The Failure of Antibody Production in the Chick Embryo

Burnet, F. M.; Stone, Joyce D; Edney, Margaret

doi:10.1038/icb.1950.29

Cited by 72 publications

(23 citation statements)

References 4 publications

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“…We have also shown that exposure to antigen during intrauterine life or during the neonatal period is not committed to develop neonatal tolerance [7]. At the same time, the self/nonself theory of the immune response, which has been regarded as a solid pillar of immunology for more than half a century, is under challenge [8]. Many researchers have recently shown that the immune system does not discriminate between self and nonself antigens.…”

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confidence: 99%

Dendritic Cells and Chronic Hepatitis Virus Carriers

Akbar

Horiike²,

Onji³

et al. 2001

Intervirology

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Many individuals infected with hepatitis B virus (HBV) and hepatitis C virus (HCV) are unable to clear these viruses following an acute infection and become chronically infected. There are more than 400 million HBV and HCV carriers in the world and a considerable number of these patients would eventually develop more severe complications like liver cirrhosis and hepatocellular carcinoma. It is not clearly known how an individual develops a chronic hepatitis virus carrier state; however, a defective immune response of the host is thought to play a critical role in the underlying pathogenetic mechanism. On the other hand, dendritic cells (DCs), the most potent antigen-presenting cells, are widely distributed in both lymphoid and nonlymphoid tissues. Recognition of the microbes or microbial antigens by DCs is one of critical events for the initiation of an immune response. DCs also play a cardinal role during the progression and termination of an immune response. The aim of this overview is to provide information regarding the role of DCs in the pathogenesis of chronic hepatitis due to HBV and HCV in humans and in animal models of HBV and HCV carrier states. First, we summarize our current understanding of the pathogenesis of hepatitis virus carrier states and also of general properties of DCs. Next, we discuss the data on the phenotypes and functions of DCs in both human and murine HBV and HCV carriers. We also discuss vaccine therapy in murine HBV carriers because activation of DCs due to vaccination-initiated HBsAg-specific immune responses in HBV transgenic mice (HBV-Tg), which in turn resulted in complete clearance of hepatitis B surface antigen and hepatitis B e antigen and decreased levels of HBV DNA in some HBV-Tg. Finally, we discuss the extracted questions and future research directions.

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confidence: 99%

Dendritic Cells and Chronic Hepatitis Virus Carriers

Akbar

Horiike²,

Onji³

et al. 2001

Intervirology

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“…, or with washed human red cells (Burnet, Stone & Edney, 1950). Moreover, there was no demonstrable change in the subsequent response of the hatched chick to the corresponding antigen.…”

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confidence: 82%

Antibody Production in Avian Embryos and Young Chicks

Buxton

1954

Journal of General Microbiology

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“…The capacity to discriminate between self and non-self is generated during embryonic and neonatal development of the immune system and specific immunological tolerance to autologous antigens is acquired [1][2][3][4][5][6].Tolerance in theT cell repertoire is achieved during development in the thymus by negative selection, i. e., deletion of potentially harmful cells [7,81. Antibody diversity in the B cell compartment is generated in two phases: one occurs by gene rearrangement of immature B cells in the primary lymphoid organs, while the other one takes place in peripheral lymphoid organs by somatic hypermutation upon antigen contact [9, 101.…”

Section: Introductionmentioning

confidence: 99%

Is there really a “lack of natural tolerance to allotypic γ‐globulins in rabbits”?

Meier¹,

Kelus²

1991

Eur J Immunol

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We present data of extended studies on the possibility of maternally derived allotype Ig inducing a state of natural immunological tolerance to a non-inherited allotype in the offspring. Rabbits homozygous at the a locus, encoding allotypes in the variable region of immunoglobulin heavy chains, and rabbits homozygous at the unliked b locus, encoding allotypes of the constant region of kappa 1 chains, were immunized at the age of 2 months against the non-inherited allotype of their heterozygous mothers to which they had been exposed in utero and in early life. As control, we immunized rabbits of the same Ig phenotype but born to homozygous mothers, and therefore not exposed to that allotype. Immunization was done in a3/a3 offspring of either a1/a3 or a3/a3 mothers, by injecting a 1 IgG, and in b6/b6 offspring of b4/b6 or b6/b6 mothers, by injecting b4 IgG. The IgG was injected either in a soluble form or emulsified in adjuvant. Injection of soluble IgG elicited only a low response, if any, revealing no differences between the various groups. All rabbits responded upon immunization with IgG in adjuvant. We have not found any good evidence for natural tolerance to a non-inherited allotype, although progeny of a1/a3 mothers had slightly decreased responses to a1. On the contrary, progeny of b4/b6 mothers responded even better than offspring of b6/b6 mothers, upon such immunization with b4. To induce tolerance experimentally, we injected newborn rabbits, either from heterozygous a1/a3 or from homozygous a3/a3 mothers, with a1 serum or IgG. Newborn of heterozygous b4/b6 or of homozygous b6/b6 mothers were injected with b4 serum or IgG in the same way. Such treatment resulted in partial tolerance to each allotype. In an attempt to amplify the tolerizing effect of the maternal a1 Ig, we injected newborn rabbits of a1/a3 mothers with the serum of their mother. The response upon subsequent immunization with a1 allotype of another individual did not differ significantly from the response of control rabbits. The response was much poorer when rabbits were injected with nonmaternal tolerogen at birth, and when the same Ig preparation was used as immunogen. In a control experiment, neonatal injection of xenogeneic proteins, human IgG or bovine serum albumin, clearly resulted in tolerance. We speculate that tolerance to allotypes is established in the T cell repertoire only but bypassed by recognition of idiotypic determinants on antigen molecules by helper T cells, which trigger anti-allotype antibody formation by allotype-specific B cells. The end result of it is a lack of natural tolerance.

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The Failure of Antibody Production in the Chick Embryo

Cited by 72 publications

References 4 publications

Dendritic Cells and Chronic Hepatitis Virus Carriers

Dendritic Cells and Chronic Hepatitis Virus Carriers

Antibody Production in Avian Embryos and Young Chicks

Is there really a “lack of natural tolerance to allotypic γ‐globulins in rabbits”?

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