No abstract

It has previously been shown that the loss of immune competence in the splenic B cell population with age may be due to auto‐anti‐idiotypic antibody regulation (M. R. Szewczuk and R. J. Campbell, Nature 1980. 286: 164). In the present study we have investigated the appearance of auto‐anti‐idiotypic antibody on immune B cells from the mucosal‐associated lymph nodes of old and young mice of the same strain. Various aged C57BL/6J male mice were immunized with 500 μg trinitrophenylated bovine gamma globulin (TNP‐BGG) in complete Freund's adjuvant (CFA) intraperitoneally. IgM, IgG and IgA anti‐TNP plaque‐forming cell (PFC) responses in the spleen, mediastinal and mesenteric lymph nodes were assayed for anti‐idiotype‐blocked, hapten‐augmentable PFC, 14 days later. It was found that 8 months or older C57BL/6J male mice produced a significantly high percentage of hapten‐augmentable IgM, IgG and IgA anti‐TNP PFC in the spleen. In contrast, there was a lack of hapten‐augmentable anti‐TNP PFC in the mesenteric and mediastinal lymph nodes with increasing age of the animal. Mice receiving antigen in the footpads and base of the tail also produced a significantly high percentage of hapten‐augmentable IgG PFC in the draining peripheral lymph nodes. TNP‐ε‐amino‐n‐caproic acid (EACA) as hapten was shown to specifically augment anti‐TNP PFC. Immune sera from 15‐month‐old mice caused a specific inhibition of anti‐TNP PFC in vitro. The inhibition of plaque formation was completely reversible by addition of TNP‐EACA as hapten. This PFC inhibitory activity in immune sera lacked anti‐TNP antibody activity, but reacted with anti‐TNP antibody of C57BL/6J origin. Immune sera from 8 month or older mice also revealed anti‐(anti‐TNP F(ab')2 IgG) titer as assayed by passive hemagglutination. Thus, the results of this study indicate a division of the immune system into regulatory compartments. Auto‐anti‐idiotypic antibody may be involved in a down‐regulation of systemic responses but with no apparent effect in the mucosal‐associated lymph nodes.

No abstract

We previously showed that the "immunologic privilege" of the anterior chamber results not from afferent blockade, but rather from induction of hapten-specific suppressor T cells that appear after anterior chamber priming with antigen. These suppressor T cells induced by anterior chamber priming differ from those induced by i.v. priming in their ability to block the efferent as well as the afferent limb of the immune response and in their lack of idiotypic surface receptors detected by rabbit anti-idiotypic antibody. We now report that intravitreal priming with haptenated syngeneic spleen cells does not result in generation of suppressor cells, but rather, can in some instances result in an enhanced systemic immunoreactivity to the priming hapten. If soluble antigenic preparations are used, however, intravitreal priming results in the generation of the suppressor T cells, which suppress subsequent DTH and CTL responses to the immunizing hapten. The suppressor cell generation after intravitreal priming is a cyclophosphamide-sensitive process. These results demonstrate that soluble products are processed differently in ocular compartments compared with cell surface coupled ligands, and further demonstrate that the generation of hapten-specific suppressor T cells is dependent, at least in part, on the form and on the specific compartment of the eye that is inoculated.