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Human polymorphonuclear leukocytes adhere to complement factor H through an interaction that involves alphaMbeta2

R G DiScipio1, P J Daffern, I U Schraufstätter

  • 1The La Jolla Institute for Experimental Medicine, CA 92037, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|April 29, 1998
PubMed
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Human complement factor H acts as an adhesion molecule for neutrophils, not eosinophils. This interaction, mediated by Mac-1, enhances neutrophil activation and adhesion to tissues.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Complement factor H (CFH) is a key regulator of the complement system.
  • Neutrophils are critical immune cells involved in inflammatory responses.

Purpose of the Study:

  • To investigate the role of human complement factor H as an adhesion ligand for human neutrophils.
  • To identify the specific receptors and mechanisms involved in neutrophil adhesion to factor H.

Main Methods:

  • Adherence assays using polymorphonuclear leukocytes (PMNs) and factor H-coated surfaces.
  • Blocking studies with monoclonal antibodies (mAbs) against integrin chains (CD11b, CD18).
  • Affinity purification and immunoprecipitation to identify factor H binding receptors.

Main Results:

Related Experiment Videos

  • Human complement factor H specifically mediates PMN adherence, not eosinophil adherence.
  • PMN adhesion to factor H is dependent on divalent metal ions and augmented by C5a and TNF-alpha.
  • Mac-1 (CD11b/CD18) was identified as the primary factor H binding receptor on PMNs.
  • Surface-bound factor H enhances PMN activation, increasing hydrogen peroxide generation.
  • Factor H interaction with glycosaminoglycans (heparin, chondroitin A) facilitates PMN adhesion.

    • Conclusions:

    • Human complement factor H functions as an adhesion molecule for human neutrophils.
    • The interaction between factor H and glycosaminoglycans may facilitate in vivo neutrophil tethering and adhesion.
    • Factor H, through Mac-1, plays a significant role in neutrophil recruitment and activation during inflammation.