The cellular immune response to antigens of Coxiella burneti

1974 ◽  
Vol 20 (5) ◽  
pp. 657-662 ◽  
Author(s):  
John P. Heggers ◽  
L. P. Mallavia ◽  
David J. Hinrichs
Keyword(s):  
Phase I ◽  
Guinea Pigs ◽  
Q Fever ◽  
Delayed Hypersensitivity ◽  
Migration Inhibition ◽  
Microagglutination Test ◽  
Cellular Immune ◽  
Antibody Levels ◽  
Circulating Antibody

Formalinized vaccines prepared from the Nine Mile, Phase I, strain of C. burneti or purified preparations of the Phase I antigen initiate a state of delayed hypersensitivity in guinea pigs as determined by the in vitro migration inhibition system. This delayed hypersensitivity is directed against the protein as well as the carbohydrate component of the Phase I antigen. Guinea pigs that had recovered from Q-fever demonstrated a similar state of delayed hypersensitivity. Circulating antibody levels as determined by the microagglutination test were readily apparent in both infected and vaccinated animals.

scholarly journals SPECIFIC IMMUNE RESPONSE GENES OF THE GUINEA PIG

1971 ◽  
Vol 134 (2) ◽  
pp. 458-470 ◽  
Author(s):  
Harry G. Bluestein ◽  
Ira Green ◽  
Baruj Benacerraf
Keyword(s):  
Guinea Pig ◽  
Glutamic Acid ◽  
Inbred Strain ◽  
Guinea Pigs ◽  
Delayed Hypersensitivity ◽  
Random Copolymers ◽  
F1 Hybrids ◽  
Antibody Levels ◽  
Dominant Genes ◽  
Circulating Antibody

The immunogenicity of three random copolymers of amino acids with L-glutamic acid and L-alanine (GA), L-glutamic acid and L-tyrosine (GT), or L-glutamic acid, L-alanine, and L-tyrosine (GAT), administered in complete Freund's adjuvant, was studied in several inbred and random-bred guinea pig strains. The animals were tested for delayed sensitivity and their sera were assayed for the presence of antibody directed against the immunizing polymer. All of the guinea pigs developing delayed hypersensitivity also had significant antibody levels in their sera. Inbred strain 2 guinea pigs responded to immunization with GA, but failed to form detectable responses to GT. Inbred strain 13 animals, on the other hand, responded to GT, but not to GA. The (2 x 13)F1 hybrids responded to both GA and GT with both delayed hypersensitivity and circulating antibody. Thus, the ability of these inbred guinea pigs to respond immunologically to GA or GT is controlled by distinct autosomal dominant genes. A variable percentage of random-bred guinea pigs, depending on their source as well as their strain, responded to immunization with GA and with GT. All guinea pigs, both inbred and random bred, responded to immunization with GAT. The ability to respond immunologically to GAT, therefore, does not seem to be under simple genetic control. However, the levels of anti-GAT antibody found in the sera of animals lacking the ability to respond to GA were much lower than those detected in GA responder animals.

scholarly journals ALLOANTISERUM-INDUCED INHIBITION OF MIGRATION INHIBITION FACTOR PRODUCTION IN IMMUNE RESPONSE GENE-CONTROLLED IMMUNE SYSTEMS

1974 ◽  
Vol 140 (2) ◽  
pp. 383-395 ◽  
Author(s):  
Shlomo Z. Ben-Sasson ◽  
Ethan Shevach ◽  
Ira Green ◽  
William E. Paul
Keyword(s):  
T Cell ◽  
Guinea Pigs ◽  
Opposite Effect ◽  
Cell Function ◽  
Migration Inhibition Factor ◽  
Immune Response Gene ◽  
Migration Inhibition ◽  
Inhibition Factor ◽  
Controlled Systems

We have previously demonstrated that alloantisera prepared by reciprocal immunization of strain 2 and strain 13 guinea pigs specifically block stimulation of in vitro DNA synthesis in genetically controlled systems. In order to determine whether this blockade extends to other T-lymphocyte functions, we examined the effect of alloantisera on the production of migration inhibition factor (MIF). (2 x 13)F1 guinea pigs were immunized with a DNP derivative of the copolymer of L-glutamic acid and L-lysine (DNP-GL) and with DNP guinea pig albumin (GPA). The response to the former is controlled by a 2-linked Ir gene while that to the latter is mainly controlled by a 13-linked Ir gene. MIF production was assayed by an indirect procedure in which the migrating cell population lacked the histocompatibility antigen against which the alloantiserum was directed. Our results showed that anti-2 serum blocked MIF production by F1 cells in response to DNP-GL but not DNP-GPA while anti-13 serum had the opposite effect. These experiments show that expression of a second major T-cell function is specifically blocked by alloantisera and suggest that Ir-gene products may act as antigen recognition substances on more than one type of T cell.

scholarly journals SPECIFICITY OF CELLULAR IMMUNE RESPONSES

1968 ◽  
Vol 127 (1) ◽  
pp. 25-42 ◽  
Author(s):  
William E. Paul ◽  
Gregory W. Siskind ◽  
Baruj Benacerraf
Keyword(s):  
Dna Synthesis ◽  
Cell Population ◽  
Guinea Pigs ◽  
Culture Fluid ◽  
Cellular Immune Responses ◽  
A Cell ◽  
Delayed Reactions ◽  
Cellular Immune

In vitro antigen stimulation of DNA synthesis in lymph node cultures from immunized guinea pigs can be obtained with very low (10–4 µg/ml) antigen concentrations in the culture fluid. Immunization with low doses of DNP-GPA leads to a cell population capable of being stimulated, on the average, by low concentration of antigen whereas immunization with large antigen doses results in a sensitive cell population requiring, on the average, high antigen concentrations for stimulation. These findings correlate well with the affinity for hapten of the serum antibodies produced by these guinea pigs. Both delayed reactions in vivo and DNA synthesis in vitro can be stimulated by hapten conjugated to proteins different from that used in primary immunization. However the immunizing conjugate is much more effective in terms of antigen concentration required for a given response. These results can be understood in terms of a thermodynamically driven interaction of antigen (or "processed" antigen) with cell-associated antibody.

scholarly journals Correlation between Ratio of Serum Doxycycline Concentration to MIC and Rapid Decline of Antibody Levels during Treatment of Q Fever Endocarditis

2005 ◽  
Vol 49 (7) ◽  
pp. 2673-2676 ◽  
Author(s):  
Jean-Marc Rolain ◽  
Areen Boulos ◽  
Marie-Noëlle Mallet ◽  
Didier Raoult
Keyword(s):  
Phase I ◽  
Q Fever ◽  
Serum Levels ◽  
Response To Treatment ◽  
Rapid Decline ◽  
Shell Vial ◽  
Real Time Quantitative Pcr ◽  
Chronic Q Fever ◽  
Antibody Levels ◽  
Quantitative Pcr Assay

ABSTRACT Endocarditis is the major clinical manifestation of chronic Q fever. Although doxycycline along with hydroxychloroquine remains the mainstay of medical therapy for Q fever endocarditis, there are wide variations in the rapidity of the patient's decline of antibody levels during such therapy. We undertook a retrospective examination of whether there was any correlation between the ratio of serum concentration to MIC of doxycycline and response to treatment in patients with Q fever endocarditis. Included herein are 16 patients from whom Coxiella burnetii was isolated from cardiac valve materials. Serology and measurement of doxycycline and hydroxychloroquine serum levels were performed and recorded after 1 year of treatment. The MIC of doxycycline for C. burnetii isolates was determined using the shell vial assay in a real-time quantitative PCR assay. At the completion of a yearlong therapy with doxycycline-hydroxychloroquine, all those that showed a low decline of antibody levels (n = 6) (i.e., <2-fold decrease in antibody titer to phase I C. burnetii antigen) had a ratio of serum doxycycline concentration to MIC between 0.5 and 1. In contrast, those having a ratio of ≥1 showed a rapid decline of phase I antibody levels (n = 9; P < 0.05). The only patient who died had a serum doxycycline-to-MIC ratio of <0.5, and the isolate of C. burnetii cultured from this patient was resistant to doxycycline (MIC = 8 μg/ml). The ratio of serum doxycycline concentration to MIC should be monitored during the course of therapy in patients with Q fever endocarditis.

scholarly journals THE COURSE OF EXPERIMENTAL AUTOALLERGIC THYROIDITIS IN INBRED GUINEA PIGS

1964 ◽  
Vol 119 (2) ◽  
pp. 327-342 ◽  
Author(s):  
Edwin M. Lerner ◽  
Philip R. B. McMaster ◽  
Eurmal D. Exum
Keyword(s):  
Guinea Pigs ◽  
Severe Disease ◽  
Low Levels ◽  
Thyroid Antigen ◽  
Antibody Levels ◽  
Relationship Of ◽  
Extent Of Disease ◽  
Experimental Allergic ◽  
Circulating Antibody

Experimental allergic thyroiditis produced in strain 13 histocompatible guinea pigs after a single immunization with thyroid extract and Freund's adjuvant was followed for more than 2 years. The disease appeared as early as 5 days and persisted for the entire period studied, although it regressed in the later stages. Circulating antithyroid antibody was detected at low levels as early as 7 days after immunization, and increased to a peak at the time of most severe disease. Thereafter, antibody decreased, but was still detectable in most animals as late as 2 years. There was no correlation between antibody levels and extent of disease except at the 7 week stage. Delayed sensitivity to thyroid antigen was found as early as 5 days after immunization, and appeared to precede the development of thyroiditis in many animals. It correlated closely with thyroiditis at 5 days and 7 weeks. At 6 months, the delayed skin reaction was decreased, and a modified type of reaction appeared which persisted as long as 26 months. The time relationship of delayed sensitivity, thyroiditis, and circulating antibody continue to confirm the role of delayed sensitivity in the pathogenesis of this disease. The accumulated data demonstrating production of thyroiditis without antibody, and the converse, tend to strengthen this view.

scholarly journals IN VITRO STUDIES OF THE SUPPRESSION OF DELAYED HYPERSENSITIVITY BY THE INDUCTION OF PARTIAL TOLERANCE

1970 ◽  
Vol 131 (3) ◽  
pp. 603-610 ◽  
Author(s):  
Yves Borel ◽  
John R. David
Keyword(s):  
In Vitro Studies ◽  
Delayed Hypersensitivity ◽  
Macrophage Migration ◽  
Factor Activity ◽  
Migration Inhibition ◽  
Macrophage Migration Inhibition ◽  
Induction Of Tolerance

Suppression of delayed hypersensitivity in vivo is correlated in vitro with the absence of macrophage migration inhibition in the presence of the antigen used to induce partial tolerance. The suppression of delayed hypersensitivity is antigen-specific in vivo as well as in vitro. The lymphocytes, and not the macrophages, are the cells involved in the induction of tolerance in terms of delayed hypersensitivity which is characterized by an absence of migratory factor activity.

Stereospecificity of flobufen metabolism in guinea pigs in vitro and in vivo: Phase I of biotransformation

Chirality ◽  
2003 ◽  
Vol 16 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Radim Kral ◽  
Lenka Skalova ◽  
Barbora Szotakova ◽  
Yogeeta N. Babu ◽  
Vladimir Wsol
Keyword(s):  
Phase I ◽  
Guinea Pigs

scholarly journals Evaluation of the immune response to CRA and FRA recombinant antigens of Trypanosoma cruzi in C57BL/6 mice

2003 ◽  
Vol 36 (4) ◽  
pp. 435-440 ◽  
Author(s):  
Valéria Rêgo Alves Pereira ◽  
Virginia Maria Barros de Lorena ◽  
Mineo Nakazawa ◽  
Ana Paula Galvão da Silva ◽  
Ulisses Montarroyos ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Immune Responses ◽  
Control Group ◽  
Mechanisms Of Resistance ◽  
Recombinant Antigens ◽  
Cellular Immune Responses ◽  
Cellular Immune ◽  
Antibody Levels ◽  
Cruzi Infection

Humoral and cellular immune responses were evaluated in 44 C57BL/6 mice immunized with the Trypanosoma cruzi recombinant antigens CRA and FRA. Both antigens induced cutaneous immediate-type hypersensitivity response. The levels of IgG1, IgG2a, IgG2b and IgG3 were high in CRA immunized mice. IgG3 was the predominant isotype. Although no difference in antibody levels was observed in FRA-immunized mice when compared to control mice, both antigens were able to induce lymphoproliferation in immunized mice. Significant differences were observed between incorporation of [³H]- thymidine by spleen cell stimulated in vitro with CRA or FRA and the control group. These results suggest that CRA and FRA could be involved in mechanisms of resistance to Trypanosoma cruzi infection.

scholarly journals STUDIES OF DELAYED HYPERSENSITIVITY IN VITRO

1957 ◽  
Vol 106 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Lowell A. Glasgow ◽  
Herbert R. Morgan
Keyword(s):  
Skin Reaction ◽  
Guinea Pigs ◽  
Viral Antigen ◽  
Intradermal Injection ◽  
Mumps Virus ◽  
Delayed Hypersensitivity ◽  
Virus Infections ◽  
Splenic Macrophages

Guinea pigs experimentally infected with mumps virus develop a delayed, hypersensitive skin reaction following the intradermal injection of heat-inactivated mumps virus. This in vivo hypersensitivity is accompanied by a state of cellular hypersensitivity which can be demonstrated in vitro by the addition of mumps viral antigen to cultures of splenic macrophages, following which they become less motile and undergo lysis. These observations support the hypothesis that the state of hypersensitivity which develops early in mumps virus infections may have a role in the pathogenesis of the disease.

scholarly journals IN VITRO DEMONSTRATION OF CELLULAR SENSITIVITY IN ALLERGIC ENCEPHALOMYELITIS

1965 ◽  
Vol 122 (6) ◽  
pp. 1161-1171 ◽  
Author(s):  
John R. David ◽  
Philip Y. Paterson
Keyword(s):  
Guinea Pigs ◽  
Nervous Tissue ◽  
Neonatal Rat ◽  
Delayed Hypersensitivity ◽  
Allergic Encephalomyelitis ◽  
Adult Rat ◽  
Peritoneal Cells ◽  
Cellular Sensitivity ◽  
Tissue Antigens

Peritoneal cells obtained from animals exhibiting delayed hypersensitivity are inhibited from migrating in vitro by specific sensitizing antigen. This test for the detection of delayed hypersensitivity was applied to the problem of cellular sensitivity in allergic encephalomyelitis (AE). The migration of peritoneal cells obtained from guinea pigs with AE was inhibited specifically by nervous tissue antigens. The specificity of this reaction was further studied. Neonatal rat nervous tissue, which was shown to lack the encephalitogenic antigen, i.e. did not produce AE when injected with complete adjuvant into guinea pigs and rats, did not inhibit the migration of cells from animals with AE. Adult rat nervous tissue, which readily produces AE, and thus contains the encephalitogenic antigen did inhibit the migration of such cells. The finding that cells from animals with AE display hypersensitivity which appears to be directed specifically to the encephalitogenic antigen strongly supports the view that such cells could play an important role in the pathogenesis of this disease.

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