Grafts of the anterior limb bud introduced at embryonic day 4 between histoincompatible chick embryos were subject to chronic, mild rejection beginning from several weeks to several months after birth. In contrast, quail wing buds similarly grafted into chickens started to be rejected at the first or second week after birth and finally autoamputated. Embryonic thymus epithelium from donor quail (before it had been colonized by hemopoietic cells) was grafted into chicks. A chimeric thymic epithelial stroma was generated in which the lymphocytes of the chick acquired the capacity to recognize the grafted limb as self either permanently or for a protracted period of time. In such thymic chimeras the grafted wings were not rejected.

Animals↗

PubMed1987

A novel method to bursectomize avian embryos and obtain quail----chick bursal chimeras. II. Immune response of bursectomized chicks and chimeras and post-natal rejection of the grafted quail bursas.

Two methods to bursectomize chick embryos before hemopoietic cell seeding of the bursa of Fabricius were compared in this work: section of the tail region at E3 including the presumptive bursal territory, and selective removal of the bursa at E5. Hatching ability is better with the former method, but survival rate and effectiveness of bursectomy are favored with the second, novel technique. Moreover, selective removal of the bursa at E5 can be followed by in situ engraftment of a quail bursa and construction of quail-chick bursal chimeras. The immune response of bursaless birds and bursal chimeras has been studied. Total absence of the bursa does not prevent a few B cells from differentiating and nonspecific Ig (IgM and/or IgG) from being secreted. As reported previously, bursaless birds, however, are unable to mount an immune response by producing specific antibodies. This immune function is restored by the graft of a quail bursa. The microenvironment of the bursa, although heterospecific, allows the expansion of the B cell population and generates the repertoire of the B cell antigen receptors. This process takes place during late embryonic and early postnatal life because the grafted quail bursal stroma is subjected to immune rejection from 2 to 3 wk after birth in all chimeras, which are, however, perfectly immunocompetent.

Age Factors↗

PubMed1986

Cell cycle control of activated, synchronized murine B lymphocytes--roles of macrophages and complement C3.

Three restriction points control the cell cycle of activated murine B lymphocytes in a synergistic way. The first is controlled by the occupancy of surface immunoglobulin either by antigen- or by immunoglobulin-specific antibodies. The second is controlled by the complement C3d receptor CR2 which can be occupied by cross-linked C3b or C3d to stimulate the entry into S phase, or by soluble C3d or a C3 alpha-chain peptide, binding to the CR2 receptor, which inhibit the entry into S phase. Macrophages produce so-called alpha factors which also control the B-cell cycle at the same point. Thus, it is suspected that macrophages produce components of the early pathway of complement activation which finally lead to cross-linking of CR2 receptors on B cells. The third restriction point is controlled by unknown receptors that recognize so-called beta factors produced by helper T lymphocytes.

Animals↗

PubMed1985

Activation and cell cycle control of murine B lymphocytes.

The cell cycle of activated murine B lymphocytes (B cells) is controlled by the occupancy of surface membrane-bound immunoglobulin (Ig) and by two types of growth factors, called alpha and beta factors. These growth factors are produced in an endocrine fashion by the interaction of helper T lymphocytes (T cells) with antigen-presenting macrophages (A cells). Antigen is taken up, processed and presented on the surface of A cells in the context of class II major histocompatibility complex (MHC) glycoproteins. Helper T cells recognize this association of antigen and class II MHC molecules. A cells produce alpha factors and T cells produce beta factors. The molecular nature of these factors and of the corresponding receptors on B cells has yet to be elucidated, although it can be shown that the complement component C3d replaces alpha factor action. Resting, G0 phase B cells are refractory to the action of alpha and beta factors. They have to be excited, i.e. rendered susceptible to the action of these factors. This can be achieved by the interaction with helper T cells that recognize antigen, bound by surface membrane Ig, in the context of class II MHC glycoproteins on the surface of resting G0 B cells. Excitation can also occur in a polyclonal fashion by cross-linking of surface Ig with immobilized, Ig-specific antibodies, or by the interaction with polyclonal activators of B cells, such as lipopolysaccharides. Entry into the cell cycle is asynchronous. Activated, cycling B cells can be synchronized by size separation, using velocity sedimentation. Synchronized B cells will retain their synchrony for several divisions, when they are stimulated by immobilized Ig-specific antibodies, alpha and beta factors. They divide every 20 h at 37 degrees C. Omission of either of the three stimuli arrests B cells, though at different points in the cell cycle. Three restriction points are found: the first occurs immediately after mitosis and is controlled by the binding of immobilized Ig-specific antibodies to surface membrane-bound Ig.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

A novel method to bursectomize avian embryos and obtain quail----chick bursal chimeras. I. Immunocytochemical analysis of such chimeras by using species-specific monoclonal antibodies.

Chick embryos were bursectomized at 5 days of incubation according to a novel surgical technique described in this article. This method yields birds that are able to hatch and are devoid of the physiologic deficiencies resulting from the previously used method, which involved resection of the cloacal and posterior embryonic region. The bursectomized embryos were grafted in situ with a quail bursa of the same age, which thereafter became chimeric through chick host hemopoietic cell invasion. By means of species-specific antibodies, the chimeric condition revealed 1) that the bursal epithelium expresses a unique antigenic determinant (MB1 determinant), until now considered to be an exclusive feature of blood vessel endothelium and hemopoietic cells, and 2) that this determinant appears in bursal epithelium at the time and site of hemopoietic cell invasion. The other point arising from this work concerns the apparent constitutive Ia expression by perifollicular blood capillary endothelial cells in normal and chimeric bursas.

Animals↗

PubMed1984

The synergism of accessory cells and of soluble alpha-factors derived from them in the activation of B cells to proliferation.

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Animals↗

PubMed1983

Requirement for macrophages or for macrophage- or T cell-derived factors in the mitogenic stimulation of murine B lymphocytes by lipopolysaccharides.

Splenic B cells from a variety of mouse strains could be depleted of accessory cells by removal of large cells through velocity sedimentation, followed by adherence to plastic and by passage over Sephadex G-10. Such accessory cell removal abolished the reactivity of the splenic B cells to the mitogen lipopolysaccharide (LPS), as measured by their capacity to polyclonally proliferate and mature to IgM-secreting cells. Accessory cells from different sources, such as peritoneal exudate cells, irradiated spleen cells, cells of the macrophage line P388 D1 and macrophages from a single colony grown from bone marrow precursors in semi-solid media in the presence of colony-stimulating factor all reconstituted LPS reactivity of the accessory cell-depleted B cells. Limiting dilutions of the cells of a single macrophage colony indicated that as little as 30 to 1000 macrophages can reconstitute the polyclonal response of 3 X 10(4) B cells to LPS. Not only activated macrophages, but also activated long-term helper T cell lines and T cell hybridomas, produced supernatant factors which could also restore responsiveness of depleted B cells to LPS.

Animals↗

PubMed1982