UMLS:C0043167 - FACTA Search

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Query: UMLS:C0043167 (pertussis)
19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in vivo effects of intravenous administration of alloantisera directed to I-J subregion coded determinants were investigated. In confirmation and extension of our previous results, anti-I-Jk [B10.A(3R) anti-B10.A(5R)] and anti-I-Js ([B10.A(3R) X B10.S(9R)]F1 anti-B10.HTT) antisera, when administered in 1 to 10 microliter amounts at the time of immunization, led to twofold increases in the IgM and IgG plaque-forming cells (PFC) responses to suboptimal doses of sheep erythrocytes in A/J (I-Jk) and SJL (I-Js) mice, respectively. To assess whether this immunopotentiation was due to a decrease in specific suppression, experiments were carried out using the polypeptide antigens random linear terpolymer of L-glutamic acid60, L-alanine30, and L-tyrosine10 (GAT) and random linear copolymer of L-glutamic acid50-L-tyrosine50 (GT), since administration of GAT to the nonresponder strain SJL, or GT to the nonresponder strain CBA fails to induce a primary PFC response and stimulates specific suppressor T cells able to prevent PFC responses to subsequent challenge with the immunogens GAT-methylated bovine serum albumin (MBSA) or GT-MBSA, respectively. The current study demonstrates that CBA (I-Jk) mice given 100 microgram GT in Maalox-pertussis adjuvant on day 0, and 10 microliter anti-I-Jk antiserum i.v. on days 0, 1, and 2, develop a significant primary specific PFC response on day 7. A similar responsiveness to 10 microgram GAT is found in SJL mice treated with 10 microliter anti-I-Js antiserum for 3 days. This same active anti-I-Js antiserum does not permit CBA mice to respond to GT, demonstrating the specificity of the anti-I-J effect. These data suggest that anti-I-J antiserum treatment at the time of antigen administration reduces suppressor responses to GAT or GT, permitting primary PFC responses. To directly demonstrate such an effect on suppressor activity, SJL or CBA mice treated, respectively, with GAT or GT to induce suppressor cells active on GAT-MBSA or GT-MBSA responses after adoptive transfer to normal syngeneic recipients were also given anti-I-J antisera (10 microliter/day) for 3 days, at which time their spleen cells were tested for suppressive activity upon transfer. Cells from such treated mice failed to show detectable suppressive activity upon transfer to syngeneic recipients challenged with GAT-MBSA or GT-MBSA, confirming the hypothesis of an in vivo effect of anti-I-J antiserum on suppressor activity.
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PMID:In vivo effects of anti-Ia alloantisera. I. Elimination of specific suppression by in vivo administration of antisera specific for I-J controlled determinants. 7 39

(Responder [R] X nonresponder [NR])F1 mice give indistinguishable primary in vitro plaque-forming cell (PFC) responses to either R or NR parental macrophages (Mphi) pulsed with the Ir-gene controlled antigen L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT). However, such (R X NR)F1 mice, if primed to GAT, retained in vitro responsiveness to GAT-R-Mphi, but no longer responded to GAT-NR-Mphi. This suggested (a) a possible Mphi-related locus for Ir gene activity in this model, and (b) the occurrence of active suppression after priming with GAT leading to a selective loss of the usual primary responsiveness of (R X NR)F1 mice to GAT-NR-Mphi. This latter interpretation was tested in the current study. [Responder C57BL/6 (H-2b) X nonresponder DBA/1 (H-2q)]F1 mice were primed with 100 microgram GAT in pertussis adjuvant. 4-8 wk later, spleen cells from such mice were tested alone or mixed with normal unprimed F1 spleen cells for PFC responses to GAT-R-Mphi and GAT-NR-Mphi. The primed cells failed to respond to GAT-NR-Mphi, and moreover, actively suppressed the normal response of unprimed F1 cells to GAT-NR-Mphi. If the primed spleen cell donor had been treated with 5 mg/kg cyclophosphamide 3 days before priming or with 5-10 microliter/day of an antiserum to the I-Jb subregion [B10.A(5R) anti B10.A(3R)] during the first 4 days postpriming (both procedures known to inhibit suppressor T-cell activity), cells from such mice responded in secondary culture to both GAT-R-Mphi and also GAT-NR-MPhi. In addition, such spleen cells no longer were capable of suppressing normal F1 cells in response to GAT-NR-Mphi. Similar data were obtained using [CBA (H-2k) X DBA/1 (H-2q)]F1. Further, it was shown that (a) primary responsiveness to GAT-NR-Mphi was not an artifact of in vitro Mphi pulsing, because in vivo GAT-pulsed Mphi showed the same activity and (b) the secondary restriction for Mphi-antigen presentation was controlled by H-2 linked genes. These data suggest an important role for suppressor T cells in H-2 restricted secondary PFC responses, and also provide additional support for the hypothesis that Ir-gene controlled differences in Mphi antigen presentation are related to both suppressor cell generation and overall responsiveness in the GAT model.
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PMID:The involvement of suppressor T cells in Ir gene regulation of secondary antibody responses of primed (responder X nonresponder)F1 mice to macrophage-bound L-glutamic acid60-L-alanine30-L-tyrosine. 10 25

Development of experimental allergic encephalomyelitis (EAE) in the SJL (H-2s) mice is associated with a T cell-dependent autoimmune response to the C-terminal part of the myelin basic protein (MBP). In this study the influence of both H-2 and non-H-2 genetic background on EAE induced with the MBP89-101 peptide is described. Analysis of different H-2q haplotype strains, B10G, B10Q, SWR and NFR/N, showed that the B10 background is relatively resistant to disease induction. Both SWR and NFR/N were susceptible to EAE showing that the H-2q haplotype is permissive for EAE development induced with MBP89-101 and that the T cell receptor (TcR) haplotype or complement C5 deficiency exert no significant influence on disease susceptibility. In a series of H-2-congenic strains on the B10 background only B10RIII (H-2r) mice were susceptible to EAE. The B10RIII mice developed a severe EAE with early onset and chronic progressive or relapsing course of disease. In addition, B10RIII mice treated with Freund's complete adjuvant and pertussis toxin alone showed an early monophasic disease. The clinical observations were confirmed by immunohistopathologic analysis of the central nervous system. In these studies, we also applied antibodies to different TcR V beta elements which showed no specific limitation of the used TcR among infiltrating T cells in the target tissue in any of the strains. It is concluded that an MBP peptide-specific disease can be induced in three different haplotypes and it is possible that shared structures between the As, Aq and Ar molecules are of importance for the trigger of encephalitogenic T cells with different TcR V elements. The presently described chronic EAE model induced in the B10RIII mice will be of value as a model for multiple sclerosis.
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PMID:Chronic experimental autoimmune encephalomyelitis induced by the 89-101 myelin basic protein peptide in B10RIII (H-2r) mice. 170 2

An EAU model has been developed in the mouse using the retinal soluble antigen (SAg), and the interphotoreceptor retinoid-binding protein (IRBP). Immunogenetic studies indicate that sensitivity to disease is H-2 dependent, but some data suggest that non-MHC genes may also contribute to the regulation of EAU. IRBP was a more potent uveitogen than SAg. Ability to mount lymphocyte and antibody responses was exhibited both by EAU-susceptible and by EAU-resistant strains, and could not be used as a predictive parameter. Dependence of disease induction on variables of immunization was studied in B10.A mice (I-Ak) immunized with IRBP. Use of Bordetella pertussis as additional adjuvant was a prerequisite for successful disease induction. Use of purified pertussis toxin (PTX), rather than a suspension of pertussis bacteria, allowed reduction of the immunization protocol to a single dose of IRBP in CFA. Severity and incidence of disease, as well as its clinical course, were directly affected by the dose of antigen and PTX, and could be controlled by varying their respective doses. A spectrum of disease, from hyperacute to chronic, could be obtained. The chronic type of EAU tended to relapse, with lesions reappearing after a brief period of essential quiescence. The special advantages of the murine EAU model for the study of ocular autoimmunity are discussed.
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PMID:The mouse as a model of experimental autoimmune uveoretinitis (EAU). 238 8

Experimental autoimmune uveoretinitis (EAU) in the mouse is a recently developed model of ocular autoimmunity. Dependence of disease induction on qualitative and quantitative parameters of immunization was studied in B10.A mice immunized with interphotoreceptor retinoid-binding protein (IRBP). It was found that use of Bordetella pertussis adjuvant as well as its mode of preparation was of critical importance for disease induction; no disease was induced if pertussis adjuvant was omitted. The minimal effective protocol for EAU induction when the vaccine form of B. pertussis adjuvant was used consisted of pretreatment with cyclophosphamide, two divided doses of IRBP in complete Freund's adjuvant (CFA), and two divided doses of B. pertussis vaccine. Any reduction in the immunization schedule resulted in reduced incidence of disease. In contrast, substituting purified B. pertussis toxin (PTX) for the vaccine allowed reduction of the immunization schedule to a single dose of IRBP in CFA and omission of the cyclophosphamide pretreatment. Severity and incidence of disease could be quantitatively controlled by varying the respective doses of IRBP and PTX. In addition, a chronic or an acute clinical course of EAU could be obtained by using either a low-dose or a high-dose immunization, respectively. Establishment of a single dose induction protocol and the quantitation of the immunopathogenic response as a function of the variables of immunization lay the foundation for the further development and utilization of this promising model of ocular autoimmunity.
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PMID:Experimental autoimmune uveoretinitis in mice. Induction by a single eliciting event and dependence on quantitative parameters of immunization. 239 17

T helper cells reactive to myelin basic protein are clearly implicated in the pathogenesis of murine EAE. We have developed a T cell line, BML-1 that (1) is reactive to the encephalitogenic amino terminal nonapeptide (1-9NAC) of MBP, (2) is I-Au restricted, and (3) induces relapsing EAE in B10.PL (H-2u) mice. Measurement of the lymphokine profile of BML-1 revealed secretion of IL-2, interferon-gamma and lymphotoxin but not IL-4. This profile is consistent with the Th1/DTH subtype. Coculture of BML-1 with MBP-primed B cells shows that BML-1 does not provide significant helper function in vitro. In addition, BML-1 secretion of interferon-gamma was found to inhibit LPS-induced anti-MBP antibody responses. This suggested that anti-MBP antibodies may not be necessary for induction of EAE. Sera from mice, in which severe disease was induced with the 1-9NAC peptide and Bordetella pertussis, showed no development of serum antibodies to MBP. These data show that MBP-reactive Th cells of the Th-1/DTH subtype can induce EAE and do not provide Th function for anti-MBP responses and that serum anti-MBP antibodies are not found in peptide 1-9NAC-induced disease. T cell lines specific for encephalitogenic epitopes and characterized for lymphokine secretion will provide a useful tool for understanding the role of T cells in the induction of EAE.
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PMID:Encephalitogenic T cells in the B10.PL model of experimental allergic encephalomyelitis (EAE) are of the Th-1 lymphokine subtype. 247

A mouse model for pertussis immunization encephalopathy has been described with features that closely resemble the severe adverse reactions occasionally seen after pertussis vaccine administration,m including seizures and a shock-like state leading to death. These reactions are produced with nearly one hundred percent efficiency provided that the mice immunized with Bordetella pertussis have 1) the appropriate major histocompatibility (H-2) genotype, 2) have been sensitized to bovine serum albumin (BSA), and 3) that the injected B. pertussis contained sufficient amounts of pertussis toxin. Antibody titres were measured in mice with haplotypes H-2d.s.k. that are highly susceptible to encephalopathy as well as in H-2b mice, that are totally resistant. Mice with H-2d.s.k. haplotypes were high responders to BSA, while H-2b (B10) mice were non-responders to BSA. Both H-2d and H-2b mice responded well to B. pertussis. Encephalopathy was induced in resistant H-2b mice with B. pertussis and passively administered anti-BSA antiserum, but not with B. pertussis and anti-(T,G)-A--L antibody. This indicated that B. pertussis and anti-BSA were absolutely required for development of encephalopathy. Encephalopathy could be induced in mice decomplemented with cobra venom factor and given BSA and B. pertussis. Several single-site mutants of B. pertussis affecting single virulence factors were induced with transposon Tn5. One of these mutants, BP357, deficient in pertussis toxin production, had a greatly reduced encephalopathic potential in the mouse model compared to the virulent strain BP 338, or to BP348, an adenylate cyclase and hemolysin double mutant, or to BP 349, a hemolysin mutant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Murine model for pertussis vaccine encephalopathy: role of the major histocompatibility complex; antibody to albumin and to Bordetella pertussis and pertussis toxin. 287 26

The mechanism by which pertussis toxin (PT) breaks the unresponsiveness of delayed-type hypersensitivity (DTH) to sheep red blood cells (SRBC) was examined in B10 mice. The unresponsiveness of DTH was induced in mice by iv injection of 10(9) SRBC and broken antigen-specifically by iv injection of 500 ng of PT into mice 1 or more days after SRBC injection. The restored DTH response in the SRBC-primed and PT-treated mice was accompanied by the appearance of Lyt-1-positive splenic T cells, capable of mediating DTH, fractionated in the low-density layers on a discontinuous bovine serum albumin density gradient. To examine the action of PT on the appearance of the DTH-effector cells, the splenic T cells from 10(9) SRBC-primed mice were treated with 100 ng/ml of PT for 60 min in vitro and then transferred into naive recipient mice. The PT-treated T cells acquired the ability to manifest DTH in the recipient mice several days after transfer. A large proportion of them were Lyt-1-positive small cells fractionated in the high-density layers before transfer and transformed into DTH-effector cells fractionated in the low-density layers in the recipient mice after transfer. Moreover, the ability of the PT-treated cells to manifest DTH on transfer was resistant to treatment with mitomycin C. These results suggest that PT acts on the sensitized, small Lyt-1-positive T cells from the unresponsive mice to differentiate them into large T-cell blasts, capable of mediating DTH, as one of the mechanisms by which PT breaks the unresponsiveness of DTH to SRBC.
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PMID:Mechanism by which pertussis toxin breaks unresponsiveness of delayed-type hypersensitivity to sheep red blood cells in mice. 309 86

The nature of primed precursor T cells (primed pre-TD), capable of differentiating into effector T cells (TD) that mediate delayed-type hypersensitivity (DTH), was investigated in B10 mice which were primed by intravenous (iv) injection of various doses of sheep red blood cells (SRBC). The presence of primed pre-TD was detected by the ability of T cells in the spleens from primed mice, which were treated in vitro with pertussis toxin and then transferred into naive recipient mice, to generate DTH in the recipient mice 14 days after transfer. The primed pre-TD were induced antigen specifically 1 day after mice were primed by iv injection of a suboptimal (10(3)), an optimal (10(5)), or supraoptimal (10(9)) dose of SRBC. They were replaced by TD 4 days after priming in optimally sensitized mice, while they were maintained without generating TD for at least 5 weeks after priming in mice primed with either a suboptimal or a supraoptimal dose of SRBC. They were L3T4-positive and dense cells, fractionated in the high-density layers on a discontinuous Percoll density gradient, and capable of transforming into less dense TD, fractionated in the low-density layers. These results indicate that primed pre-TD, which are induced by an antigen signal and then can be activated by a nonspecific stimulus, are present not only in responsive mice but also in unresponsive mice, suggesting that either the generation of TD from primed pre-TD or primed pre-TD alone is the decisive factor for either responsiveness or unresponsiveness.
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PMID:Studies on primed precursors of effector T cells involved in delayed-type hypersensitivity to sheep red blood cells in mice. 349 71

The expression of acute experimental autoimmune encephalomyelitis (EAE) in mice is controlled by several dominant genes, H-2 and histamine sensitization genes. SJL/J and SWR/J, which are H-2s and H-2q, respectively, are susceptible to EAE and sensitive to Bordetella pertussis histamine-sensitizing factor (HSF), which produces a vasoactive amine hypersensitivity. Other H-2s or H-2q strains such as A.SW, B10.Q and several others do not develop acute EAE and are not sensitive to B. pertussis HSF. One strain tested, DDD (KsIsD?) is HSF sensitive but does not develop EAE (presumably because it lacks the appropriate responder H-2 haplotype). However, F1 hybrids between B10.S and DDD are sensitive to HSF and develop EAE. The induction and effector phases of acute EAE are apparently controlled by the combination of H-2 and HSF genes. A combination of the correct H-2 hapotype and histamine sensitivity is required for the development of acute EAE.
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PMID:Acute autoimmune encephalomyelitis in mice. II. Susceptibility is controlled by the combination of H-2 and histamine sensitization genes. 680 29

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