AbstractMice, selected for high (H) and low (L) antibody responses to xenogeneic erythro‐cytes (Biozzi mice, selection I), have been tested for their immune responsiveness to lysozymes. The anti‐ring‐necked pheasant egg‐white lysozyme (REL) and anti‐hen egg‐white lysozyme (HEL) primary plaque‐forming cell responses are 20 to 40‐fold lower in L than in H mice. The heterogeneity of anti‐HEL antibodies in the secondary response, as analyzed by isoelectric focusing, is highly reduced in L as compared to H mice. Thein vitroanti‐HEL plaque‐forming cell secondary response of (H × L)F1lymph node (LN) cells is induced by HEL‐pulsed macrophages (Mϕ) from H, but not from L, mice. Therefore, genetic differences affecting antibody responsiveness in H and L mice are expressed at the level of antigen‐presenting cells. This genetic defect observed in L cells has been studied in more detail using an antigen‐specific, T cell‐dependent LN cell proliferative assay. After HEL‐complete Freund's adjuvant (CFA) priming, LN cells from H or (H × L)F1mice respond to HEL, REL (which is cross‐reactive with HEL) and purified protein derivative of tuberculin (PPD), whereas LN cells from L mice do not respond to HEL or REL but proliferate in the presence of PPD. Proliferation of HEL‐CFA primed (H × L)F1LN cells is induced by HEL‐ or REL‐pulsed Mϕ from H but not from L mice, whereas PPD‐pulsed Mϕ from H or L mice give similar proliferative responses. By increasing 50‐fold the concentration of HEL used to pulse Mϕ from H and L mice, a comparable proliferative response is obtained when HEL‐CFA‐primed (H × L)F1LN cells are stimulated with HEL‐pulsed Mϕ from either line. This finding indicates that the genetic defect at the antigen‐presenting cell level in L mice is not absolute, but rather
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