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PMID: 1346398 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Generation of signals activating neutrophil functions by leukocyte integrins: LFA-1 and gp150/95, but not CR3, are able to stimulate the respiratory burst of human neutrophils.

The Journal of cell biology ·Vol. 116 ·No. 4 ·1992-02-00 ·Pages 1007-17

Berton G, Laudanna C, Sorio C, Rossi F

Abstract

To address the question whether leukocyte integrins are able to generate signals activating neutrophil functions, we investigated the capability of mAbs against the common beta chain (CD18), or the distinct alpha chains of CR3, LFA-1, or gp150/95, to activate neutrophil respiratory burst. These investigations were performed with mAbs bound to protein A immobilized to tissue culture polystyrene. Neutrophils plated in wells coated with the anti-CD18 mAbs IB4 and 60.3 released H2O2; H2O2 release did not occur when neutrophils were plated in wells coated with an irrelevant, isotype-matched mAb (OKDR), or with mAbs against other molecules (CD16, beta 2-microglobulin) expressed on the neutrophil surface at the same density of CD18. Four different mAbs, OKM1, OKM9, OKM10, 60.1, which recognize distinct epitopes of CR3 were unable to trigger H2O2 or O2- release from neutrophils. However, mAbs against LFA-1 or gp150/95 triggered both H2O2 and O2- release from neutrophils. Stimulation of neutrophils respiratory burst by both anti-CD18, and anti-LFA-1 or gp150/95 mAbs was totally inhibited by the microfilaments disrupting agent, cytochalasin B, and by a permeable cAMP analogue. While the capability to activate neutrophil respiratory burst was restricted to anti-LFA-1 and gp150/95 mAbs, we observed that mAbs against all members of leukocyte integrins, including CR3, were able to trigger neutrophil spreading. These findings indicate that, in neutrophils, all three leukocyte integrins can generate signals activating spreading, but only LFA-1 and gp150/95 can generate signals involved in activation of the respiratory burst. This observation can be relevant to understand the mechanisms responsible for the activation of neutrophil respiratory burst by tumor necrosis factor-alpha, which has been shown to be strictly dependent on expression of leukocyte integrins (Nathan, C., S. Srimal, C. Farber, E. Sanchez, L. Kabbash, A. Asch, J. Gailit, and S. Wright. 1989. J. Cell Biol. 109:13411349.

MeSH Terms
Antibodies, Monoclonal/immunology Antigens, CD/immunology,physiology CD18 Antigens Humans Hydrogen Peroxide/metabolism Integrin alphaXbeta2/immunology,physiology Lymphocyte Function-Associated Antigen-1/immunology,physiology Macrophage-1 Antigen/immunology,physiology Neutrophils/immunology,metabolism Respiratory Burst Superoxides/metabolism
Chemicals
Antibodies, Monoclonal Antigens, CD CD18 Antigens Integrin alphaXbeta2 Lymphocyte Function-Associated Antigen-1 Macrophage-1 Antigen Superoxides Hydrogen Peroxide
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Berton G
Institute of General Pathology, University of Verona, Italy.
Laudanna C
Sorio C
Rossi F
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Article Info
Journal
The Journal of cell biology
Abbr.
J Cell Biol
ISSN
0021-9525
Published
1992-02-00
Pages
1007-17
Language
English
Region
United States
NLM ID
0375356
PMCID
PMC2289342
Subset
IM
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