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C J Bellone

Publications and source records attributed to C J Bellone.

43 records · Page 3Linked to original sources
PubMed1980

Anti-phenyltrimethylamino immunity in mice. II. L-Tyrosine-p-azophenyltrimethylammonium-induced suppressor T cells selectively inhibit the expression of B-cell clones bearing a cross-reactive idiotype.

The anti-phenyltrimethylamino (TMA) response in A/J mice is characterized by a cross-reactive idiotype(s) (CRI) that appears linked to the Ig-Ie allotype. These findings made it attractive to look for a CRI on T cells reactive to the same TMA determinant. Thus a suppressor T-cell (Ts) assay specific for L-tyrosine-p-azophenyltrimethylammonium [tyr(TMA)] was developed. A/J mice were primed with either tyr(TMA) in complete Freund's adjuvant (CFA), L-tyrosine-azobenzenearsonate [tyr(ABA)] in CFA, or with CFA alone. 6 wk later all mice were inoculated with TMA-bovine serum albumin (BSA) in CFA, boosted with soluble TMA-BSA 3 wk later, and plaqued 7 d after the soluble boost. Priming with tyr(TMA) in CFA resulted in 66% suppression of anti-TMA plaque-forming cells (PFC) as compared with control groups primed with tyr(ABA) in CFA or CFA alone. The suppression was shown to be mediated by Ts, as only T cells but not B cells from suppressed animals transfer the suppression in adoptive cell transfer experiments into lethally irradiated recipients. The profile of the anti-TMA PFC in the suppressed and nonsuppressed animals was examined via incorporation of anti-idiotypic sera (specific for CRI-TMA) into the plaquing medium. The results of these experiments indicate that the suppression of the major CRI+-TMA PFC was virtually complete, whereas the CRI--TMA PFC are left intact. When A/J mice were primed with idiotypic antisera (anti-Id) or normal rabbit serum (NRS) rather than with the antigen on CFA alone, and the same protocol was followed thereafter, the anti-Id-inoculated mice were suppressed by 63% when compared with the NRS-primed controls. Again the suppression could be accounted for by the exclusive elimination of CRI+ anti-TMA PFC. The possibility that the antigen-induced idiotype suppression may result from idiotypic restrictions between interacting CRI+-Ts and CRT+-B cells will be discussed.

Animals↗
PubMed1980

Extensive cross-reactive idiotypy among guinea-pig anti-TMA antibodies.

The extensive cross-reactivity of the immune response by strain 13 (S-13) and outbred guinea-pigs (GP) to either the bivalent antigen L-tyrosine-p-azophenyltrimethylammonium (tyr(TMA)) [H-L-tyr(TMA)-NH-(CH2)3]2 (T-S-T) or the conjugate 3-(p-trimethylphenylazo)-N-acetyl-L-tyrosylglycylglycine-bovine serum albumin (T-S-B) was examined. Antibody (Ab) isolated from a single T-S-B immune S-13 animal by affinity chromatography (proband) was used to induce anti-sera (anti-Id) in a rabbit and a syngeneic S-13 GP. These anti-Ids were both shown to be idiotype specific by means of a tube binding radioimmunoassay (TBRIA). A series of S-13 anti-(T-S-B), S-13 anti-(T-S-T), and outbred anti-(T-S-B) antisera were tested as inhibitors in the TBRIA through a range of 6-200 ng of anti-TMA Ab equivalent. Each was found to inhibit extensively, indicating a considerable amount of cross-reactivity of idiotypes present in the sera. In general, the rabbit anti-Id recognized more cross-reactivity among the various antisera than did the GP reagent, particularly among those from T-S-B immune S-13 animals. Addition of free "hapten" tyr(TMA) as an inhibitor specifically displaced 55% of the label from the rabbit reagent at 10(-5)M, while only 25% of binding of the proband to GP anti-Id was inhibitable at this concentration. These findings suggest that the rabbit and GP anti-Ids are directed predominantly to different determinants, the rabbit recognizing the less variant, hapten-binding portion of the GP Ab more than does the syngeneic GP reagent. Data from isoelectric focus patterns support the impression of a highly restricted Ab response to TMA. While each serum gives a distinct binding pattern, several bands appear shared by all responders.

Animals↗
PubMed1977

Inhibition of T-antigen-binding cells by idiotypic antisera.

Shared idiotypy between B- and T-cell receptors specific for the antigen L-tyrosine-p-azophenyltrimethylammonium [tyr(TMA)] was studied in an antigen-binding assay using idiotypic antisera. These idiotypic reagents were prepared by inoculation of rabbits with purified anti-tyr(TMA) antibody raised in strain 13 guinea pigs. The antisera blocked 78-83% of the antigen-binding T cells (T-ABC) and 50-55% of the antigen-binding B cells (B-ABC) from tyr(TMA)-immune strain 13 and outbred lymph node cells (LNC). An excess of normal guinea pig Ig in the ABC assay did not affect the ability of the idiotypic antisera to block T- and B-ABC. Nylon wool-passed tyr(TMA)-immune LNC were trypsin treated resulting in a 75% loss of T-ABC. The trypsin-treated population was then cultured for 16 h which resulted in a return of T-ABC to 92% of pretrypsin values. 77% of these regenerated T-ABC could be blocked with idiotypic antisera. Specificity of the idiotypic antisera was tested in L-tyrosine-p-azobenzenearsonate-immune guinea pig LNC. Neither T- nor B-ABC were blocked in this heterologous system. Further blocking experiments were performed to characterize the nature of the T-ABC receptor. A variety of anti-Ig reagents, some of which block B-ABC, do not inhibit T-ABC suggesting that variable regions on T cells are not linked to Ig Constant regions.

Animals↗
PubMed1977

Antigen-binding lymphocytes in guinea pigs. I.B cell expansion to the monovalent antigen L-tyrosine-p-azophenyl trimethylammonium (tyr(TMA)) in the absence of antibody production.

The monofunctional antigen L-tyrosine-p-azophenyltrimethylammonium chloride, tyr(TMA), and the polyfunctional antigen, TMA-human gamma-globulin (TMA-HGG), were used to investigate the antigen structural requirements necessary for clonal proliferation of B cells. This clonal expansion was characterized with respect to receptor immunoglobulin class and affinity maturation. Antigen-binding analysis revealed that inoculation of tyr(TMA), although only of m.w. 344, triggers clonal expansion of B lymphocytes 9-fold in the absence of any apparent antibody production. There does not appear to be any maturation with respect to antibody class since greater than 90% of the tyr(TMA)-specific B cells bear the micron receptor in the nonimmune and immune state. However, the average avidity of the B cells for this antigen increases with time after immunization. In contrast, immunization with TMA-HGG results in an 18-fold increase in B lymphocytes with significant amounts of anti-TMA antibody production. With time after immunization, both maturation of average avidity and class of Ig receptor (micron leads to gamma shift) occur. These findings indicate that the functionally T cell-specific antigen tyr(TMA) can trigger clonal B cell expansion and affinity maturation at the receptor level in the absence of detectable antibody production.

Animals↗
PubMed1976

In vivo host immune to a tumor-specific transplantation antigen induced by Rous sarcoma virus.

We examined the host immune response to a tumor-specific transplantation antigen (TSTA) induced by Rous sarcoma virus (RSV) In vivo. In contrast to previous in vitro studies, the present investigation demonstrated in vivo host immunity of the TSTA 10-55 days after tumor inoculation. Immunity to the TSTA appeared specific, since the homologous RSV tumor was rejected. whereas the heterologous tumor grew progressively. No generalized suppression of cell-mediated or hymoral immunity was shown, because tumor-bearing hosts retained the ability to reject heterologous tumor cells and mounted a normal plaque response to sheep red blood cells. Although alpha-globulin levels were elevated, they did not appear to affect the host's immunity to the growing tumor or to heterologous antigens. Assoicated with the progressively growing tumor was the appearance in the serum of a fetal antigen with characteristics of an alpha-2 acute phase protein.

Alpha-Globulins↗