BALB/c mice were injected neonatally with monoclonal antibody against a T15 idiotope, MaId5-4, and the immune potential of splenic lymphocytes against phosphorylcholine (PC) was studied by stimulation with S. pneumoniae R36a (Pn) in vitro. The total number of PC-specific plaque-forming cells (PFC) and the proportion of PFC expressing the MaId5-4 idiotope (Id' PFC), as well as two other distinct (nonhomologous) idiotypes of the T15 family recognized by monoclonal antibodies AB1-2 and B36-82, was determined by plaque assay against PC-coupled red blood cells. The magnitude of the total PFC response of splenocytes from age-matched normal and MaId5-4-suppressed mice was comparable but all three Id(s) which were expressed on >70% PFC from normal splenocytes were below detection level in splenocytes from suppressed mice. Depletion of T cells lowered the total PFC response to a comparable degree in both mice. Normal B cells (BN) stimulated by Pn expressed all three Id(s) much like the normal splenocytes. B cells from MaId5-4suppressed mice (Bs) always failed to express MaId5-4 but they occasionally did express the B36-82 or Abl-2. The reciprocal mixing of B and T cells followed by Pn stimulation revealed that both normal T cells (TN) and T cells from MaId.5-4-suppressed mice (T,) provided equal help to either BN or Bs in regard to total PFC number. Ts consistently inhibited the expression of MaId5-4 in BN cultures, but only rarely the expression of Abl-2 and B36-82. Bs cocultured with TN never expressed MaId5-4 but they sometimes did express one or both of the other two Id. These results show that neonatal application of a monoclonal anti-Id suppresses the expression of the Id determinant which is recognized by the antibody, as well as other determinants. The mechanism of the suppression of the target Id (MaId5-4) involves both B cell tolerance and active suppression. The mechanism of cosuppression (idiotopes AB1-2 and B36-82) is variable, apparently involving a B cell tolerance, lack of Id-specific help, and/or active suppression.
Pertusis toxin (PTX) has been shown to potentiate autoimmunity in experimental autoimmune disease. The exact mechanism of this effect has not been determined; however, the modification of G proteins by ADP-ribosylation has been suggested. Here it is demonstrated that this modification may contribute to autoimmunity by the abrogation of transforming growth factor-β (TGF-β) growth-inhibitory signals. Anti-TGF-β demonstrated the same effect on lymphocytes as high concentrations of PTX in vitro.
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