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Biomedical subjects

A K Abbas

Publications and source records attributed to A K Abbas.

At least 127 records · Page 7Linked to original sources
PubMed1978

Antigen-antibody complexes suppress antibody production by mouse plasmacytoma cells in vitro.

Preformed complexes of 2,4-dinitrophenylated keyhole limpet hemocyanin (DNP-KLH) and anti-DNP or anti-KLH antibodies selectively, suppressed the production of anti-DNP IgA by the plasmacytoma cell line, MOPC 315, in vitro. Compexes made with DNP8.5KLH (8.5 moles DNP/10(5) daltons carrier) inhibited the secretion of IgA but not its synthesis, whereas complexes prepared with the more highly substituted DNP20KLH inhibited synthesis as well. Moreover, complexes of DNP-KLH and anti-DNP F(ab')2 fragments were as suppressive as those made with IgG antibodies, suggesting that the mode of presentation of antigenic determinants and not surface Fe receptors may play a major role in this phenomenon.

Animals↗
PubMed1977

Mechanisms of B cell tolerance: I. Dynamic nature of the induction of hapten-specific unresponsiveness by hapten-conjugated pneumococcal polysaccharide.

Exposure of 2,4-dinitrophenyl (DNP)-hemocyanin-primed spleen cells to DNP-conjugated pneumococcal polysaccharide (DNP-S3) in vivo or in vitro renders such cells unresponsive to DNP-hemocyanin challenge following adoptive transfer. The unresponsiveness is hapten-specific, independent of the presence of T cells and adherent cells, and not due to either toxic effect of S3 or carry-over of tolerogenic amounts of cell-bound DNP-S3, and thus presumably represents a model of B cell tolerance. The degree of suppression induced depends upon the dose of the tolerogen and most strikingly on the duration of exposure of cells to the tolerogen. Thus 2 to 6 h exposure to DNP-S3 has an insignificant effect on anti-DNP responses, while 24 and 48 h exposures in vitro and in vivo are highly suppressive. Such a dynamic process of tolerance induction suggests a "multiple hit" phenomenon, implying the generation of suppressive signals by repeated cycles of tolerogen-receptor interactions. The process can be interrupted by removal of extracellular DNP-S3, although this does not reverse the unresponsiveness that has already been induced.

Animals↗
PubMed1977

Inhibition of antibody production in plasmacytoma cells by antigen.

Tissue culture-adapted MOPC 315 mouse plasmacytoma cells which secrete monoclonal anti-DNP IgA antibody, were cultured with a variety of DNP-carrier conjugates and the production of IgA measured by pulse labeling with [3H]leucine and by plaque-forming cell assays. DNP-coupled bovine, human and rabbit gamma-globulins (containing 9 to 12 DNP groups per 50 000 mol wt of carrier) inhibited the synthesis and secretion of IgA by 40 to 80%. This inhibition was specific, since unconjugated globulins were ineffective, non-IgA proteins and DNA synthesis remained unaffected, and DNP-globulins had no effect on X5563 cells which do not bind DNP. The degree of suppression of antibody production dependen on the concentration and epitone density of the antigen and on the duration of exposure of cells to it, and was no attributable to absorption of secreted antibody by cell-bound antigen. Comparably substituted DNP conjugates of F(ab')2 and intact globulins were equally inhibitory. The inhibition of antibody synthesis by DNP-BGG was reversible following removal of the antigen. This phenomenon is similar in many respects to the antigen-induced blockade of normal antibody-secreting cells, and provides a valuable model system for analyzing the mechanisms of antigen-mediated cellular inactivation.

Animals↗
PubMed1976

Fatal pulmonary reaction from low doses of bleomycin. An idiosyncratic tissue response.

There were two cases of fatal interstitial pneumonia secondary to bleomycin sulfate administration. Although bleomycin pulmonary toxicity is generally thought to be dose-related and occurs infrequently with a total cummulative dose less than 300 to 400 units, the two reactions reported here occurred with doses of 105 and 165 units. Fatal bleomycin-induced pneumonia has been previously reported at these low dosages, and physicians should be aware that this toxic reaction may occur as an idiosyncratic response. Previous thoracic irradiation may be a predisposing factor. Patients receiving bleomycin should be meticulously monitored by interrogation for cough, dyspnea, and chest pain; by auscultation for rales; by serial chest roentgenograms; and by determinations of vital capacity and single-breath carbon monoxide diffusing capacity.

Adenocarcinoma↗
PubMed1976

The distribution of Ia antigens on the surfaces of lymphocytes.

The distribution of Ia antigens was studied on murine spleen lymphocytes by an ultrastructural technique employing deep freeze-etched replicas. Ia antigens were labeled on cells from appropriate congenic and recombinant strains of mice by incubating the cells with FITC-conjugated anti-Iak antibody, followed by ferritin-coupled Fab anti-FITC. Ia antigens were detected predominantly on immunoglobulin (Ig)-bearing B lymphocytes. Antigens coded for by the entire Ik region were present on the surfaces of 95% of the positive cells (from B10.BR mice) in densely packed microclusters. Ia specificities coded for by the I-A and I-C subregions (on 4R and B10.HTT mice) exhibited a more variable pattern, with 30 to 35% of the labeled cells having sparsely distributed Ia antigens in relatively discrete microclusters. Binding of anti-Iak antibody at 37 degrees C led to patch formation but not to capping. Modulation of surface Ig left Ia antigens diffusely distributed on the cell surface, indicating that these two membrane proteins are independent molecules.

Animals↗
PubMed1975

Modification of the rat alloimmune response by enhancing antibodies and the role of blocking factors in the survival of renal grafts.

Correlation of morphological and immunological events ocurring in control and passively enhanced rat renal allograft recipients has revealed an important role for vasculitis in rejection, whereas the tempo and severity of graft lymphocyte infiltration and tubular damage was comparable in both groups during the first 5 days. Thereafter, the degree of cellular infiltration in enhanced allografts progressed and actually exceeded that in control grafts. 2-Mercaptoethanol-sensitive lymphocytotoxic antibodies were present in both groups with comparable titers and appearance times; however, the presence of a severe IgG-containing necrotizing arteritis and glomerulitis in control, but not enhanced, grafts suggests that passive enhancement protects by interfereing with the cooperative T cell-dependent inductive response. Further support for this possibility comes from the fact that the development of cytotoxic lymphocytes against donor target cells was delayed for 48 hr in the enhanced group. While controls died at days 9-11, enhanced animals entered a period of prolonged survival with stable renal function. This state of "autoenhancement" was characterized by a low degree of cell-mediated cytotoxicity and the appearance of serum factors that blocked the in vitro cellular assay. Blocking factors have a low affinity for the attacking cell population, suggesting that they are immune complexes or anti-idiotypic antibodies, and not free alloantibody of high affinity.

Animals↗
PubMed1975

Non-random distribution of surface immunoglobulins on murine B lymphocytes.

An indirect labeling technique was used to map the surface immunoglobulin (Ig) on murine splenic B lymphocytes by freeze-etching. Cells were labeled first with fluorescein conjugates of monovalent (papain-digested) anti-Ig antibody followed by monovalent anti-fluorescein antibody coupled to ferritin. The technique avoids cross-linking and aggregation of surface Ig. Freeze-etched replicas of cells labeled at 4 degrees C, as well as of cells prefixed with paraformaldehyde showed that surface Ig was distributed in small clusters with interconnecting networks. The observed pattern was analyzed statistically by comparing it with the expected random (Poisson) distribution and shown to be non-random to a high degree of statistical significance. The deviation from randomness could be explained by the presence of clusters and relative excesses of bare membrane. Such an observed distribution of surface Ig suggests that this membrane macromolecule may be organized in a specific manner. The distribution may also play a role in the function of surface Ig as the antigen receptor on B lymphocytes.

Animals↗
PubMed1975

Immunologic enhancement of rat renal allografts. III. Immunopathologic lesions and rejection in long-surviving passively enhanced grafts.

Immunologic enhancement of renal allografts from (Lewis times Brown Norway) F1 to Lewis rats was achieved by administering a single dose of antidonor serum at the time of transplantation. A series of grafts functioning for 1 to 4 months after transplantation were examined by light and immunofluorescence microscopy to evaluate the long-term protective effects of the enhancing serum and to determine if previously unobserved lesions appeared in long survivors. Despite the absence of detectable circulating cytotoxic alloantibody, long-term allografts showed necrotizing glomerular and arterial lesions which resembled those seen in acutely rejecting grafts and were compatible with humoral rejection. Thus, in this model, there is a late decline in the ability of passive enhancement to inhibit humoral rejection. Long-term grafts also developed tubular lesions with deposition of immunoglobulin and complement on the tubular basement membranes (TBM). Anti-TBM antibodies were demonstrated in recipients' sera and found to be organ specific but not major histocompatibility antigen or species specific. This tubular lesion is therefore a unique form of allograft injury in which the immune response is directed against tissue antigen(s) which are distinct from the major histocompatibility antigens that induce rejection.

Animals↗
PubMed1975

Interrelationships of surface immunoglobulin and Fc receptors on mouse B lymphocytes.

Receptors for the Fc portion of immunoglobulin (Ig) molecules have been detected on mouse B lymphocytes by an immunofluorescence technique, employing immune complexes of fluorescein-conjugated KLH and rabbit anti-KLH antibody. At 37 degrees C, membrane-bound complexes rapidly undergo capping and clearing from the surface. Modulation of Fc receptors does not alter the amount of distribution of surface Ig, indicating that these two molecules are independent moieties. However, capping of surface Ig by intact or pepsin-digested anti-Ig antibody leads to co-capping of Fc receptors. These results suggest that ligand binding to surface Ig induces some alteration which allows the Ig to enter into an association with Fc receptors.

Animals↗
PubMed1974

Immunologic enhancement of rat renal allografts. I. Comparative morphology of acutely rejecting and passively enhanced grafts.

The acute unmodified rejection of (Lewis x Brown Norway) F(1) to Lewis renal allografts is characterized by an early and progressive lymphoid cell infiltrate, glomerular necrosis, necrotizing arteritis and ischemic cortical necrosis leading to graft destruction. A single low dose of enhancing antiserum given at the time of transplantation prolongs graft survival by abrogating the necrotizing lesions in glomeruli and arteries and the subsequent cortical necrosis. Passive enhancement in this model is interpreted as representing predominantly a block in the humoral antibody-mediated rejection response. It is suggested that the block is effected mainly, peripherally, ie, at the level of the transplanted kidney itself.

Animals↗
PubMed1974

Immunologic enhancement of rat renal allografts. II. Immunohistology of acutely rejecting and passively enhanced grafts.

Unmodified renal transplants from (Lewis x Brown Norway) F(1) hybrids to Lewis rats show deposition of immunoglobulin (IgG) and complement in the arteries, which cause an acute necrotizing arteritis with ischemic necrosis of the grafts. Treatment with a single dose of enhancing antiserum at the time of transplantation prevents the arterial deposition of IgG and complement, and the vascular lesions. The enhancing antibody probably acts peripherally by blocking crucial antigenic sites in the graft vasculature, since cytotoxic alloantibody is detectable in the circulation of both control and enhanced recipients. Unmodified allografts also show deposition of IgG in glomeruli accompanied by glomerular necrosis. Immunofluorescent studies indicate that these glomerular lesions are mediated by complexes of antigen and alloantibody, and at least partially also by a nonhistocompatibility antibody directed against antigens in glomerular endothelial cells. Enhancing antiserum treatment reduces glomerular IgG deposition and thus greatly mitigates the glomerular lesion as well.

Animals↗