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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A hyperacute form of experimental autoimmune encephalomyelitis (HEAE) was induced in Lewis rats using small doses (3.2 mug) of guinea pig myelin basic protein as immunogen and B. pertussis vaccine as adjuvant. Myelin basic proteins from species other than guinea pig (rat, man, monkey, pig, ox, rabbit and sheep) induced only ordinary EAE with this adjuvant. HEAE was more readily distinguished from ordinary EAE by clinical criteria (early onset, with a rapid and severe course, and high incidence of cerebral signs and mortality) than by histologic signs which, although characteristic of HEAE. were not pathognomonic for HEAE, HEAE was transferred to x-irradiated syngeneic recipient rats with lymph node cells from appropriately immunized donors. The Brown Norway (BN) strain of rat was found susceptible to induction of ordinary EAE, but not HEAE, using large doses of either rat or guinea pig myelin basic proteins. The unique immunogenicity of the guinea pig basic protein must be due to a different antigenic determinant from the determinant(s) which is shared by rat and guinea pig myelin basic proteins and which without B. pertussis induces ordinary EAE. The adjuvant action of B. pertussis in inducing HEAE in the Lewis rat is most likely mediated through an immunocompetent T lymphocyte.
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PMID:Antigen, host and adjuvant requirements for induction of hyperacute experimental autoimmune encephalomyelitis. 6 74

Several parameters of the in vitro lymphocyte proliferative response to myelin basic protein (BP) in Lewis (Le) and Brown Norway (BN) rats were examined. The results demonstrate that BN rats, a strain normally resistant to BP-induced experimental allergic encephalomyelitis, and Le rats, a strain readily susceptible to the disease, have similar patterns of the proliferative response to BP. An important difference, however, is that BN lymphocytes, although responding significantly to BP, are unable to proliferate to the same level as Le lymphocytes. In experiments measuring the lymphocyte response as a function of antigenic stimulus, days of culture, or type of adjuvant used, the BN rat peak response was in general 70% or less of the Le rat peak response. Furthermore, the BN lymphocyte response was reduced when B cells were removed whereas there was no effect in the Le rat. A negative feedback mechanism, possibly suppressor cells, has been suggested to explain these differences.
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PMID:Kinetics of the in vitro lymphocyte response to myelin basic protein in the the Lewis and Brown Norway strains of rat. 7 6

Brown Norway (BN) rats are much less susceptible to experimental allergic encephalomyelitis (EAE) than Lewis rats. Nevertheless, BN rats developed severe EAE, even paralysis, when immunized with rat spinal cord and carbonyl iron adjuvant. Complete Freund's adjuvant (CFA) was much less effective. The use of both CFA and pertussis vaccine with rat cord was moderately, but not consistently, effective. Guinea pig spinal cord was weakly encephalitogenic to BN rats with all adjuvant combinations. We were not able to produce EAE in BN rats with purified myelin basic protein from either rat or guinea pig. Inoculations directly into lymph nodes or into the blood stream proved that the low susceptibility of BN rats was not due to lack of absorption from the site of inoculation, but may be related to peculiarities of processing antigen in draining lymph nodes. The severity of EAE in F1 hybrids was intermediate between the BN and Lewis parental strains when tested with an immunizing procedure of appropriate strength. The fact that F1 hybrids were less reactive than Lewis mandates modification of the theory that susceptibility to EAE is inherited through a single autosomal dominant gene.
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PMID:Allergic encephalomyelitis in the reputedly resistant Brown Norway strain of rats. 112 Sep 1

Nervous tissue expression of immunological signal and recognition molecules, as well as lymphoid tissue immune responses after facial nerve trauma was studied in male rats of the Lewis and Brown Norway (BN) strains. In both rat strains nerve transection caused within four days the appearance of IFN-gamma-like immunoreactivity in the cytoplasm of axotomized motor neurons and an induction of MHC class I and II, and CD4 molecules on surrounding glial cells to a similar extent. T lymphocytes also infiltrated the facial nuclei ipsilateral to the axotomy in all animals. The number of autoreactive T cells in superficial cervical lymph nodes, which in response to whole myelin or peptides of myelin basic protein (MBP) secreted IFN-gamma increased markedly after axotomy. This response was more conspicuous in Lewis rats, which are susceptible to experimental allergic encephalomyelitis (EAE), than in BN rats, which are EAE resistant. A proportion of the axotomized Lewis rats also developed widespread perivascular infiltration of mononuclear cells in the CNS, reminiscent of EAE. Hypothetically, a strong expansion of myelin autoreactive IFN-gamma producing T cells secondary to nerve trauma may have immunopathological consequences in genetically predisposed individuals. It is also possible that myelin reactive T cells, whether recruited to the lesioned nerve, could have impact on macrophage function during Wallerian degeneration in the distal stump.
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PMID:Facial nerve transection causes expansion of myelin autoreactive T cells in regional lymph nodes and T cell homing to the facial nucleus. 128 78

Fischer 344 rats, immunized with the synthetic encephalitogenic myelin basic protein peptide YS49 (YGSLPQKAQRPQDENG), produced heteroclitic antibodies that reacted much more extensively and with a much higher affinity with the cross-reacting encephalitogenic guinea pig sequence S49S (GSLPQKSQRSQDENG) than they did with the immunogenic YS49. On the other hand, antisera against S49S reacted in a normal manner with homologous S49S and cross-reacted only poorly with YS49. The phenomenon of heteroclisis in Fischer 344 rats correlated with the greater encephalitogenic potency of the cross-reacting entity. Kibler et al. (J. Exp. Med., 146 (1977) 1323-1331), by comparing the encephalitogenic guinea pig sequence to a less potent analog, had also previously observed what now would be termed a heteroclitic phenomenon at the T cell level in Lewis rats. In their hands, however, as well as in ours Lewis rat antisera against the encephalitogenic peptide region were much too complex to be analyzed with respect to heteroclisis. It was shown in the present experiments that by utilizing the Fischer 344 system one may also readily obtain heteroclisis at the B cell level against encephalitogenic peptides. Neither YS49 nor S49S as immunogen produced detectable antibody in Brown Norway (BN) rats with exception of two immunized with YS49. In those two cases heteroclitic antibodies were obtained that had a very low significant (greater than 3 SD above baseline) antigen binding capacity for S49S and no detectable reactivity for the homologous YS49 ligand.
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PMID:Heteroclitic antibodies in Fischer 344 rats to a synthetic encephalitogenic myelin basic protein peptide. 242 34

Lewis and Brown Norway rats were infected at different ages with the neurotropic murine coronavirus strain, JHM and the resultant central nervous system diseases were studied. Suckling rats of both strains came down with a fatal, acute encephalomyelitis. Weanling Lewis rats developed a subacute demyelinating encephalomyelitis which neuropathologically revealed changes of an immunopathologic reaction. In contrast, Brown Norway rats developed a clinically silent subacute demyelinating encephalomyelitis with a persistent JHM virus infection which was less severe and quite different from the subacute demyelinating encephalomyelitis in Lewis rats with respect to size, distribution, and localization of the demyelinating plaques as well as the type of infiltrating cells. In addition, infected Lewis rats showed a pronounced lymphocyte proliferation to myelin basic protein and JHM virus whereas lymphocytes from infected Brown Norway rats did not react to these two antigens. These observations demonstrate the pathogenetic importance of host factors in the development of virus-induced demyelination.
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PMID:Comparative analysis of coronavirus JHM-induced demyelinating encephalomyelitis in Lewis and Brown Norway rats. 244 66

Experimental allergic encephalomyelitis (EAE)-susceptible Lew and EAE-resistant Brown Norway (BN) rats and the corresponding MHC congenic strains were examined for their ability to develop clinical and histologic EAE. The ability of T cells from these animals to proliferate in vitro in response to whole guinea pig (GP) myelin basic protein (MBP), rat MBP, and to the major encephalitogenic peptide of GP MBP 66-88 (GP 68-88) was also assessed. We found that Lewis (Lew) was highly susceptible and showed good T cell responses to GP, MBP, rat MBP, and GP 68-88. Lew.1N (BN MHC on Lew background) and BN were not susceptible and T cells from these strains showed significant responses to GP MBP, but not to rat MBP or GP 68-88. Although BN.B1 (Lew MHC on BN background) was not susceptible to actively induced EAE, MBP-specific Lew T cells could transfer severe disease to BN.B1. BN.B1 T cells showed responses to GP-MBP, rat MBP, and GP 68-88 and, when transferred to naive BN.B1 or Lew, induced only mild clinical EAE in both strains. Increasing the number of T cells from BN.B1 had no effect on the severity of clinical symptoms in either recipient, suggesting some deficiency in the T cell repertoire that is necessary for induction of severe EAE. These results suggest that 1) the T cell response to rat MBP and GP68-88 (but not to sites other than 68-88 in GP MBP) is necessary for susceptibility to EAE; 2) the ability to respond to both rat MBP and GP 68-88 is determined by the MHC gene products on APC; and 3) given a permissive MHC, the T cell response that results in EAE is influenced by non-MHC genes.
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PMID:Genetic control of the development of experimental allergic encephalomyelitis in rats. Separation of MHC and non-MHC gene effects. 245 18

Conjugates of horseradish peroxidase with myelin basic protein (BP) of guinea pig or Lewis rat were used to identify antibody-containing cells in draining lymph nodes during experimental allergic encephalomyelitis (EAE). Peroxidase activity was revealed for light and electron microscopic preparations with the diaminobenzidine reaction of Graham and Karnovsky. Basic proteins (BP) were also iodinated with (125)I for determination of circulating antibody against BP by radio-immunoassay of (125)I BP using coprecipitation with antirat IgG or with antirat serum proteins. Encephalitogenicity was lost after conjugation of guinea pig BP or Lewis rat BP with peroxidase, whereas iodination did not affect the encephalitogenicity of guinea pig or Lewis rat BPs. EAE was induced in Lewis rats with guinea pig or Lewis rat spinal cord BPs in complete Freund's adjuvant. Draining lymph nodes were studied by light and electron microscopy during the course of the immune reaction, and cells with specific antibody against BP were identified with the use of BP-horseradish peroxidase conjugates. Lymph node sections from animals immunized with high antigen doses (500 mug) showed numerous plasma cells with intracellular antibody against BP in medullary cords 10 days after immunization and 4 days prior to histologic appearance of EAE. Numbers of positive cells correlated with levels of circulating antibody against BP. Immunization with a low antigen dose (5 mug) resulted in EAE, few or no antibody-containing cells, and significantly lower levels of circulating antibody. Brown Norwegian rats, a strain resistant to EAE, immunized with 500 mug of BP had positive cells in draining lymph nodes and high levels of circulating antibody against BP in the absence of histologic evidence of EAE. Lewis rats injected with Lewis rat small BP failed to develop EAE. Nevertheless, these animals showed levels of circulating antibody and antibody-containing cells similar to those of animals which developed EAE after injection of the mixture of Lewis rat large and small BP. It is concluded that although the BP-peroxidase labeling method reveals cells with specific anti-BP antibody, these cells are probably unrelated to EAE. The lack of correlation between EAE induced by low antigen doses and levels of circulating anti-BP antibody (determined with the use of highly encephalitogenic (125)I-BP) suggests that effector cells can be stimulated at low antigen doses, but higher antigen doses are required to induce the production of levels of circulating antibody detectable by the method of immune coprecipitation.
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PMID:The significance of circulating and cell-bound antibodies in experimental allergic encephalomyelitis. 454 31

Silicone, previously thought to be a biologically inert and harmless material, has now been reported to elicit antibody response and to be responsible for adjuvant disease in humans. The present study was designed to evaluate the immune function of forty individuals who had undergone silicone breast augmentation for a period of longer than ten years and who were compared with 40 sex and age-matched controls. The following immunological functions were studied: lymphocyte subset analysis, lymphocyte mitogenic response, NK cytotoxic activity and markers for autoimmunity such as ANA, rheumatoid factor immune complexes such as smooth muscle, myelin, and thyroid, and tissue antibodies. Results of lymphocyte subpopulation analysis showed significantly elevated T helper/suppressor ratio in 60% and significantly decreased T helper/suppressor ratio in 7.5% of the silicone implant group, while the control group showed increased helper/suppressor ratio only in 10% of tested individuals and no significant decrease in the T helper/suppressor ratio. There was 20% inhibition in T cell mitogenic responses in the silicone implant group, which is significant when compared to the controls. When NK cytotoxic activity was compared between the two groups, significant inhibition in the ability of lymphocytes to kill tumor target cells was observed in the silicone implant group. This inability of target cell lysis was attributed to the demonstrated lack of granularity of NK cells from the silicone implant group. There was significant increase in: immune complexes, anti-nuclear antibodies, anti-thyroid antibodies, anti-striated muscle cell antibody, and anti-myelin basic protein antibodies. These immunological abnormalities in individuals who underwent silicone breast augmentation indicate a mechanism of tissue injury to these patients, causing autoimmune diseases or syndromes. Since autoimmunity in some other conditions is associated with abnormalities in the HLA serotyping system, and since some collagen vascular diseases have been associated with a higher incidence of the HLA serotyping system, it is recommended that HLA studies be included in future investigations of immune-mediated abnormalities associated with silicone breast augmentation. Our findings here show definite abnormalities of the T helper/suppressor ratio, increased autoimmunity, as well as increased production of immune complexes. Silicone implants have been used in cosmetic and reconstructive surgery more than 30 years (Brown et al., 1960). The gel used in the implant is produced from silicone, which is then related with methyl chloride and polymerized to form stable polydimethylsiloxane (Brown, et al., 1960). There have been a number of reports describing the occurrence of connective tissue disease in patients after the implantation of silicone.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immune functional impairment in patients with clinical abnormalities and silicone breast implants. 757 Jun 22

Myelin basic protein (MBP) is a major protein of central nervous system myelin which can induce experimental autoimmune encephalomyelitis (EAE) in susceptible laboratory animals. The role of T cells in the induction of EAE has been extensively studied, but the antibody response to MBP has not been well characterized. In the present work, we immunized rats with encephalitogenic guinea-pig MBP and mapped autoreactive antibodies binding to peptides in the rat MBP sequence. We studied the responses of the Lewis rat strain, susceptible to EAE, and the responses of the Fischer and Brown-Norway (BN) rats, resistant to EAE. We found that Lewis rats immunized to guinea-pig MBP develop antibodies to a diversity of MBP epitopes with a dominance of MBP peptide p11-30 and peptides in the 71-140 region. Fischer rats showed a similar pattern of antibody specificities, but with higher titers than the Lewis rats. BN rats, in contrast, developed a very low titer of antibodies and lacked a response to p11-30. Thus, there is no clear correlation between the nature of the anti-MBP antibody response and the state of susceptibility or resistance to EAE induction in the different rat strains.
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PMID:Diversity of the B cell repertoire to myelin basic protein in rat strains susceptible and resistant to EAE. 1002 18


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