Development of Rheumatoid Factors and Anti-F(ab′)2 Antibodies in Guinea Pigs Immunized with Type II Bovine Collagen

1986 ◽  
Vol 80 (2) ◽  
pp. 214-220 ◽  
Author(s):  
Benjamin Wolf ◽  
Reza I. Bashey ◽  
Charles D. Newton ◽  
Sergio A. Jimenez
Keyword(s):  
Guinea Pigs ◽  
Type Ii ◽  
Rheumatoid Factors ◽  
Bovine Collagen

scholarly journals THE RELATION BETWEEN ANTIANAPHYLAXIS AND ANTIBODY BALANCE

1936 ◽  
Vol 64 (4) ◽  
pp. 657-672 ◽  
Author(s):  
Marion C. Morris
Keyword(s):  
Guinea Pigs ◽  
Horse Serum ◽  
Type Ii ◽  
Partial Saturation ◽  
Type B ◽  
True Nature ◽  
Humoral Antibodies ◽  
Antigen Antibody ◽  
Circulating Antibody

It has been shown that antianaphylaxis is not caused by a partial saturation of cellular or humoral antibodies by the following facts. 1. Guinea pigs passively sensitized with anti-horse or antipneumococcus serum and specifically desensitized do not manifest as great a reactivity upon resensitization with the same antiserum as upon the original sensitization. 2. Guinea pigs passively sensitized with anti-Friedländer Type B serum or antipneumococcus Type II serum and specifically desensitized do not attain the same degree of reactivity as normal animals when passively sensitized with anti-horse serum. 3. Guinea pigs passively sensitized with anti-Friedländer Type B serum and desensitized with the specific carbohydrate remain as resistant to infection with Friedlander's bacillus Type B as undesensitized guinea pigs. Since in this case, at least, it is agreed that type-specific immunity and type-specific hypersensitiveness are due to the same type-specific antibody, a change in anaphylactic response should be accompanied by a change in immune response, provided this change depends on antibody balance. 4. A determination of the antibody content of the serum of sensitized as well as of desensitized guinea pigs by mouse protection tests indicates that a loss of reactivity in desensitized animals cannot be adequately accounted for on the basis of depletion of circulating antibody. These experiments suggest that hypersensitiveness and resistance are different manifestations of the same antigen-antibody reaction while antianaphylaxis is a state of refractoriness which is due neither to excess of circulating antibody nor to antibody depletion, but is the result of secondary changes the true nature of which is still not definitely established.

Two types of cells with central innervation in pineal gland of guinea pigs

1987 ◽  
Vol 252 (4) ◽  
pp. C369-C377 ◽  
Author(s):  
H. C. Parkington ◽  
I. McCance ◽  
H. A. Coleman
Keyword(s):  
Guinea Pigs ◽  
Young Male ◽  
Type I ◽  
Type Ii ◽  
Alpha Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Central Innervation ◽  
Intracellular Microelectrodes ◽  
Cervical Ganglia ◽  
Beta Adrenoceptor Blockers

Cells within pineal glands isolated from young, male guinea pigs were impaled with intracellular microelectrodes and their responses to stimulate the nerve supply to the gland were studied. Two types of cells were identified. The response of cells of type I was a depolarization on which spikes were superimposed. Blockers of alpha-adrenoceptors abolished the spikes while beta-adrenoceptor blockers reduced the depolarization to 27%, leaving a small tetrodotoxin-sensitive depolarization. After bilateral removal of the superior cervical ganglia (SCG) the beta-mediated depolarization was not observed while the spikes and the smaller depolarization persisted. The response of cells of type II was an initial large, transient depolarization followed by a smaller depolarization. Both components were reversibly blocked by tetrodotoxin. The only agents found to have any effect on these cells were oxytocin, vasopressin, and vasotocin. These peptides caused depolarization similar in amplitude to the larger response to nerve stimulation, although more prolonged. The large depolarization was not observed following ganglionectomy, but the smaller one persisted. It is concluded that cells of type I and II both receive inputs from nerves whose cell bodies lie in the SCG. Cells of both types are also innervated through another pathway.

Type II Collagen Induced Tympanosclerosis Model in Guinea Pigs

1985 ◽  
Vol 12 ◽  
pp. S200-S202 ◽  
Author(s):  
Yoshiro Yazawa ◽  
Tai-Jun Yoo ◽  
Tsukasa Ishibe ◽  
Koichi Tomoda
Keyword(s):  
Guinea Pigs ◽  
Type Ii Collagen ◽  
Type Ii

Type II Collagen-Induced Autoimmune Inner Ear Lesions in Guinea Pigs

1984 ◽  
Vol 93 (5_suppl) ◽  
pp. 3-5 ◽  
Author(s):  
T. J. Yoo ◽  
K. Tomoda ◽  
A. D. Hernandez
Keyword(s):  
Inner Ear ◽  
Guinea Pigs ◽  
Type Ii Collagen ◽  
Type Ii

Electrocochleographic Changes in Endolymphatic Hydrops Induced by Type II Collagen Immunization through the Stylomastoid Foramen

1989 ◽  
Vol 98 (7) ◽  
pp. 556-562 ◽  
Author(s):  
Toru Ohashi ◽  
Koichi Tomoda ◽  
Nobuo Yoshie
Keyword(s):  
Ganglion Cell ◽  
Guinea Pigs ◽  
Endolymphatic Hydrops ◽  
Spiral Ganglion ◽  
Type Ii Collagen ◽  
Ménière’S Disease ◽  
Type Ii ◽  
Cell Degeneration ◽  
Stylomastoid Foramen ◽  
Spiral Ganglion Cell

Changes in action potential (AP) and summating potential (SP) were investigated in guinea pigs immunized with type II collagen through the stylomastoid foramen. Endolymphatic hydrops could be induced in four of 11 guinea pigs. The striking feature of the electrocochleographic waveform in guinea pigs with endolymphatic hydrops was the negative SP recording in response to high frequency tone bursts. Furthermore, abnormal changes in AP were observed in three of four hydropic guinea pigs. Morphologic study of the cochleas in these three guinea pigs with light microscopy revealed spiral ganglion cell degeneration in addition to endolymphatic hydrops and almost normal sensory hair cells. These results suggest that guinea pigs with hydrops as produced by our procedure can serve as a useful model of Meniere's disease, that autoimmune response may play an important role in the etiopathogenesis of Meniere's disease, and that spiral ganglion cell degeneration together with endolymphatic hydrops seems to contribute to abnormal changes in AP.

scholarly journals ANAPHYLAXIS WITH THE TYPE-SPECIFIC CARBOHYDRATES OF PNEUMOCOCCUS

1929 ◽  
Vol 49 (2) ◽  
pp. 251-266 ◽  
Author(s):  
Oswald T. Avery ◽  
William S. Tillett
Keyword(s):  
Guinea Pigs ◽  
Anaphylactic Shock ◽  
Horse Serum ◽  
Free Form ◽  
Rabbit Serum ◽  
Type Ii ◽  
Type Iii ◽  
Positive Results ◽  
Anaphylactic Response ◽  
Immune Rabbit

1. The type-specific carbohydrates (haptens) of Pneumococcus Types I, II and III, when isolated in protein-free form, are devoid of the property of inducing active anaphylactic sensitization in guinea pigs. 2. The bacterial carbohydrates of Pneumococcus, of which the Type II and Type III substances are nitrogen-free, produce rapid and fatal anaphylactic shock in guinea pigs passively sensitized with the precipitating serum of rabbits immunized with pneumococci of the homologous type; the reactions induced are type-specific. 3. In contrast to the positive results with immune rabbit serum, there is a complete absence of anaphylactic response to pneumococcus carbohydrate in guinea pigs passively sensitized with antipneumococcus horse serum.

The natural soluble form of IL-18 receptor β exacerbates collagen-induced arthritis via modulation of T-cell immune responses

2009 ◽  
Vol 69 (01) ◽  
pp. 276-283 ◽  
Author(s):  
S Veenbergen ◽  
R L Smeets ◽  
M B Bennink ◽  
O J Arntz ◽  
L A B Joosten ◽  
...  
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Bone Erosion ◽  
Biological Activities ◽  
Type Ii Collagen ◽  
Histological Evaluation ◽  
Soluble Form ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Bovine Collagen

Objective:IL-18 is a pluripotent cytokine that has been implicated in the development of rheumatoid arthritis. A soluble form of the IL-18 receptor accessory protein (sIL-18Rβ) with unknown function has recently been identified. This study examined the ability of sIL-18Rβ to inhibit IL-18 biological activities and to modulate immune responses during collagen-induced arthritis (CIA).Methods:Adenoviruses encoding sIL-18Rβ were administered intravenously in type II collagen-immunised DBA/1 mice. Humoral responses were analysed by determining anti-bovine collagen type II (BCII) antibody levels by ELISA. Cytokine production by splenic T cells and cytokine levels in serum were measured by Luminex multi-analyte technology. CD4+CD25+Foxp3+ regulatory T cells (Treg) were measured by flow cytometry.Results:Intravenous delivery of Ad5.sIL-18Rβ in collagen-immunised mice led to enhanced transgene expression in splenic antigen-presenting cells (APC). A co-culture of these sIL-18Rβ-transduced APC with purified splenic CD3+ T cells led to a marked inhibition of IL-18-induced IFNγ, IL-4 and IL-17 production by CD3+ T cells. Remarkably, systemic treatment with Ad5.sIL-18Rβ caused an exacerbation of arthritis, and histological evaluation of knee joints showed increased cartilage and bone erosion. No significant differences were observed in anti-BCII antibodies, but the aggravation was accompanied by decreased IFNγ (−30%) and IL-4 (−44%) and increased IL-17 (+84%) production by splenic CD3+ T cells. In addition, reduced circulating levels of CD4+CD25+Foxp3+ Treg and anti-inflammatory IL-10 were shown.Conclusion:This study identifies sIL-18Rβ as a novel IL-18 inhibitor, which promotes CIA after intravenous overexpression by affecting Treg levels and supporting a T helper type 17 response.

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