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A M Stall

Publications and source records attributed to A M Stall.

44 records · Page 3Linked to original sources
PubMed1986

Immunoglobulin-bearing B cells reconstitute and maintain the murine Ly-1 B cell lineage.

Previous reconstitution studies in irradiated mice distinguished Ly-1 B from other B cells. The predominant B cell populations in spleen and lymph node are readily reconstituted from progenitors present in adult bone marrow. Ly-1 B cells, in contrast, are reconstituted from cells in peritoneum rather than bone marrow. Further studies, presented here, demonstrate that Ly-1 B populations are reconstituted from peritoneal cells that already express both surface immunoglobulin (IgM) and Ly-1, that is, Ly-1 B. Such cells reconstitute and maintain the Ly-1 B population in irradiated recipients for at least 6 months.

Animals↗
PubMed1984

Allotypic specificities of murine IgD and IgM recognized by monoclonal antibodies.

Hybridomas generated from mice immunized with allotype and H-2-incompatible spleen cells were screened by flow cytometry. Monoclonal antibodies (MAb) to four of the five known specificities of IgD were identified. The location of these specificities on the IgD molecule was determined by the ability of a given MAb to bind to cells stripped of the Fab fragment by trypsin proteolysis. Igh-5.1 (present on IgDa and IgDe) and Igh-5.5 (unique to IgDe) were both located on the Fab fragment. Results from cross-blocking experiments suggest that, except for Igh-5.3, MAb which recognize the same specificity bind to the same antigenic determinant. Both the trypsin digest and blocking studies indicate that Igh-5.3 is composed of at least two antigenic determinants. AF6-78.25, a MAb specific for IgM of the b, d, and n haplotypes, was also identified; this MAb defines a new specificity, Igh-6.6. On the basis of the reactivities of these MAb, it appears that although the Igh-Ce and Igh-Cd haplotypes are virtually identical at the Igh-3(gamma 2b), Igh-1(gamma 2a), and Igh-2(alpha) loci, they are highly divergent at the Igh-5(delta) and Igh-6(mu) loci. This indicates that the Igh-Cd haplotype may have resulted from a recombination between Igh-Ce and another haplotype.

Animals↗
PubMed1982

I-A antigens on cloned alloreactive murine T lymphocytes are acquired passively.

Cloned lines of alloreactive cytolytic and amplifier T lymphocytes have been examined for expression of I-A antigens. Using flow cytofluorometry and monoclonal antibodies, MHC antigens representing both I-A and H-2K or D determinants were reproducibly detected on the cell surface of these cloned T lymphocytes. All cloned lines examined expressed H-2K or D antigens representing the MHC haplotype appropriate to their strain of origin. However, I-A as well as H-2K or D antigens appeared to be acquired passively from the stimulating cell population. Within the lower limits of detection using the fluorescence-activated cell sorter, evidence suggesting endogenous synthesis of I-A antigens by these cloned T lymphocytes could not be demonstrated. Further, the observed binding appeared to be nonspecific, because material originating from allogeneic, syngeneic, or third-party stimulating cells could be observed under appropriate conditions.

Animals↗
PubMed1978

The effect of inhibitors of protein synthesis on the reexpression of surface immunoglobulin following antigenic modulation.

P3, a cell line derived from the plasmacytoma MOPC-21 secretes IgG1 (K) and is sensitive to complement (C')-mediated lysis by antibody directed against gamma1 or K. Sensitivity is attributed to the presence of immunoglobulin molecules on the surface membrane, designed Ig-mem. This sensitivity is abolished by antigenic modulation of Ig-mem. Modulated cells, when incubated in the absence of antibody, recover sensitivity to lysis in 4 hr. By measuring the rate of recovery, it has been possible to study the effects of various drugs on the reexpression of Ig-mem. Treatment of modulated cells with cycloheximide (Cx), pactamycin Pc), anisomycin (An), homoharringtonine (Ha) or sparsomycin (Sm), each a specific inhibitor of a different step in protein synthesis, produces a significant reduction in the rate of recovery. Paradoxically, puromycin (Pm), also a specific inhibitor of protein synthesis, does not reduce the rate of recovery. Studies were performed using Pm together with each of the other drugs to gain an understanding of the relationship between protein synthesis and recovery from modulation. Based upon these studies, we conclude that continued operation of the initiation cycle of protein synthesis is required for reexpression of Ig-mem in the absence of de novo protein formation.

Anisomycin↗
PubMedDate not supplied

Depletion of the predominant B-cell population in immunoglobulin mu heavy-chain transgenic mice.

The transgenic mouse line M54 was generated by introducing a functionally-rearranged immunoglobulin mu heavy-chain gene into the germ line of a C57B1/6 inbred mouse. Previous examination of the antibodies produced by B-cell hybridomas derived from transgenic M54 mice showed that the presence of the mu transgene grossly altered the immunoglobulin repertoire of unimmunized animals, suggesting that these mice suffer from a serious immunoregulatory perturbation. Studies presented here introduce a new perspective on this functional defect. We show that the lymphoid tissues from these transgenic mice lack virtually all conventional bone-marrow-derived B cells, which constitute the predominant B-cell population in normal mice and which typically produce primary and secondary antibody responses to T-cell-dependent antigens. Moreover, the bone marrow from transgenic M54 mice is depleted of pre-B lymphocytes, indicating a serious defect in early B-cell lymphopoiesis. In contrast, CD5 (Ly-1) B cells, a second B-cell population displaying a characteristic set of cell surface markers which are derived from distinct precursors in the peritoneum, are represented at normal frequencies in these transgenic mice. Thus, the presence of the rearranged immunoglobulin heavy-chain transgene in M54 mice results in an unexpected selective developmental defect that impairs the development of bone-marrow-derived pre-B and B cells without affecting Ly-1 B cells.

Animals↗
PubMedDate not supplied

A major peritoneal reservoir of precursors for intestinal IgA plasma cells.

Studies presented examine the origin of IgA plasma cells in B lineage chimeric mice constructed by reconstituting lethally irradiated mice with a mixture of syngeneic bone marrow cells and peritoneal cells from Ig heavy chain allotype congenic donors. In these mice, essentially all B cells in spleen and Peyer's patches are derived from the bone marrow donor; however Ly-1 B lineage cells which have been mainly detected in the peritoneum are derived from the peritoneal cell donor. Surprisingly, roughly half of the IgA plasma cells in the lamina propria of the gut are also derived from the peritoneal cell donor, suggesting an important role for peritoneally-derived B cells in the mucosal immune response.

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