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S Fuchs

Publications and source records attributed to S Fuchs.

At least 163 records · Page 9Linked to original sources
PubMed1977

Cytophilic antibodies in experimental autoimmune myasthenia gravis.

Macrophage-cytophilic antibodies, with acetylcholine receptor specificity, are present in rabbits with experimental autoimmune myasthenia gravis (EAMG). Such antibodies may have a significant role in the immunologic mechanism involved in the pathogenesis of myasthenia gravis. The induction of EAMG in rabbits was performed by injection of purified AChR from the electric organ of Torpedo californica. Both the binding of AChR specific cytophilic antibodies to normal macrophages and the presence of such antibodies bound in vivo to macrophages of sick animals were demonstrated in vitro. The amount of cytophilic antibodies was determined by measuring cell-associated radioactivity after the addition of 125I-AChR. Cytophilic antibodies capable of binding to normal alveolar macrophages were detected in all animals 14 days after immunization, and were maintained through the severe stages of the disease. In addition, cytophilic anti-AChR antibodies were shown to be bound in vivo to alveolar macrophages drawn from severely sick rabbits, as was measured by a direct 125I-AChR binding to such macrophages. The role of cytophilic antibodies and in particular of macrophage-associated cytophilic antibodies in the pathogenesis of autoimmune diseases is not clear yet. The availability of AChR specific cytophilic antibodies can now be utilized for studying their role in the immunopathogenesis of EAMG.

Acetylcholine↗
PubMed1976

The effect of antisynaptosomal plasma membrane antibodies on memory.

Antisynaptosomal plasma membrane antibodies were introduced through an infusion cannula into rat brain and their effects on behaviour were tested. Four different learning paradigms were used, two appetitively and two aversively motivated, to show impairment in memory retrieval. No effects were found on aquisition, motor activity, or motivation.

Animals↗
PubMed1976

Immunosuppression of experimental autoimmune myasthenia gravis by hydrocortisone and azathioprine.

Experimental autoimmune myasthenia gravis (EAMG), induced in rabbits by injection of acetylcholine receptor (AChR) from Torpedo californica, was suppressed by appropriate treatment with hydrocortisone or with azathioprine. Administration of hydrocortisone in gradually increasing doses, starting at the time of immunization with the receptor, prevented exacerbation of the disease in the early stages of treatment, as was the case when hydrocortisone was administered in high doses from the beginning. Prolonged administration of the antimetabolite azathioprine (Imuran) prevented the appearance of EAMG, for at least 4 months, in rabbits immunized with AChR. Cell-mediated immunity to AChR was demonstrated to be significantly decreased in such treated animals. The effects of hydrocortisone and azathioprine on EAMG support the view that the disease involves an immunologically cell-mediated mechanism and indicate that the experimental disease can serve as a useful model for chemotherapy of the human disease.

Acetylcholine↗
PubMed1975

X-ray microanalysis of calcium binding sites in Paramecium with special reference to exocytosis.

In Paramecium cells Ca++-stimulated triggering of the exocytosis of secretory vesicles ("trichocysts") was achieved by ionophores X-537 A or A 23187. Under triggering conditions electron dense deposits were present in some "resting" trichocysts and regularly in discharging trichocysts; upon subsequent fixation deposits occurred on the trichocyst membrane (on the inner side or within the membrane) and on the "inner lamellar sheath" from where deposits seemed to "radiate" into the secretory materials. Similar results were obtained with glutardialdehyde fixation alone which also triggers exocytosis but only at low concentrations. Element analysis by energy dispersive x-ray microanalysis ascertained the presence of Ca and P in deposits occurring in trichocysts. Those "resting" trichocysts which were devoid of deposits did not contain Ca or P enriched. Hence, an abrupt Ca++-influx into individual trichocysts just before exocytosis seems to be involved in the triggering mechanism, possible in combination with the sudden activation of an ATPase system localized at those sites of the trichocysts which primarily contain the deposits. When paramecia were treated only with Ca++ and then fixed with OsO4 plus oxalate or merely with glutardialdehyde, electron scattering deposits were formed also on the inner side of the cell membrane and within the ciliary shaft (but rarely in trichocysts). Deposits obtained on cilia (including "ciliary granule plaques") also contained Ca, P and S. Cells contain osmiophilic "calcium-storing vacuoles" which were selectively rich in Ca and S but devoid of P.

Animals↗
PubMed1975

Passive transfer of experimental autoimmune myasthenia by lymph node cells in inbred guinea pigs.

Passive transfer of experimental autoimmune myasthenia (EAM) was performed with lymph node cells from donor guinea pigs immunized with purified acetylcholine receptor (AChR) from Torpedo californica. Recipient animals revealed the same clinical signs and electromyographic patterns as observed in actively challenged animals. These phenomena are parallel to the clinical manifestations of the human disease myasthenia gravis, in which cellular response to AChR was recently demonstrated.

Acetylcholine↗
PubMed1975

Humoral antibodies to acetylcholine receptor in patients with myasthenia gravis.

Sera from patients with myasthenia gravis (M.G.) were studied by the quantitative micro-scale complement-fixation assay for the presence of humoral antibodies against acetylcholine receptor (AChR). The purified receptor was extracted from the electrogenic tissue of the electric ray, Torpedo californica. A significant difference in the antibody titres was observed between myasthenic and non-myasthenic patients. Out of fifteen patients with myasthenia gravis, at least 12 (80%) had antibodies against AChR. Only one case out of twenty-four controls had an indication of anti-receptor antibodies. In view of observations on the role of AChR as the autoantigen in myasthenia gravis, such antibodies may have significance in producing the neuro-muscular block characteristic of the disease.

Acetylcholine↗
PubMed1975

Myasthenia gravis and acetylcholine receptor. Effect of steroids in clinical course and cellular immune response to acetylcholine receptor.

Lymphocytes from patients with myasthenia gravis (MG) were transformed when cultured in vitro with an acetylcholine receptor fraction extracted from the electric organ of an electric eel. Marked diminution of the cellular response to acetylcholine was shown in patients who improved clinically with prednisone treatment. The transient clinical deterioration during the first days of prednisone treatment was accompanied by a transient increase in lymphocyte response. These findings that an in vivo sensitization of lymphocytes to self-acetylcholine receptor may occur in MG, and that a cell-mediated autoimmune mechanism may be important in the pathogenesis of the neuromuscular block. The present observations indicate that prednisone provides a measure of immunosuppression in MG. The transient clinical deterioration during the first days of prednisone therapy may reflect an enhancement of cell reactivity by this drug.

Acetylcholine↗
PubMed1975

The effect of the thymus-independent antigens, collagen and synthetic collagen-like polypeptide, on the requirement of cell cooperation in the immune response to thymus-dependent antigens.

The effect of thymus-independent antigens on the need for cell cooperation in the immune response to thymus-dependent antigens was investigated. Irradiated recipient mice transplanted with either bone marrow cells or a mixture of bone marrow and thymus cells, were immunized with the thymus-independent antigen (Pro-Gly-Pro)n covalently conjugated to the thymus-dependent ovalbumin, or with a mixture of (Pro-Gly-Pro)n and ovalbumin. In both cases an effective response towards ovalbumin was observed in the absence of thymus cells as was found for the thymus-independent (Pro-Gly-Pro)n. The same effect on ovalbumin was demonstrated when a mixture of the thymus-independent collagen and ovalbumin was used for immunization. On the other hand, when irradiated reconstituted mice were immunized with a mixture of ovalbumin and the thymus-dependent gelatin, which is the denatured product of collagen, cell-to-cell cooperation was required for an immune response to both immunogens. The effect of (Pro-Gly-Pro)n and collagen on the response to the thymus-dependent ovalbumin in vivo was observed in in vitro experiments using sheep red blood cells (SRBC) as the immunogen as well. In the presence of reduced and carboxymethylated (RCM) Ascaris collagen and (Pro-Gly-Pro)n, nude spleen cells could produce significant numbers of plaque-forming cells towards SRBC. Thus, (Pro-Gly-Pro)n and collagen can deliver the signal required to stimulate B cells to produce antibody towards thymus-dependent antigens in the absence of T cells. In contrast to the results with (Pro-Gly-Pro)n and collagen, the thymus-independent synthetic polypeptide poly(DTyr, DGlu-)-poly(DPro)--poly(DLys) did not affect the requirement for cell cooperation of the thymus-dependent immunogens, ovalbumin and SRCB. It thus appears that the ability to substitute for T cells for antibody production towards thymus-dependent immunogens is not a general characteristic of thymus-independent antigens.

Animals↗
PubMed1975

Differential cytotoxic acitivity of anticollagen serum on rat osteoblasts and fibroblasts in tissue culture.

Rat skin fibroblasts grown in tissue culture were lysed by anti-rat-tail collagen serum and antibodies to the ordered collagen-like synthetic polymer (Pro-Gly-Pro)-n. This cytotoxic effect is complement-dependent and occurs only if the fibroblasts were pretreated with trypsin. These anti-sera have very little cytotoxicity on cultured rat osteoblasts. This differential cytotoxicity is not due to differential binding of anticollagen serum to the cells. Both osteoblasts and skin fibroblasts bind the anticollagen serum as was demonstrated by fluorescent immunoglobulin.

Animals↗
PubMed1975

Immunological relationship between acetylcholine receptor and thymus: a possible significance in myasthenia gravis.

A defined immunological cross-reaction was observed between acetylcholine receptor fraction from the electric eel, Electrophorus electricus, and two calf thymus fractions. The cross-reaction was demonstrated on the cellular level by means of the lymphocyte transformation technique, and on the humoral level, by means of the microcomplement fixation assay. In the human disease myasthenia gravis both acetylcholine receptor at the neuromuscular junction and the thymus are affected, probably by an autoimmune mechanism. The immunological cross-reaction between acetylcholine receptor and thymic components may explain the association between endplate and thymus disorders in myasthenia gravis.

Acetylcholine↗
PubMed1975

The nature of murine immune response to nucleic acids.

The antibody response of mice to nucleic acids appears to be genetically regulated, and may show varying patterns. SJL/J mice and AKR/Cu mice are high responders to denatured DNA complexed with MBSA and produce 7S as well as 19S antibodies. DBA/2 mice respond with low titers to this immunogen which consists of 19S antibody exclusively. C57BL/6 mice are high responders to denatured DNA, but produce only 19S antibodies. Denatured DNA-MBSA is immunogenic when injected without complete Freund's adjuvant, thereby suggesting that this antigen might be thymus independent. The pattern of immune responses of some strains to the polyribonucleotides poly(I)-poly(C) and poly(A)-poly(U) is opposite to that observed with denatured DNA. Thus, DBA/2 mice are high responders and SJL/J mice are low responders. However, the low responders SJL/J mice produce 7S as well as 19S antibody which suggests that different mechanisms operate for the regulation of immune responses to the two types of nucleic acids. Whereas no antibody is elicited upon immunization with DNA in the absence of a carrier protein, poly(A)-poly(U) and poly(I)-poly(C) are immunogenic when injected without MBSA. Immunization with complexes of the polyribonucleotides and MBSA enhanced the responses to these immunogens; however, the strain differences were not completely abolished. Poly(A)-poly(U) did not enhance the low immune responses of DBA/2 mice to denatured DNA when injected i.v. following immunization with the DNA-MBSA. However, simultaneous immunization of DBA/2 and SJL/J mice with poly(A)-poly(U) and denatured DNA-MBSA resulted in high antibody titers to both immunogens in either mouse strain.

Animals↗