Vitamin A deficiency severely compromises the magnitude of the primary and secondary antibody response to tetanus toxoid (TT) but does not impair the development of immunologic memory. To further characterize this immunodeficiency in antibody production, we have quantified the immunoglobulin G (IgG) subclasses (IgG1, IgG2a, IgG2b, and IgG2c) during the primary and secondary response to TT in normal, vitamin A-deficient, and retinol-repleted rats. In the primary response in normal rats, anti-TT IgG1 and IgG2b predominated. In vitamin A-deficient rats the production of anti- TT IgG2b was severely impaired, with little change in either IgG1 or IgG2a. In the secondary response vitamin A-deficient rats produced low levels of all anti-TT IgG subclasses. However, when vitamin A-deficient rats were repleted with retinol 2 days before reimmunization their secondary anti-TT IgG response was normal both in magnitude and IgG subclass distribution. This result implies that although vitamin A deficiency during the primary antibody response impaired anti-TT IgG2b production, it did not inhibit Ig heavy chain recombination or the differentiation of lymphocytes that formed memory B cells for each subclass; furthermore, these cells were activated in the secondary response after vitamin A status was improved. Thus, these experiments further support the concept that memory cell formation remains normal during vitamin A deficiency despite low levels of antibody production.
All Science Journal Classification (ASJC) codes
- Molecular Biology