Retinoic acid receptor status in mouse spleen during a primary immune response against beta-galactosidase

Endocr Regul. 2000 Sep;34(3):113-8.

Abstract

Objective: Evaluation of the dynamics of all-trans retinoic acid receptor binding properties in mouse spleen nuclear extracts during a primary immune response against beta-galactosidase.

Methods: Female BALB/c mice, aged between 5 and 6 weeks were immunized intradermally into the shaved back (4 spots each) with 100 microg beta-galactosidase in 100 microl sterile phosphate buffered saline (pH 7.2) and blood was taken by tail bleeding on days 0 (preimmune serum), 4 and 6. Production of antibody in serum and the detection of cytokines (IL-4, IFN-gamma) from proliferation supernatants were determined by ELISA. Antigen-specific proliferation assay of isolated spleen cells was based on [3H]-thymidine incorporation measured in a liquid scintillation counter. Both, the maximal binding capacity (Bmax) and the affinity (Ka) of all-trans retinoic acid nuclear receptors (RAR) were evaluated according to Brtko (1994).

Results and conclusions: Injection of beta-galactosidase induced the first detectable antibody responses on day 4 (IgM) and on day 6 (IgG). These points of time, reflecting the early and the mature immune response served to measure the antigen-specific proliferation and production of IL-4 and IFN-gamma in the supernatants of the proliferation cultures as well as all-trans retinoic acid receptor (RAR) binding characteristics in spleen nuclear proteins. The RAR Bmax was significantly (P<0.05) decreased only at the time of the first specific IgG antibody production.

Conclusions: The data obtained indicate the involvement of RAR in the late phase of an in vivo immune response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibody Formation*
  • Antigens / immunology
  • Antigens / metabolism
  • Cell Division
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Immunity, Cellular
  • Immunization
  • Immunoglobulin G / biosynthesis
  • Immunoglobulin M / biosynthesis
  • Interferon-gamma / biosynthesis
  • Interleukin-4 / biosynthesis
  • Mice
  • Mice, Inbred BALB C
  • Receptors, Retinoic Acid / metabolism*
  • Spleen / immunology*
  • Spleen / metabolism*
  • Spleen / ultrastructure
  • Tretinoin / metabolism
  • beta-Galactosidase / immunology*

Substances

  • Antigens
  • Immunoglobulin G
  • Immunoglobulin M
  • Receptors, Retinoic Acid
  • Interleukin-4
  • Tretinoin
  • Interferon-gamma
  • beta-Galactosidase