Purification of human C3b inactivator by monoclonal-antibody affinity chromatography

Hsiung, Li-min; Barclay, A. Neil; Brandon, Malcolm R.; Sim, Edith; Porter, Roy

doi:10.1042/bj2030293

Cited by 113 publications

(65 citation statements)

References 23 publications

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“…One day before oral infection with 20 cysts from the Pru-␤-gal strain, LEW and BN rats were injected intraperitoneally with 5 mg of anti-gamma interferon (anti-IFN-␥) MAb (DB1) (31), and they were then injected with 3 mg of DB1 at days 0, 2, and 4 postinfection. Control rats were injected intraperitoneally with isotype control MAb (OX21) (15).…”

Section: Methodsmentioning

confidence: 99%

Innate Refractoriness of the Lewis Rat to Toxoplasmosis Is a Dominant Trait That Is Intrinsic to Bone Marrow-Derived Cells

et al. 2005

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Toxoplasmosis is a ubiquitous parasitic infection causing a wide spectrum of diseases. It is usually asymptomatic but can lead to severe ocular and neurological disorders. Among the small-animal models available to study factors that determine susceptibility to toxoplasmosis, the rat appears to be rather similar to humans, particularly in terms of resistance to acute infection. Here, we demonstrate that the Lewis (LEW) rat strain displays an unexpected refractoriness to Toxoplasma infection. Complete resistance was assessed by both negative anti-Toxoplasma serology and lack of detection of the parasite during the course of infection. In this model, sex, age, major histocompatibility complex, and inoculum size had no effect on resistance. Interestingly, progeny from F 1 hybrid crosses between Fischer (F344) or Brown Norway susceptible rats and LEW resistant rats were also fully resistant, showing a dominant effect of the gene or set of genes. Furthermore, resistance of the LEW rat was shown to be dependent on hematopoietic cells and partially abrogated by neutralization of endogenous gamma interferon. To our knowledge, this is the first observation of a rodent strain that is refractory to Toxoplasma infection. This model is therefore an attractive and powerful tool to dissect host genetic factors involved in susceptibility to toxoplasmosis.Toxoplasma gondii is an obligate, intracellular parasite which can infect all mammals, including humans. In natural oral infection, the parasite initially crosses the intestinal barrier and disseminates, during the acute disease, as replicating cytolytic tachyzoites. The development of a vigorous immune response leads to a chronic infection characterized by the persistence of encysted parasites within the host's muscular and nervous tissues.In the human population, toxoplasmosis is usually asymptomatic, and substantial morbidity and mortality are most often found in immunocompromised patients (e.g., in those with AIDS, with organ transplants, or who received anticancer therapies) and in congenitally infected infants (10). Despite the fact that the host immunologic status is known to be critical in the outcome of Toxoplasma infection (7, 12), the severity of the disease caused by Toxoplasma infection varies widely depending on the host species (8, 30, 33) and remains unpredictable among individuals.Up to now, genetic studies on susceptibility to toxoplasmosis have been confined to the mouse model (2, 3, 23). A limitation of this model is the high susceptibility of certain strains of mice to toxoplasmosis, with a high rate of mortality during acute infection. Interestingly, in respect to clinical course and in utero transmission, toxoplasmoses in rats and humans are similar, and the infection in rats can serve as a model for human toxoplasmosis (6,26,(33)(34)(35). Hence, like humans, rats do not succumb to acute toxoplasmosis even with a high inoculum of Toxoplasma strains that are highly virulent in mice. In a comparative study using various strains of rats, we have previously s...

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Section: Methodsmentioning

confidence: 99%

Innate Refractoriness of the Lewis Rat to Toxoplasmosis Is a Dominant Trait That Is Intrinsic to Bone Marrow-Derived Cells

et al. 2005

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“…The following mouse IgG1 Abs were tissue culture supernatants produced from hybridomas in the Medical Research Council Cellular Immunology Unit (Oxford, U.K.) by Mike Puklavec: OX8 (anti-rat CD8␣) (11), OX22 (anti-rat CD45RC) (12,13), OX32 (anti-rat CD45RC, noncompetitive with OX22) (13,14), OX39 (anti-rat CD25) (15), NDS62 (anti-rat CD25, noncompetitive with OX39) (16), W3/25 (anti-rat CD4) (17), OX21 (isotype control mouse IgG1, reactive with human factor I) (18), OKT4 (anti-human CD4) (19), and OKT8 (anti-human CD8) (20). Some of these Abs were purified and biotinylated using standard methods.…”

Section: Antibodiesmentioning

confidence: 99%

CD25 Is a Marker for CD4+ Thymocytes That Prevent Autoimmune Diabetes in Rats, But Peripheral T Cells with This Function Are Found in Both CD25+ and CD25− Subpopulations

Stephens

Mason

2000

The Journal of Immunology

286

199

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Previously we have shown that autoimmune diabetes, induced in rats by a protocol of adult thymectomy and split-dose gamma irradiation, can be prevented by the transfer of a subset of CD4+ T cells with a memory phenotype (CD45RC−), as well as by CD4+CD8− thymocytes, from syngeneic donors. Further studies now reveal that in the thymus the regulatory cells are observed in the CD25+ subset of CD4+CD8− cells, whereas transfer of the corresponding CD25− thymocyte subset leads to acceleration of disease onset in prediabetic recipients. However, in the periphery, not all regulatory T cells were found to be CD25+. In thoracic duct lymph, cells that could prevent diabetes were found in both CD25− and CD25+ subsets of CD4+CD45RC− cells. Further, CD25− regulatory T cells were also present within the CD4+CD45RC− cell subset from spleen and lymph nodes, but were effective in preventing diabetes only after the removal of CD25− recent thymic emigrants. Phenotypic analysis of human thymocytes showed the presence of CD25+ cells in the same proportions as in rat thymus. The possible developmental relationship between CD25+ and CD25− regulatory T cells is discussed.

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“…The mAbs used in this study were as follows: W3/25 (anti-rat CD4) (23), OX6 (anti-rat MHC class II) (24), OX8 (anti-rat CD8) (25), OX12 (anti-rat -light chain) (26), OX21 (anti-human C3b inactivator) (27), OX22 (antirat CD45RC) (7), R73 (anti-rat TCR␣␤) (28), V65 (anti-rat TCR␥␦) (29), JJ319 (anti-rat CD28) (30), and 10.78 (anti-rat NKR-P1) (31). The hybridomas OX6, OX8, OX12, OX21, OX22, and W3/25 were kindly provided by Dr. D. Mason (Oxford, U.K.).…”

Section: Antibodiesmentioning

confidence: 99%

The Balance Between CD45RChigh and CD45RClow CD4 T Cells in Rats Is Intrinsic to Bone Marrow-Derived Cells and Is Genetically Controlled

Subra

Cautain

Xystrakis

et al. 2001

The Journal of Immunology

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The level of CD45RC expression differentiates rat CD4 T cells in two subpopulations, CD45RChigh and CD45RClow, that have different cytokine profiles and functions. Interestingly, Lewis (LEW) and Brown Norway (BN) rats, two strains that differ in their ability to mount type 1 and type 2 immune responses and in their susceptibility to autoimmune diseases, exhibit distinct CD45RChigh/CD45RClow CD4 T cell ratios. The CD45RChigh subpopulation predominates in LEW rats, and the CD45RClow subpopulation in BN rats. In this study, we found that the antiinflammatory cytokines, IL-4, IL-10, and IL-13, are exclusively produced by the CD45RClow CD4 T cells. Using bone marrow chimeras, we showed that the difference in the CD45RChigh/CD45RClow CD4 T cell ratio between naive LEW and BN rats is intrinsic to hemopoietic cells. Furthermore, a genome-wide search for loci controlling the balance between T cell subpopulations was conducted in a (LEW × BN) F2 intercross. Genome scanning identified one quantitative trait locus on chromosome 9 (∼17 centiMorgan (cM); log of the odds ratio (LOD) score 3.9). In addition, two regions on chromosomes 10 (∼28 cM; LOD score 3.1) and 20 (∼40 cM; LOD ratio score 3) that contain, respectively, a cytokine gene cluster and the MHC region were suggestive for linkage. Interestingly, overlapping regions on these chromosomes have been implicated in the susceptibility to various immune-mediated disorders. The identification and functional characterization of genes in these regions controlling the CD45RChigh/CD45RClow Th cell subpopulations may shed light on key regulatory mechanisms of pathogenic immune responses.

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Purification of human C3b inactivator by monoclonal-antibody affinity chromatography

Cited by 113 publications

References 23 publications

Innate Refractoriness of the Lewis Rat to Toxoplasmosis Is a Dominant Trait That Is Intrinsic to Bone Marrow-Derived Cells

Innate Refractoriness of the Lewis Rat to Toxoplasmosis Is a Dominant Trait That Is Intrinsic to Bone Marrow-Derived Cells

CD25 Is a Marker for CD4+ Thymocytes That Prevent Autoimmune Diabetes in Rats, But Peripheral T Cells with This Function Are Found in Both CD25+ and CD25− Subpopulations

The Balance Between CD45RChigh and CD45RClow CD4 T Cells in Rats Is Intrinsic to Bone Marrow-Derived Cells and Is Genetically Controlled

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