Multiple Serum Protein Deficiencies in Congenital and Acquired Agammaglobulinemia 1

Gitlin, David; Hitzig, W. H.; Janeway, Charles A.

doi:10.1172/jci103374

Cited by 89 publications

(28 citation statements)

References 5 publications

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“…We would like to consider, in an analogy to the immunologic memory (27)(28)(29)(30)(31), that the period shortly before and after birth might be the key in also understanding autoimmunity. Because at this phase of development the immune system is relatively incompetent, transferable maternal immunologic memory is essential for the survival of the fetus, newborn, and infant (32).…”

Section: Maternal Autoimmune Imprinting Predisposes Offspring To T1dmentioning

confidence: 99%

Early and Quantal (by Litter) Expression of Insulin Autoantibodies in the Nonobese Diabetic Mice Predict Early Diabetes Onset

Melanitou

Devendra

Liu

et al. 2004

The Journal of Immunology

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International audienceAiming to study the early stages of type 1 diabetes phenotype, before insulitis appears, we measured insulin autoantibodies (IAA) between 3 and 5 wk of age in the NOD mouse (early-IAA (E-IAA)). We report that IAA are found as early as at 3 wk of age, at weaning, and their expression is a quantal phenotype. Maternal autoantibody status influences this early phenotype, because animals of litters issued from IAA-positive ante partum mothers develop E-IAA with a significantly higher incidence than animals issued from IAA-negative mothers. These E-IAA represent synthesized rather than transplacental autoantibodies, as evidenced by higher levels in many offspring compared with maternal IAA, and negative as well as positive offspring in the same litters and it correlates with early diabetes onset, defining the first autoimmune window in diabetes pathogenesis. Therefore, autoimmune processes leading to type 1 diabetes initiate early in life, are influenced by maternal autoantibody status, and can be revealed by the presence of IAA. Our data suggest that the mechanisms responsible for the breakdown of self-tolerance are subjected not only to genetic predisposition, but also to the physiological status of the mother. Pathological progression to autoimmunity is marked by the presence of immunological windows relating early steps with final disease onset

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Section: Maternal Autoimmune Imprinting Predisposes Offspring To T1dmentioning

confidence: 99%

Early and Quantal (by Litter) Expression of Insulin Autoantibodies in the Nonobese Diabetic Mice Predict Early Diabetes Onset

Melanitou

Devendra

Liu

et al. 2004

The Journal of Immunology

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show abstract

“…My father was the first to identify a series of infants that failed to make any class of antibody or immunoglobulins. In fact, it was from the study of his patients that it was realized that the adaptive humoral immune response could be broken down into the major classes of Ig (13). He accumulated 17 patients with no circulating antibody or Ig, all of whom had recurrent infection with pyogenic (pus-forming) bacteria.…”

Section: The Adaptive Immune System Interacts With the Innate Immune mentioning

confidence: 99%

How the immune system works to protect the host from infection: A personal view

Janeway

2001

Proc. Natl. Acad. Sci. U.S.A.

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296

144

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“…Larsson/Hagclquist/Costcr 51 might also question whether the name agammaglobulinaemia or hypogammaglobulinaemia really is adequate, since G itlin et al have shown that in these conditions there is also a reduction of two beta-globulins (13,14) and since the absence of isohaemagglutinins, one third of which belong to the electrophoretic beta-globulin frac tion (30), is regarded as a criterion of hypogammaglobulinaemia (5,9,49,62). Young et al (64) have also claimed that the defect should preferably be described as immunoglobulin deficiency, and Barandun et al (3,4) have called the condition AntikorpcrMangelsyndrom.…”

Section: Introductionmentioning

confidence: 99%