PubMed1985
We have compared the in vitro and in vivo mitogenic and polyclonal antibody (IgM-, IgG-, IgA- and IgM anti-SRBC-secreting PFC) and autoantibody (IgM anti-ssDNA-, anti-bromelin-treated [HB]- and anti-intact mouse RBC-secreting PFC) responses to peptidoglycan (PG), LPS, protein A, PWM, PHA and Con A in young (4-7 weeks) and old (7-8 months) normal (BALB/c, CBA/H, C57BL/6) and autoimmune (NZB, NZB X NZW F1, BXSB, MRL/1; old BXSB and MRL/1 were 4-5 months) mice. Our results demonstrated that: lymphocytes from young and old autoimmune mice (except old BXSB) could be further polyclonally activated in vitro by PG or LPS as well as or better than lymphocytes from young and old normal mice; lymphocytes from young or old autoimmune mice were less polyclonally activated in vitro by protein A or PWM, respectively, than lymphocytes from young or old normal mice; PG and LPS were equally effective polyclonal activators in vitro; in vivo, LPS was a stronger stimulant than PG; in vivo, LPS could induce polyclonal activation in both young and old normal and autoimmune mice, whereas, PG could only induce polyclonal activation in vivo in young and old normal mice, but did not induce further activation in young and old autoimmune mice; only some tests (anti-ssDNA and IgG PFC in vivo, and IgA and anti-HB MRBC PFC in vitro) revealed higher responses in autoimmune than in normal mice, and these higher responses were seen more often in vivo than in vitro; both autoimmune and normal mice had a high frequency of autoantibody (especially anti-ssDNA) secreting cells in polyclonal activation in vitro, whereas a high frequency of these cells in vivo was only found in autoimmune mice; in most cases in vitro, polyclonal activators did not change the frequency of autoantibody and heteroantibody secreting cells, but in vivo, both PG and LPS increased the frequency of anti-ssDNA antibody secreting cells in normal, but not in autoimmune, mice; LPS increased the in vivo, but not in vitro, frequency of cells secreting anti-HB MRBC antibodies in some strains of mice; old mice had lower mitogenic responsiveness than young mice in both autoimmune and normal strains; autoimmune mice had similar, higher or lower mitogenic responses than normal mice, depending on the strain and the age, but in most cases consistent for both B and T cell mitogens; and there was no correlation between the patterns of increased or decreased mitogenic and polyclonal antibody responses in normal and autoimmune mice.4+.