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Biomedical subjects

C C Bernard

Publications and source records attributed to C C Bernard.

At least 109 records · Page 6Linked to original sources
PubMed1983

Immunopathology of murine experimental allergic orchitis.

Experimental allergic orchitis (EAO) was induced consistently in BALB/c mice by immunization with homologous testicular tissue homogenate emulsified in complete Freund's adjuvant (CFA) providing that the animals had received simultaneously at least 1 microgram of an extract of Bordetella pertussis rich in pertussigen. All animals thus treated developed orchitis and serum antibody to testicular antigens within 20 days after immunization. The lesions were located in testis (100%), rete testis (37%), cauda epididymis (21%), and vas deferens (37%). Ductus efferentes and caput epididymis were only rarely affected. Early lesions in the seminiferous tubules were characterized by peritubular and/or intratubular accumulation of eosinophils, neutrophils, lymphocytes, and macrophages. This was followed by aspermatogenesis. Late lesions included massive necrosis and extensive fibrosis of the seminiferous tubules. Disruption of blood-testis barrier on day 20 was evidenced by the detection of 1) perfused lanthanum deposits between Sertoli cells and surrounding inflammatory cells inside the seminiferous tubules, 2) deposits of endogenous mouse IgG in germinal epithelium, and 3) probable immune complexes (granular C3) surrounding seminiferous tubules. Murine EAO differed from that of the guinea pig in the lack of involvement of the ductus efferentes, the extensive necrosis, the abundant polymorphonuclear eosinophils in the lesion, and the exquisite requirement of concomitant injection of B. pertussis extract.

Animals↗
PubMed1982

Experimental autoimmune encephalomyelitis. An anatomically-based explanation of clinical progression in rodents.

Lactate accumulation was measured soon after decapitation in three adjacent lower spinal cord regions of rats with EAE. Results indicate that during EAE, and in correlation with the onset of clinical signs of both initial attack and short-term relapse, a differential focal increase in lactate accumulation occurs in rat spinal cord compared to Freund's Complete Adjuvant controls, with greater increase occurring in more caudal segments. A [14C]antipyrine method of estimating relative spinal cord blood flow failed to find evidence that the lactate accumulations were due to focal ischemia. Subsequent measurement of isotopic water and total protein increases in the same cord regions indicated that a slight but significant increase in vasogenic edema occurs in correlation with the increase in lactate accumulation and the onset of EAE clinical signs. The data are interpreted as lending support to a speculative theory of paralysis induced by edema during EAE, in which nerve root endoneurium is postulated as the functionally vulnerable site. More specifically, it is hypothesized that the ascending progression of clinical signs of EAE in rodents can be explained on an anatomical basis by progressive disturbance of the nodes of Ranvier in nerve root myelinated fibers.

Animals↗
PubMed1982

Gm allotypes and multiple sclerosis.

Immunoglobulin allotypes (Gm) were analysed in 40 multiple sclerosis (MS) patients and the distribution of phenotypes compared to that in 1220 healthy controls. The frequencies of GM(1) and Gm(1, 2) are significantly increased inthe patients suggesting that the presence of the Gm3;5, 13, 14 haplotype confers a resistance to the development of MS.

Female↗
PubMed1981

Hind-limb motor ability in Lewis rats during the onset and recovery phases of experimental autoimmune encephalomyelitis.

Hind-limb motor function in adult female Lewis rats with experimental autoimmune encephalomyelitis (EAE) was investigated using an objective behavioral measurement of motor ability. Rats were pretrained to avoid falling from the external surface of a power-driven running wheel. The performance of EAE-group rats on the wheel was then compared with that of saline and adjuvant controls immediately prior to the onset of clinical signs of EAE, and within 3 days of apparent recovery from EAE. Results indicate no apparent hind-limb motor deficit in the absence of overt clinical signs of EAE, despite histological evidence of severe inflammatory lesions persisting in the central nervous system (CNS) at the time of the post-recovery test. The remarkably transient nature of motor impairment is discussed within the context of a continuing search for the underlying cause(s) of clinical signs of EAE.

Animals↗
PubMed1981

Genetic control of T helper cell function in the clawed toad Xenopus laevis.

The genetic control of the collaboration between Xenopus T and B cells has been analyzed in vivo using cells from five strains of major histocompatibility complex-defined Xenopus. When carrier (fowl gamma-globulin)-primed T cells and hapten (dinitrophenylated keyhole limpet hemocyanin)-primed B cells differed by minor histocompatibility antigens or by only one haplotype of the major histocompatibility complex, the collaboration was efficient in the sense that large numbers of plaques, low-molecular weight antibodies and high-affinity IgM antibodies could be recorded in the cultures challenged with dinitrophenylated fowl gamma-globulin. However, when T and B cells differed at both alleles of the major histocompatibility complex, lower numbers of plaques were obtained, no low-molecular weight anti-hapten antibodies could be detected, and the IgM antibodies that were sometimes synthesized were of low affinity. This suggests that the major histocompatibility complex, or a gene linked with it, affects the collaboration between Xenopus T and B cells in a way perhaps similar to that described in mammals.

Animals↗
PubMed1981

Antibody to myelin basic protein in extracts of multiple sclerosis brain.

Autoimmunity to a neural antigen is a suspected cause of multiple sclerosis (MS), and a candidate autoantigen is myelin basic protein (MBP). Accordingly, saline extracts of brain from patients with MS and other diseases were prepared and the content of immunoglobulin (Ig) determined. Antibody to MBP was measured with a highly-sensitive solid-phase radioimmunoassay using 125I-staphylococcal Protein A. Anti-MBP activity was detected in brain extracts of all eleven MS patients, and in seven out of the eight brain extracts from the patients with other diseases; however the level of anti-MBP activity was significantly higher in the MS extracts (P less than 0.01). Analysis of the MS brain extracts after purification by affinity chromatography columns revealed that the anti-MBP activity was specifically mediated by IgG and resided in the IgG1, IgG2, and/or IgG4 subclasses.

Adult↗
PubMed1980

In vitro evidence for T-B lymphocyte collaboration in the clawed toad, Xenopus.

Requirements for an in vitro secondary antibody response to the soluble antigens dinitrophenylated keyhole limpet hemocyanin and dinitrophenylated flow gamma-globulin are described for the clawed toad, Xenopus. Priming of both hapten and carrier-specific cells is required in order to obtain good responses to the hapten. The carrier-reactive ("helper") cells do not adhere to nylon wool, are X ray-resistant and surface Ig-negative. The cell adherence and X ray sensitivity characteristics of these Xenopus "T" cells and their ability to generate a mixed lymphocyte response, allogeneic cytotoxic and helper activities, are identical to those of thymus-derived (T) cells in higher vertebrates. The hapten-reactive, antibody-secreting cell precursors are nylon-adherent, X ray-sensitive and surface Ig-positive. In the absence of other distinguishing serological markers for T cells in frogs, and considering the thymus dependency of the helper activity described here, the evidence presented is interpreted as demonstrating the requirement for antigen-specific T-B cell cooperation in response to soluble protein antigens in vitro for Xenopus.

Animals↗
PubMed1980

Active suppression of the allogeneic histocompatibility reactions during the metamorphosis of the clawed toad Xenopus.

Metamorphosis is a privileged period for the induction of tolerance to allografts. Transfer of lymphocytes from metamorphosing Xenopus into isogenic adults prevented the rejection of a skin graft differing from the adult host by minor histocompatibility antigens. This implies that active suppression is involved at one step of the induction of tolerance to the self-antigens that differentiate at the time of metamorphosis. The reciprocal experiments of preventing tolerance induction by transfer of normal adult cells into metamorphosing animals failed. However, passive transfer of anti-graft immunity in tolerant animals was partially observed, provided that a transfer of primed cells was done simultaneously with the challenging graft. Thus, memory cells are not as sensitive to the suppression as are the cells that respond in a first set reaction.

Animals↗
PubMed1979

Ontogeny of immunity in amphibians: changes in antibody repertoires and appearance of adult major histocompatibility antigens in Xenopus.

Larval Xenopus anti-2,4-dinitrophenyl antibodies of the low-molecular weight type can be analyzed by isoelectric focusing (IEF). Within a clone of genetically identical animals, tadpoles make antibodies whose IEF spectrotypes are shared by most of the individuals. Adults of the same clone also make antibodies of identical spectrotype, but the adult pattern can be very different from the larval one, although both responses are heterogeneous. The larval spectrotypes that one cannot see in a primary adult response can be found if the adult has been primed during larval life and boosted after metamorphosis. The heterogeneity of the response is somewhat lower in tadpoles (up to 12 antibody IEF bands) than in adults (up to 20 antibody IEF bands). The change in the repertoire occurs during metamorphosis at the time of the appearance of two major histocompatibility complex antigens. One, a lymphocyte antigen, appears 10-15 days before the end of metamorphosis, the other, present on red cells (and presumably also on lymphocytes), appears 1.5 month after the end of metamorphosis, as determined by immunofluorescence analysis. During the same period, the syngeneic mixed leukocyte reaction switches from a larval anti-adult to an adult anti-larval reaction.

Animals↗
PubMed1979

The New York City-HIP contract.

With the signing of a contract not to exceed $25 million, the Health Insurance Plan of New York (HIP) and the City of New York applied the concept of the Health Maintenance Organization (HMO) on a scale never before attempted. Beginning in January 1978, as many as 100,000 Medicaid eligible individuals and families were enrolled in a prepaid group medical plan as participants in an experiment whose success or failure depended largely upon the City health system's ability to adapt to change. It also depended upon the support of the major health interests in this unique effort at rational, systemwide health planning.

Health Maintenance Organizations↗
PubMed1978

A search for the "multiple sclerosis virus"--lack of effect of brain extracts on myelin development in chickens, mice and rats.

Attempts were made to transmit possible infectious agents from tissue of MS patients into three animal species, under conditions designed to enhance the development of such an agent. Myelination was monitored by measuring CNPase activity and myelin basic protein. Although no significant effects were observed, the usefulness of a new assay for CNPase was demonstrated. Nude mice were found to have a lower level of CNPase than their heterozygous littermates.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1978

Localization of genetic control in mice over response to liver-specific F antigen.

Antibody production to the liver-specific F antigen was tested in recombinant strains of mice of different H-2 types to determine whether a histocompatibility-linked immune response (Ir) gene controlled responsiveness to this antigen. Responseiveness was found to be controlled by an Ir gene located in the K end (K and/or I-A subregions) of the H-2 complex.

Animals↗
PubMed1978

Experimental autoimmune orchitis in T-cell-deficient mice.

Experimental autoimmune orchitis (EAO) was induced in inbred strains of mice by injection of mouse testis homogenate (MTH) in Freund's complete adjuvant with pertussis vaccine. Although all mice injected with MTH and adjuvants developed signs of EAO, there were marked strain variations in susceptibility to EAO suggesting that genetic factors may be involved in the response to antigen or to adjuvants. Studies in hypothymic BALB/c. nu/nu mice indicated that a source of T cell was required for induction of EAO. Thus BALB/c. nu/nu mice were not able to develop EAO, despite adequate orchitogenic challenge; reconstitution of nu/nu mice with syngeneic thymocytes completely restored the capacity of such mice to develop orchitis. Transfer of EAO was effected in nu/nu mice with lymphoid cells from appropriately immunized donors but not with immune serum. However, both T cells and antibodies may be necessary in the effector stages of the disease since the capacity of lymphoid cells to transfer EAO was only partially inhibited by anti-Thy-1.2 treatment.

Animals↗
PubMed1977

Binding properties of radiolabeled basic protein of myelin: reassessment in relation to diagnostic immunoassays.

The binding of radioiodinated basic protein of myelin ([125I]BPM) to a sheep lymphocyte cell pellet, sheep erythrocytes, and cell-free tubes used in the assay was investigated as a possible diagnostic procedure in multiple sclerosis. [125I]BPM apparently bound to 5 x 10(6) sheep lymphocytes incrementally with no plateau, up to 300 ng, and also to sheep erythrocytes; when cells were transferred to fresh tubes, over 90% of the radioactivity remained on the original tube, regardless of the tube surface. Various substances, including BPM and unrelated basic proteins, competitively inhibited the binding of basic protein of myelin to sheep cells and assay tubes. Binding was inhibited by sera from patients with multiple sclerosis, but equally so by normal sera. The large capacity of BPM to bind nonspecifically could limit its use in the above type of binding assay and would need to be allowed for in conventional radioimmunoassays.

Erythrocytes↗
PubMed1977

Experimental autoimmune encephalomyelitis in mice: antigen binding lymphocytes to basic protein of myelin in susceptible and resistant strains.

Antigen-binding lymphocytes (ABL) to basic protein of myelin (BPM) were demonstrable in the thymus and spleen of various strains of mice. Counts of ABL did not differ in strains resistant and susceptible to EAE, and did not differ when human or murine 125I-labelled BPM was used as a labelled antigen to detect ABL. After injection with mouse spinal cord and adjuvants, under conditions known to be immunogenic and encephalitogenic for susceptible strains of mice, counts of ABL increased two- to four-fold in suceptible strains but did not icnrease in resistant strains. Antigen binding could not be accounted for by the attachment to cells of cytophilic antibody with specificity for BPM, because such antibody was seldom demonstrable even after immunization. Inferences from the study were: (i) that tolerate (non-responsiveness) to certain autoantigens at least must depend on control over continually present antigen-reactive lymphocytes rather than on any lack of capacity to recognize antigen; (ii) differences in susceptible and resistant strains are evident after, rather than before, immunization.

Animals↗
PubMed1977

Anti-T cell activity of niridazole in experimental autoimmune encephalomyelitis.

The antischistosomal drug niridazole, known to selectively depress cell-mediated immune function, was assessed in experimental autoimmune encephalomyelitis (EAE) in mice. EAE results from an immune attack by activated T lymphocytes on the central nervous system. Niridazole given orally at a dose of 100 mg/kg body weight three times a week and starting either before or after immunization caused a significant suppression of signs and histological lesions of EAE, lasting up to ten weeks after cessation of treatment. There was no effect of niridazole on either release of macrophage migration inhibition factor in response to specific neural antigen, production of antibody, or on the nonspecific inflammatory reaction to adjuvant. Niridazole presumably acts by preventing release of lymphokines by activated T cells after contact with antigens.

Animals↗