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CD40 stimulation promotes human secondary immunoglobulin responses in HuPBL-SCID chimeras

  1. Author:
    Murphy, W. J.
    Funakoshi, S.
    Fanslow, W. C.
    Rager, H. C.
    Taub, D. D.
    Longo, D. L.

  2. Author Address

    Murphy WJ NCI, Lab Leukocyte Biol, Div Basic Sci, SAIC Frederick,Frederick Canc Res & Dev Ctr Bldg 567,Room 210 Frederick, MD 21702 USA NCI, Lab Leukocyte Biol, Div Basic Sci, SAIC Frederick,Frederick Canc Res & Dev Ctr Frederick, MD 21702 USA NCI, Intramural Res Support Program, SAIC Frederick, Frederick Canc Res & Dev Ctr Frederick, MD 21702 USA NCI, Clin Serv Program, SAIC Frederick, Frederick Canc Res & Dev Ctr Frederick, MD 21702 USA Immunex Corp Seattle, WA USA NIA Baltimore, MD 21224 USA
    1. Year: 1999
  2. Journal: Clinical Immunology
    1. 90
    2. 1
    3. Pages: 22-27
  4. Type of Article: Article
  1. Abstract:

    Antibodies to CD40 have been demonstrated to promote B-cell, growth and differentiation in vitro. In order to determine if CD40 stimulation could promote antigen-specific human immunoglobulin (Ig) production in vivo we examined the effects of anti-human CD40 MoAb in an in vivo system where human peripheral blood lymphocytes (huPBL) were engrafted into mice with severe combined immune deficiency (SCID). The huPBL-SCID mice were then given various doses of diphtheria-tetanus toroid (DT) vaccine and were examined for the presence of human DT-specific antibodies by ELISA. Surprisingly treatment with anti-CD40 significantly lowered background DT responses versus untreated chimeras in unimmunized huPBL-SCID mice. However, after immunization, huPBL-SCID mice treated with anti-CDBO MoAb responded to a significantly greater extent in response 60 the vaccine compared with control huPBL-SCID mice, although total Ig levels were sometimes lower in anti-CD40-treated mice. The predominant Ig isotype induced after immunization was IgG. Thus, CD40 stimulation promotes human secondary IgG responses in huPBL-SCID mice. These data demonstrate that CD40 stimulation is capable of promoting antigen-specific human B-cell responses in vice. (C) 1999 Academic Press. [References: 21]

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