A thymocyte proliferative response assay was used to compare spontaneous and lipopolysaccharide (LPS)-induced interleukin-1 (IL-1) release by alveolar macrophage (AM) in asthmatic patients and normal subjects. Twelve asthmatic patients and seven nonsmoking healthy subjects underwent a bronchoalveolar lavage (BAL). All asthmatic patients had a reversible airway obstruction and 7/12 were allergic. BAL AM were separated by adherence on tissue culture plates in medium RPMI-1640 supplemented with antibiotics and fetal calf serum, and were incubated with or without 10 μg/ml LPS for 20 h. Free-cell supernatants were tested by C3H/HeJ mice thymocyte proliferative assay. Unstimulated AM supernatant IL-1 activity was significantly higher in asthmatic patients (mean ± SEM: 47.8 ± 11.9 units/106 AM) in comparison with healthy subjects (4.8 ± 2.3 units/106 AM; p < 0.05, Mann-Whitney U test) but did not significantly differ between allergic (42.2 ± 15.5 units/106 AM) and intrinsic asthmatic patients (55.8 ± 20.7 units/106 AM). For healthy subjects, IL-1 activity was significantly higher in LPS-stimulated AM supernatants (85 ± 20 units/106 AM, p < 0.05; Mann-Whitney U test) in comparison with unstimulated ones; for asthmatic patients, unstimulated and LPS-stimulated AM supernatant IL-1 activity did not significantly differ. This finding is in accordance with previous work suggesting that AM from asthmatic patients have a weak suppressive activity upon lymphocyte proliferation and emphasize the enhanced AM releasability in asthma.
Placenta‐eluted gamma globulins (PEGG) have been recently and successfully used in the treatment of patients with rheumatoid arthritis. PEGG, eluted at acid pH from large pools of human placentas, contained 99% IgG material. Sephacryl S300 gel filtration revealed a main fraction (76%) of native IgG accompanied by 10% aggregates and 14% digested fragments (as identified by sodium dodecyl sulfate—polyacrylamide gel electrophoresis and immunoelectrophoresis with specific antisera). Previous in vitro data had suggested that alloantibodies to class II HLA antigens were present in this preparation. This study confirms that PEGG and F(ab')2 fragments were able to inhibit stimulating cells in mixed lymphocyte reactions. Additional findings showed that: (a) IgG from PEGG were cytotoxic for the non—T cell population; (b) IgG or F(ab')2 from PEGG bound only to class II HLA—bearing cells; (c) F(ab')2 from PEGG were able to block the complement‐mediated cytotoxicity of anti—HLA—DR and anti‐DQw1 alloantibodies. These data confirm the presence of class II HLA alloantibodies in PEGG. These antibodies may account for the clinical improvement reported in patients with rheumatoid arthritis. Our findings are similar to recent data showing that the injection of anti‐Ia antibodies in experimental animal models decreases the autoimmune process.
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