and its ligand intercellular adhesion molecule-1 (ICAM-1) are cell adhesion molecules that play an important role in the capacity of mononuclear phagocytes (MPs) to present antigens to T lymphocytes. Since in pulmonary sarcoidosis (PS) this capacity is increased at sites of disease activity, we studied the expression of LFA-1 and ICAM-1 on peripheral blood monocytes (BMs) and alveolar macrophages (AM) obtained by bronchoalveolar lavage (BAL) from normal subjects (n=7) and patients with PS (n=14). To accomplish this, immunocytochemical stainings were made on cytocentrifuge preparations using anti-LFA-1 (anti-CD 11a) and anti-ICAM-1 (anti-CD 54) monoclonal antibodies (MoAbs). Normal and sarcoid BMs displayed a high percentage of positivity with both MoAbs with no difference between study groups (LFA-1: control BM 87.8±8.8 percent; sarcoid BM 84.7±9.5 percent; ICAM-1: control BM 80.8±10 percent; sarcoid BM 88.0±4.2 percent; p=NS for all comparisons). In both groups the percentage of cells expressing LFA-1 and ICAM-1 molecules among AMs was lower than among autologous BMs (LFA-1: control AM 46.5±13.2 percent, p<0.001 vs control BM; sarcoid AM 64.2±15.9; p<0.001 vs sarcoid BM) (ICAM-1: control AM 42.7±8.5 percent, p<0.001 vs control BM; sarcoid AM 72.1±10.6, p<0.001 vs sarcoid BM). AMs from patients with PS showed a higher degree of positivity for LFA-1 and ICAM-1 than normal AMs (p<0.02 and p<0.001, respectively). The positivity for LFA-1 and ICAM-1 molecules on sarcoid AMs was not correlated with the positivity for two different BM-associated markers (ie, the CD 11b and the CD 14 molecules) and was not correlated with the percentage of T lymphocytes in BAL, selected as a marker of the intensity of the alveolitis. These results suggest that the increased ability of sarcoid AMs to induce the proliferation of T lymphocytes may be related, at least in part, to the increased expression of LFA-1 and ICAM-1 molecules on their surfaces. (literal)
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