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A humanized CD18 antibody can block function without cell destruction

M J Sims1, D G Hassal, S Brett

  • 1Department of Cell Biology, Wellcome Research Laboratories, Beckenham, United Kingdom.

Journal of Immunology (Baltimore, Md. : 1950)
|August 15, 1993
PubMed
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Researchers developed a humanized antibody to block leukocyte integrin interactions, crucial for cell adhesion and immune responses. This antibody effectively inhibits key functions without causing cell death.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Leukocyte integrins, specifically LFA-1 (leukocyte functional antigen-1), mediate leukocyte adhesion to endothelium and cell-cell interactions.
  • These interactions are critical for leukocyte extravasation and immune cell activation.
  • Targeting leukocyte integrins offers therapeutic potential for inflammatory and immune-related diseases.

Purpose of the Study:

  • To analyze the inhibitory capacity of monoclonal antibodies (mAbs) against human CD11a and CD18 (LFA-1 subunits).
  • To develop and characterize a humanized version of a potent blocking anti-CD18 mAb.
  • To assess the functional properties of the humanized antibody, including binding, blocking activity, and effector functions.

Main Methods:

  • Screening of seven anti-CD11a and two anti-CD18 mAbs for inhibition of LFA-1-mediated interactions.

Related Experiment Videos

  • Humanization of the lead anti-CD18 mAb (YFC51.1) using complementarity-determining region (CDR) grafting.
  • Characterization of the humanized mAb's binding affinity to CD18 and its functional blocking capabilities, including assessment of complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC).

    • Main Results:

    • A rat anti-human CD18 mAb (YFC51.1) demonstrated superior blocking activity.
    • The humanized version of YFC51.1 retained binding to human CD18 and maintained functional blocking characteristics.
    • The humanized IgG1 mAb did not mediate cell killing (CDC or ADCC) and did not bind human C1q.

    Conclusions:

    • A humanized anti-CD18 mAb has been successfully developed, preserving the potent blocking activity of its parental rat antibody.
    • This humanized antibody is a promising therapeutic candidate for modulating leukocyte adhesion in inflammatory conditions.
    • The lack of effector functions (CDC/ADCC) in the humanized IgG1 isotype enhances its safety profile for clinical applications.