Xx/Xy Lymphoid Chimærism in Congenital Immunological Deficiency Syndrome With Thymic Alymphoplasia

Kadowaki, Junichi; Thompson, R N; Zuelzer, Wolf W.; Woolley, P V; Brough, A. Joseph; Gruber, Dinah

doi:10.1016/s0140-6736(65)92559-6

Cited by 191 publications

(41 citation statements)

References 20 publications

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“…In one case, they were able to demonstrate the presence of emboli of what appeared to be chorionic cell detritus in the umbilical vein and an arteriole of the brain. Human chimeras have been described by Taylor and Polani (1965) and Kadowaki, Thompson, Zuelzer, Woolley, Brough, and Gruber (1965) The inumunoglobulins at 1 year of age were of a similar order to those found by Soothill et al (1966) in 4 of their cases of rubella; that is, low IgG level and raised IgM. However, the loss of lymphoid tissue in this case was much more striking, especially in the thymus and alimentary tract, than in our cases of congenital rubella.…”

Section: Discussionsupporting

confidence: 85%

“…Evidence in support of this hypothesis would be the finding of negative lymphocyte transfer tests (Gray and Russell, 1963) or tolerance of maternal skin grafts. In addition, it is possible that the case of Kadowaki et al (1965) was due to situation (iii) of Nisbet and Heslop (1962). A second alternative, and the borderline between this and the first hypothesis is indistinct, is that the runting disease is due to the virus itself.…”

Section: Discussionmentioning

confidence: 99%

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Pathology of congenital rubella in Jamaica.

Thorburn¹,

Miller²

1967

Archives of Disease in Childhood

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The clinical, virological, and haematological features of the congenital rubella syndrome have been well documented in the recent American paediatric literature, as a result of the epidemic which occurred in 1964. However, apart from isolated case reports (Lambert, Stern, and Wellsteed, 1965; Stern and Williams, 1966;Menser, Dorman, Reye, and Reid, 1966) pathological data have been limited to descriptions of certain organs or tissues as part of larger series of clinical studies (Plotkin,

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Pathology of congenital rubella in Jamaica.

Thorburn¹,

Miller²

1967

Archives of Disease in Childhood

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“…Complete monosomy of a group 17,18 chromosome has not been reported as a constitutional anomaly, but in a case of probably XX/XY lymphoid chimaerism the bone marrow shortly before death contained a cell-line lacking a group 17, 18 chromosome and having a staining reaction which the authors associated with acute leukaemia (Kadowaki et al, 1965). No other evidence of neoplastic change was found in this remarkable case.…”

Section: Experimental Evidencementioning

confidence: 63%

A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia

Spiers¹,

Baikie²

1970

Br J Cancer

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The hypothesis is advanced that abnormalities of the chromosome group 17,18 play a special role in the genesis and/or evolution of some reticuloendothelial neoplasms. Aberrations of the group 17,18 chromosomes in tumour cells exceed in variety the reported anomaliesof any other chromosome. Both the frequency of these aberrations and their nature make them most unlikely to be due to chance. They appear to be non-random, often occurring in every cell of a tumour, and like the Ph 1 anomaly in chronic granulocytic leukaemia, mightpossess aetiological significance. The Ep- and Eqchromosomal anomalies resemble the Ph 1 in being fine structural modifications, which occur as acquired lesions only in neoplasms, often in tumour cells with otherwise normal karyotypes. Aberration of the group 17,18 chromosomes may sometimes be secondary to neoplasia but nevertheless of evolutionary significance for the tumour cells. Changes leading to relative or absolute excess of long-arm material of chromosome 18 may confer survival advantage upon cells, particularly if a normal complement of short-arm material is simultaneously retained. However, specific deletion of the distal part of the long arms of No. 18 may also favour cell survival. The short arms of chromosome 18 may carry genes limiting cell reproduction, while the long arms carry material promoting proliferation. More distally on the long arms, there may be genes which also limit reproduction. Disturbances affecting the balance between these components of the genome may be important in inception of neoplasia or subsequent evolution of tumour cell lines.

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“…The remaining one-third of each litter served as controls. We previously determined that injection of either 40 X 106 syngeneic lymph node cells at birth (5) or 0.2 ml of alloantiserum on postnatal days [11][12][13] The publication costs ofthis article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact.…”

Section: Methodsmentioning

confidence: 99%

Manipulation of brain DNA synthesis is achieved by using a systemic immunological disease.

Griffin¹,

Crom²,

Head³

1982

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

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Previously, we showed that as early as postnatal day 11 an immunological disease, graft-versus-host disease, induced by grafting allogeneic lymph node cells into an immunoincompetent neonatal rat significantly decreases cerebellar histogenesis-i.e., DNA synthesis and the number of newly formed neurons. Here, we report that, subsequent to successful immunotherapy, there was a reversal of the deleterious graft-versushost disease-induced alterations in DNA synthesis in individual cerebellar germinal cells. Immunotherapy involved treating the diseased rats on postnatal days 11, 12, and 13 with alloantiserum specifically directed against the grafted lymph node cells injected on the day of birth. On postnatal day 14, diseased, serum-treated, and control littermates were injected with [3H]thymidine and, 15 min later, the cerebella were excised and autoradiographed. A 0.72-mm segment of the external granular layer in the cerebellar fissure between lobules VIB and C was searched for labeled cells. The control group had the greatest number-of labeled cells, defined by the presence of six or more autoradiographic grains, (43 + 4, mean ± SEM) and the greatest number of grains per cell (9.5 ± 0.2). Rats with the disease had few labeled cells (4 ± 2) and the number of grains per cell was low (6.6 ± 0.6); however, serum treatment increased both the number of labeled cells (26 ± 8) and the number of grains per cell (7.4 ± 0.2). These results show that without mononuclear infiltrates or inflammation in the cerebellum, a systemic immunological disease can dramatically decrease DNA synthesis per germinal cell and, moreover, that halting the disease by alloantiserum therapy can reverse this effect. These findings emphasize the sensitive plastic nature of neuronal cell acquisition in the normally developing brain.To determine the extent to which neural tissue can repair, by cellular proliferation, after a period ofarrested growth or injury, manipulation of DNA synthesis is necessary-i.e., a relatively rapid (a few days) suppression and subsequent restoration of DNA synthesis paralleled by a decrease and subsequent increase in the formation of identifiable neuronal cell types. Graft-versus-host disease (GVHD), which can be arrested by treatment of host animals with alloantiserum, provides such a manipulatory process (1). Because newborn rodents are not competent to recognize foreign tissues, immunocompetent allogeneic lymph node cells grafted on the day of birth (day 0) attack and destroy host lymphomyeloid cells, thus inducing the systemic immune syndrome, GVHD (2, 3). In the course of the disease, a decrease in cell proliferation in a number of vital organs occurs (4). Furthermore, an altered gait, suggestive ofcentral nervous system involvement, is known to be one of the manifestations of GVHD. The cerebellum is indeed one of the organs adversely affected by neonatally induced GVHD, as indicated by a dramatic decrease in DNA synthesis, by postnatal day 11, an event that precedes the wasting process characterizing the late...

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Xx/Xy Lymphoid Chimærism in Congenital Immunological Deficiency Syndrome With Thymic Alymphoplasia

Cited by 191 publications

References 20 publications

Pathology of congenital rubella in Jamaica.

Pathology of congenital rubella in Jamaica.

A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia

Manipulation of brain DNA synthesis is achieved by using a systemic immunological disease.

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