Publications by authors named "Thorbecke G"

A study was made of bovine serum albumin density gradient-separated bursa cells with respect to their distribution on the gradients, % cytoxicity with anti-Ig + complement (C) or anti-mu + C, and localization of fractions in irradiated syngeneic recipients. Layer A showed a higher cytotoxicity with anti-Ig + C or anti-mu + C than the others; layer D showed the lowest % cytotoxicity, although a large % of the cells not killed by anti-Ig were killed by anti-bursa serum + C. The C + D layers contained a much larger fraction of the Ig+ cells from the bursa in the 1--4-week-old than in the 6--12-week-old animals, suggesting a relative shift towards lower density of Ig+ bursa cells with age.

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Transfer of lymphoid cells from agammaglobulinemic donor chickens into 3- to 4-week-old irradiated recipients that had been surgically bursectomized at 2 to 3 weeks of age significantly depressed the ability of the antibody-forming apparatus to recover from irradiation. Antibody production to Brucella abortus and sheep erythrocytes remained much below control levels in BX donor-cell recipients of both chicken strains studied (SC and FP). Progressive loss of serum IgM and IgG was observed primarily in the FP strain resulting in complete agammaglobulinemia within 4 to 6 weeks after transfer of BX donor spleen cells.

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Incubation of trinitrophenylated hemocyanin (TNP-KLH)-primed spleen cells with microgram amounts of 2,4-dinitrophenyl (DNP) or 2,4,6-trinitrophenyl (TNP) conjugates of pneumococcal polysaccharide type 3 (SIII) for as little as 5 min at 4 degrees C results in a specific "block" of the 19 S and 7 S adoptive memory response to TNP-KLH. This hapten-SIII-induced block of anti-hapten memory B cell responsiveness seems to be an example of specific receptor blockade. The block is specific and can be prevented by simultaneous incubation of the primed cells with hapten-protein conjugates which presumably compete with the hapten-polysaccharide for attachment to the B cell surface via anti-hapten Ig receptors.

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Graft versus host (GVH) reactivity of parental lymph node (LN) cells was assayed by measurements of 3H-thymidine incorporation in vivo. Mitomycin (Mit.) treatment of parental cells abolished their proliferative activity but the combination of such Mit.

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Adoptive anti-trinitrophenyl (Tnp) responses were elicited from Tnp-hemocyanin (Tnp-KLH)-primed cells by challenge with an immune complex of KLH and a Tnp conjugate of the Fab fragment of rabbit anti-KLH. Removal of T cells by treatment with anti-Thy 1.2 (phi C3H) + complement abolished this effect.

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Serially transferred LAF spleen cells show a deficient 7S PFC response to TNP-Brucella when Tx as compared to normal irradiated intermediate hosts are used. This defect can be corrected by combining the spleen cells with lymph node cells from the Tx intermediate hosts. It is concluded that T helper cells, residing primarily in lymph node, are needed for efficient 19S leads to 7S conversion in the immune response.

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Homing of 3-H-adenosine-labeled bursa cells to follicles in the chickens spleen was greatly reduced by prior incubation of the transferred cells with rabbit anti-chicken-immunoglobulin sera. This effect was transient, being present 6 hr after cell transfer but gone by 18 hr, when incubation was at 0 degreesC without complement. The inhibition persisted until at least 18 hr after incubation at 37 degrees C with complement.

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Spleens from LAF1 mice injected intravenously with sheep erythrocytes (SE) are relatively rich in memory T cells early in the immune response (1 to 3 days) and rich in memory B cells as the response progresses (2 weeks or more). Marked cooperation for the secondary immune response in vitro was obtained by combining 10(6) spleen cells from LAF1 mice, taken 2 days after intravenous priming with SE, with 10(7) spleen cells from day 14 primed mice. The results indicate relative deficiencies in the spleen for B memory cells on days 1 to 2 and for T memory cells on day 14 after priming.

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Cells from reticulum-cell sarcomas (RCS), tumors with a probable B-cell origin in the SJL/J mouse strain, induced a high degree of proliferation in O-bearing syngeneic lymph-node and thymus cells obtained from young non-tumours mice. Although of considerably lower magnitude, a proliferation of SJL/J thymus cells to syngeneic normal lymph-node cells was also noted. Sera from normal syngeneic mice did not block either of these proliferative responses.

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