Lack of age‐associated auto‐anti‐idiotypic antibody regulation in mucosal‐associated lymph nodes

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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.

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