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Immune responsiveness of guinea pigs to dinitrophenyl-poly-L-lysine and to the lysine rich random co-polymer of L-glutamic acid and L-lysine are both controlled by a single gene, the `poly-L-Iysine gene'. This paper reviews recent experiments which demonstrate that these two antigens specifically compete with one another for being presented to T cells by the same antigen-presenting cells. This finding is interpreted to mean that antigens to which responsiveness is controlled by the same single gene compete for the Ir gene product of antigen-presenting cells. The review discusses if the products of the immune response genes-presumably the Ia antigens-may constitute a third specific antigen recognition system. It further speculates if this idea may help to provide insight into the phenomenon of histocompatibility-restriction and into the nature of the mixed leucocyte reaction. [ABSTRACT FROM AUTHOR]

This paper reviews the present knowledge of B-L antigens encoded by the chicken B complex as regards to the following aspects: (1) identification and cellular expression, (2) structural studies, (3) evidence for two distinct populations of B-L antigens, (4) mapping of B-L loci of the B complex, (5) B-L and immune response, and (6) the role of the B-L antigens for the control of mixed lymphocyte reactions (M LR) and graft-versus-host (GVH) reactions. It is concluded that B-L antigens of the chicken exhibit extensive homology with mammalian La antigens. A genetic map of the B complex is presented. [ABSTRACT FROM AUTHOR]

The role of complement component C5 in the immune response of mice to sheep red blood cells (SRBC) was investigated. Congenic C5-sufficient and C5-deficient B10.D2 mice and genetically C5-defficient DBA/2 mice, as such or supplemented with C5-suffcient serum, were used as experimental animals, C5-substitution of the C5-deficient mice resulted in measurable C5 levels for days. The functional half-life of C5 in C5-deficicnt DBA/2 mice was about 21 h. No significant differences between the IgM-responses of C5 bearing and naive C5-deficient animals were observed. This suggests that C5 does not play a major role in the primary humoral immune response of mice in vivo, although C5 seems to do so in in vitro experiments, even with the same antigen. Antigen-induced C5-produclion by C5-deficient mice as one of the explanations of the in vitro, in vivo discrepancy could not be confirmed experimentally. [ABSTRACT FROM AUTHOR]

We have examined the immunological activity of five affinity-purified protein antigens from Mycobacterium tuberculosis in seven inbred and one outbred guinea pig strains. The test systems were measurements of delayed-type hypersensitivity (Dth) responses, lymphocyte stimulation assays (LS), and antibody response measurements. The results showed significant differences in the immunogenicity of the single-protein antigens and, when the antigens were considered separately, highly significant guinea pig strain differences. The outbred guinea pig strain behaved as a Dth high responder to all antigens studied. The order of magnitude of the Dth responses was not usually correlated with that of the corresponding antibody responses for the individual guinea pig strain-antigen combinations. In particular, when compared with the other strains, strain 2 guinea pigs generally gave the lowest Dth, but the highest antibody responses. A 38,000 molecular weight protein, possessing M. tuberculosis complex-specific B-cell determinants, appeared immunodominant in 5 out of 7 strains. Our Dth data in the inbred strains further suggest the presence of an M. tuberculosis-specific T-cell epitope. A T-cell line, 11D9, derived from the high-responder guinea pig strain 13 reactive to this protein, was shown to be able to confer a tuberculin-like skin reaction in vivo. LS assays with recombinant 38-kDa protein and truncated versions of the protein mapped the 11D9-defined T-cell epitope to the middle part of the molecule. [ABSTRACT FROM AUTHOR]

The plaque-forming antibody response of C57BL/6 mice to rabbit gamma globulin (RGG) decreases as a function of age. RGG in tolerogenic form induces tolerance of young mice but sensitizes older animals. If antigen is administered together with lipopolysaccharide, the age-dependent decline in immune responsiveness is not observed, nor are older animals sensitized by tolerogen. The age-dependent decline in immune responsiveness is due to a loss of T helper capacity; sensitization by tolerogen is attributable to a subpopulation of B cells which becomes sensitized by the tolerogen. Older animals, treated with tolerogen, show a degree of central tolerance of T cells and a relatively slight, age-dependent diminution in colchicine- or cyclophosphamide-sensitive precursors of suppressor cells. [ABSTRACT FROM AUTHOR]

The present experiments were undertaken to delineate the role of LD and SD antigens in terms of memory in cell-mediated immune response (CML), Using recombinants that differ for either the H-2K or H-2D determinants (SD-different) and other recombinants differing for the central region of H-2 (LD different), we have investigated this question. The results indicate that priming to SD determinants leads to a more rapid and higher response when cells are restimulated in vitro with either the same SD antigt-n alone or the same SD plus an LD antigen and tested on target cells that possess either the SD antigen alone or both the LD and SD antigens. Antigens in the central regions of H-2, which includes LD, serve as the stimulus both for the helper T cells and for the c)'totoxic T lymphocjtes. Priming with a high dose of LD antigt-ns leads to memory in the cytotoxic T lymphocyte recognizing the cytotoxic target antigens coded by the central region of H-2. Nevertheless, memory could not be detected when priming was done under the same conditions as for SD antigens. Moreover, a primed helper T-cell response does not facilitate the development of increased CML on restimulation in vitro with the LD antigen used for priming and a new SD antigen. Thus, it seems that memory in CML is in the cytotoxic T lymphocyte and not in the proliferating helper cells. [ABSTRACT FROM AUTHOR]

Spleen cells from bovine serum albumin (BSA)-primed CBA mice were exposed to proteolysis by papain and pronase under conditions where cell recovery and viability were not impaired but surface Ig and antigen-binding were greatly reduced. The ability of the cells to respond to BSA was tested by a modified Farr assay of serum taken 10 days after adoptive transfer of cells to lethally irradiated syngeneic recipients. Cells not exposed to enzymes were able to respond to BSA either in vitro before adoptive transfer or in vivo after transfer. Cells exposed to papain and pronase were unable to respond in vitro, but normal antibody production was approached when the cells were exposed to antigen in vivo. Thus, after removal of much surface Ig the cells were temporarily unresponsive to antigen but were still functional, as demonstrated by their ability to recover responsiveness in vivo. [ABSTRACT FROM AUTHOR]

Evidence is presented that significant numbers of specific anti body-forming cells are released from the spleen into the circulation on the 4th day of the secondary-immune response to sheep erythrocytes. This release results in a transient appearance of specific antibody-forming cells in the blood and implicates a dissemination of specific anti body-forming cells from the spleen to different parts of the body. Also specific antigen-binding cells are released from the spleen, with a peak release on the 4th day of the immune response. [ABSTRACT FROM AUTHOR]