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S K Pierce

Publications and source records attributed to S K Pierce.

118 records · Page 7Linked to original sources
PubMed1976

Allogeneic carrier-specific enhancement of hapten-specific secondary B-cell responses.

We have analyzed the capacity of carrier-specific T cells to enhance the immune response of hapten-specific secondary B cells which do not share genes in the H-2 complex with the T cells. For this analysis we have used the in vitro splenic focus technique which allows assessment of monoclonal responses of B cells isolated in splenic fragment cultures of irradiated reconstituted carrier primed mice. A previous report from this laboratory demonstrated that syngeny in the I region of the H-2 complex was necessary between collaborating hapten-specific primary (nonimmune) B cells and carrier-specific T cells for responses yielding IgG1 but not IgM antibody. These findings lead up to postulate that the expression of I-region gene products on the surface of primary B cells and I-region syngeny with collaborating carrier-specific T cells were essential elements in the triggering events leading to IgG1 synthesis by primary B cells. The results presented in the present report indicate that, unlike primary B cells, the majority of secondary B cells can be stimulated to produce IgG1 antibody in carrier-primed allogeneic recipients. Although the enhancement of secondary IgG1 responses is slightly greater with syngeneic T cells, the allogeneic collaborative interaction requires both carrier priming of recipient mice and stimulation with the homologous hapten-carrier complex and thus appears to be specific. These findings clearly discriminate secondary from primary B cells and indicate that the mechanism of stimulation of secondary B cells to yield IgG1-producing clones differs fundamentally from the stimulation of primary B cells in that the requisite for I-region syngeny is obviated.

Animals↗
PubMed1975

The allogeneic bisection of carrier-specific enhancement of monoclonal B-cell responses.

The ability of T cells to enhance the response of syngeneic and allogeneic B cells to thymus-dependent hapten-carrier conjugates was analyzed. This analysis was carried out on individual primary B cells in splenic fragment cultures derived from irradiated reconstituted mice. This system has several advantages: (a) the response of the B cells is entirely dependent on carrier priming of the irradiated recipient; (b) this B-cell response can be quantitated in terms of the number of responding cells; and (c) very small B-cell responses can be readily detected and analyzed. The results indicate that the majority of hapten-specific B cells were stimulated in allogeneic and syngeneic recipients only if these recipients were previously carrier primed. The number of B cells responding in carrier-primed allogeneic recipients was 60-70% of that in syngeneic carrier-primed recipients. The antibody-forming cell clones resulting from B cells stimulated in the allogeneic environment produced small amounts of antibody and antibody solely of the IgM immunoglobulin class, while the larger responses in syngeneic recipients were predominantly IgG1 or IgM plus IgG1. The capacity of collaborative interactions between carrier-primed T cells and primary B cells to yield IgG1 antibody-producing clones was shown to be dependent on syngeny between these cells in the H-2 gene complex. It is concluded that: (a) B cells can be triggered by T-dependent antigens to clone formation through collaboration with T cells which differ at the H-2 complex as long as these T cells recognize the antigen; (b) the immunoglobulin class produced by the progeny of stimulated B cells generally depends on the nature of the stimulatory event rather than the nature of the B cell itself; and (c) stimulation to IgG1 production is dependent on syngeny between the collaborating T and B cells probably within the Ir-1A region. The role of the Ia antigens in the formation of IgG1-producing clones is not yet clear; Ia identity could permit IgG1 production or, conversely, nonidentity of Ia could induce all allogeneic interactions which prohibit IgG1 production.

Animals↗
PubMedDate not supplied

The response of contractile and non-contractile vacuoles of Paramecium calkinsi to widely varying salinities.

Paramecium calkinsi from tidal marshes survive a wide salinity range. Fluid output of contractile vacuoles of these cells decreased as salinity of the medium to which they were acclimated increased, and both pulse rate and vacuole volume were used to regulate output. When cells were first exposed to more dilute medium, contractile vacuoles greatly increased volume so that fluid output increased even though pulse rate decreased. In cells shifted to a more concentrated medium, contractile vacuole output decreased by decreasing pulse rate. The contractile vacuole is surrounded by a set of collecting structures which change form as the salinity changes. Distensible ampullae are found in media of low salinity and collecting canals are found in media of high salinity. When cells are shifted from high salinity to low, the number of ampullae increases and the number of canals decreases. When cells are shifted from low salinity to high, the number of ampullae decreases and the number of canals decreases. Other non-contracting vacuoles also appear in response to a hypoosmotic shock. These include vacuoles within the cell as well as "blisters" on the surface. The number and frequency of blisters increases with the size of the hypoosmotic shock. They detach from cells without resulting in any visible loss of cytoplasm. Non-contractile vacuoles may play a role in sequestering and removing excess water that the contractile vacuoles cannot handle.

Adaptation, Physiological↗
PubMedDate not supplied

Assessing B cell diversification by antigen receptor and precursor cell analysis.

A major element in the understanding of B cell specificity diversification is the extent of diversity present in mature and in developing B cell populations. Two general methods are currently used for assessing the specificity repertoire: (a) the enumeration of cells whose receptors can bind a specific antigen, and (b) the enumeration of cells which can respond to antigenic stimulation by antibody-forming cell clone production. Our laboratory has utilized the latter method to establish the frequency of B cells responsive to a wide variety of antigenic determinants. The findings indicate that: (a) the primary murine B cell specificity repertoire probably includes more than 10(7) clonotypes; (b) some clonotypes are represented by numerous B cells (40,000 TEPC 15 precursors per BALB/c mouse) while most are represented by fewer than to B cells per mouse; (c) the acquisition of the repertoire is apparently antigen-independent since germfree mice have repertoires similar to conventional mice and secondary B cells are easily distinguished from primary B cells; (d) the neonatal repertoire appears to contain only 10(4) clonotypes at birth, each represented by perhaps 200-400 cells; (e) the diversification process from neonatal to adult repertorie appears highly ordered and reproducible. Antigen binding cell studies have now used in conjunction with the splenic focus assay in an attempt to correlate these two techniques. The results indicate that the efficiency of the splenic focus assay used for precursor cell anlysis it 4-5% for both primary and secondary B cells and is similar to the percent of donor B cells lodged in recipient spleens. For certain antigens (DNP-BSA) the number of antigen-binding cells can represent 4% of the total B cells, and this number directly correlates with the concentration of antigen used; stimulation, on the other hand, appears to have an affinity threshold achieved by only 0,02% of the DNP-specific B cells. In contrast, PC-BSA antigen-binding cell and splenic focus precursor cell frequencies are identical. These findings are interpreted to indicate that antigen-binding cell analyses confirm the validity of the calculations used to estimate precursor frequencies in the splenic focus technique. However, for some antigens binding to cell receptors, one detects a large number of cells belonging either to a nonstimulatable B cell subclass or whose receptor affinity is too low to permit stimulation.

Animals↗