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Two main ideas have been put forward lo explain the unexpectedly low anti-hapten antibody titres which can result from pre-priming a mouse with carrier before hapten-carrier immunization. The first involves the interaction of a network of idiotype-specific suppressor T cells, the second instead arguing for the role of intrinsie B-cell anergy. This paper proposes that the data available can equally be interpreted as reflecting the suboptimal interaction between T and B cells at differing stages of maturity, provided that memory B cells can be divided into two subsets. Further, it is suggested that these considerations must be taken into account in the analysis of B-cell anergy in receptor transgenic mice. [ABSTRACT FROM AUTHOR]

As perhaps the staunchest advocates of repertoire purging as the central mechanism of immunological tolerance, we note with satisfaction a spate of recent, elegant papers which suggest an intrathymic clonal abortion model as the explanation for at least some examples of T-cell tolerance. This view agrees with the classical formulation of the Billingham-Brent-Medawar school of tolerance as a specific, central failure of immune responsiveness. Repertoire purging within the B-lymphocyte compartment remains much more controversial. There is no doubt that experimental models exist where the B cell is the reversible target of tolerance induction. The question is, in view of the ease of inducing autoantibody formation both in vivo and in vitro, just how relevant are such clonal anergy mechanisms to authentic self-tolerance? Arguments are presented that there must be two windows of tolerance susceptibility in the ontogeny of the B cell; one while it is maturing in the bone marrow, to prevent autoreactivity of high affinity to important accessible self-antigens; and a second soon after activation of pre-memory cells by exogenous antigen, to prevent fortuitous mutations towards high-affinity anti-self-reactivity establishing a forbidden clone. [ABSTRACT FROM AUTHOR]

CD2 is expressed on murine B cells, probably as a result of a chromosomal translocation event during speciation. There are no activating antibodies to mouse CD2, but when activated non-specifically, only T cells up-regulate their expression of CD2. We investigated the expression and function of CD2 on B cells using mice transgenic for human CD2 under the control of a modified version of the autologous promoter/enhancer that included the immunoglobulin enhancer. This construction directs expression of human CD2 to the B cell compartment as well as to the T cell compartment. In this paper, we confirm that activating pairs of anti-CD2 monoclonal antibodies are mitogenic for mouse T cells transgenic for human CD2. In contrast, mouse B cells that express similar amounts of human CD2 are not stimulated to proliferate by equivalent doses of these antibodies. We were also unable to show any functional consequence for these B cells as a result of CD2 ligation. [ABSTRACT FROM AUTHOR]

The article discusses the relationship between the nature of the blood group and the type of antibody response in the adaptive immunity and blood transfusion. It states that the T cells, B cells, and antigen-presenting cells (APCs) are the key players for the formation of antibodies. It adds that after migrating the progenitor cells from the circulation into the epithelial thymus, T and B cells with their T-cell receptor (TCR) and B-cell receptor (BCR) may respond to antigens.

Two distinct murine B-cell differentiation factors, designated B 151 -TRY 1 and B 151-TRF2, were described originally as B151 K12 T-cell hybridoma-derived lymphokines that induce immunoglobulin (Ig) secretion by antigen-activated B cells and unstimulated B cells, respectively. In the present study, we found that a highly purified B1 51-TRF1 fraction prepared by reversed-phase high-performance liquid chromatography (RP-H PLC) also has the ability to cause a polyclonal differentiation of unstimulated B cells into IgM-secreting cells in the apparent absence of co- stimulant. The activity of the B151-TRF1 fraction but not the B151-TRF2 fraction on unstimulated B cells was markedly inhibited by addition of a monoclonal antibody (mAb) specific for the B151- TRF 1/IL-S to the culture. To determine whether 8151 -TRF 1/IL-S and 8151 -TRF2 act on distinct populations among unstimulated B cells, the responsiveness of neonatal B cells and adult B cells that had been fractionated by Percoll density gradient centrifugation was assessed. B15 l-TRFI/IL-5 predominantly acted on lower density B cells, which appeared around 3 weeks after birth in the spleen. In contrast, B151-TRF2 could activate both lower and higher density B cells almost equally and B 151 -TRF2-responsive B cells were already present by 1 week of age. Thus, these results suggest that B151-TRFI/IL-5 and B151-TRF2 act on distinct subpopulations among antigen-unprimed normal B cells to induce IgM-secreting cells. [ABSTRACT FROM AUTHOR]

Antibody production to influenza A strain virus X31 (H3N2) was measured in cultures of peripheral blood mononuclear cells (PBMC) stimulated with either antigen (X31) or pokeweed mitogen (PWM). With some donors, X31 antibody was produced in response to antigenic stimulation, but not as part of the polyclonal response to PWM, suggesting that antigen and PWM may be acting on different B-cell subpopulations. To test this hypothesis, T-cell depleted PBMC (E-) cells were fractionated on discontinuous Percoll gradients and assayed for antibody production in response to antigen or PWM. Fraction I (FrI = SC < 1.070) cultured in the presence of T cells responded well to PWM, but not at all to X31. FrII (1070 < SG < 1.075) and FrIII (SG > 1.075) cultured in the presence of T cells both responded well to X31, but only the medium-density B cells (FrII) were able to make specific antibody when T cells were replaced with T-cell replacing factor (TRF). Specific X31 antibody responses by medium- and high-density B cells (FrII and FrIII) were suppressed equally by the addition of allogeneic T-suppressor (Ts) cells. When allo-activated Ts cells were inactivated by irradiation, allogeneic T-helper (Th) cells were able to collaborate with both FrII and FrIII B cells in specific antibody responses to X31. Since TRF was not able to substitute for T cells in specific antibody responses by FrIII B cells, this result shows that allogeneic T-cell help was not mediated by non-specific 'allogeneic effect' factors and apparently requires cognate T cell-B cell interactions. [ABSTRACT FROM AUTHOR]

Lectin-free supernatants obtained from PWM-stimulated lymphocytes, enable B cells to proliferate and secrete immunoglobulin. Both functions arc augmented by the addition of irradiated T cells. In the presence of antigen, these supernatants also enhance specific anti-tetanus toxoid antibody production. The components of the supernatant responsible for these activities have a molecular weight between 30,000 and 60,000, and have the characteristics of non-specific factors: they are genetically unrestricted, and do not bind to either antigen or anti-DR affinity columns. There is no evidence that the partial T dependency of these factors is an indication that their target is a T cell. Instead, T cells appear necessary to move the B cell into a state of activation in which it becomes responsive to the factor. Alternative activation signals such as Staph. A. Cowan can substitute for T cell help in the proliferative response, but not for immunoglobulin or antibody synthesis. The implications of these results for the approaches used to detect and classify B cell growth factors are discussed. [ABSTRACT FROM AUTHOR]

Unlike the suppression of a primary response to a thymus-dependent antigen, pretreatment of mice with anti-IgD serum has no effect on the response to a thymus-independent (TI) antigen. It has also been shown that anti-IgD serum injected parenterally into mice 2 days previously, has no suppressive effect on non-specific responsiveness to an intraperitoneal injection of LPS. There is a similar lack of effect on the non-specific element of responsiveness to a TI antigen. These results provide in vivo confirmation of the results of previous in vitro experimentation. [ABSTRACT FROM AUTHOR]

Antigen-antibody complexes efficiently inhibit the induction of antibody formation. Using Mishell-Dutton cultures, it can be demonstrated that neither T cells nor their products are required for this inhibition of IgM PFC formation. The blockade is at the level of B cells and cannot be overcome by LPS or TRF. The data demonstrate that cross-linking of antigen- and Fc-receptors by antigen-antibody complexes is a blocking signal for B cells. [ABSTRACT FROM AUTHOR]

Comparative study of two T-cell subpopulations, killers and MIF producers, immune to H-2 antigens, was performed using the in vitro micro-techniques of cell-mediated cytolysis and inhibition of macrophage migration. T-dependence of MIF production was shown in this system by lymphocyte separation onto T- and B-cells and by inactivation of MIF producers with anti-θ serum. At least part of MIF producers appeared to be more sensitive than killers to the action of anti-θ antibodies in the presence of complement. Production of MIF as compared to the cytotoxic activity was revealed in regional lymph node cells earlier and preserved longer after immunization with allogeneic tumour cells. Immune lymph node cells were shown to produce MIF when incubated with spleen cells of congenic and recombinant strains of mice possessing either private or public H-2 specificities of the immunizing complex, but they did not produce MIF when incubated with syngeneic spleen cells. Removal of killers by absorption on the relevant target cells did not reduce the ability of non-adherent lymphocytes to produce MIF. Unlike cytotoxic activity, MIF production is inhibited by pre-treatment of immune lymphocytes with pronase. The data obtained are indicative of essential differences in effector T-cell subpopulations which exert the cytotoxic effect and produce MIF in the H-2 system. The implications of these data for studies on T-cell differentiation under the action of H-2 antigens are discussed. [ABSTRACT FROM AUTHOR]

The article offers information on two forms of lymphocyte-like cells in lamprey which express distinct variable lymphocyte receptors (VLR) locus and share basic properties with B and T cells. As cited, two forms of lymphocyte like cell include VLRA-expressing cells which proliferate in response to antigen but did not secrete soluble antibodies and VLRB cells which not only proliferate but also secreted soluble antibodies. As reported, reciprocal cell-communication occurs between T and B cells.