Differentiation of precursor T lymphocytes in man and delineation of the selective abnormalities in severe combined immune deficiency disease

1982 ◽  
Vol 25 (3) ◽  
pp. 303-315 ◽  
Author(s):  
Erwin W. Gelfand ◽  
Hans-Michael Dosch
Keyword(s):  
Immune Deficiency ◽  
T Lymphocytes ◽  
Deficiency Disease ◽  
Severe Combined Immune Deficiency ◽  
Combined Immune Deficiency

Human RANTES induces the migration of human T lymphocytes into the peripheral tissues of mice with severe combined immune deficiency

1994 ◽  
Vol 24 (8) ◽  
pp. 1823-1827 ◽  
Author(s):  
William J. Murphy ◽  
Dennis D. Taubu ◽  
Miriam Anveru ◽  
Kevin Conlonu ◽  
Joost J. Oppenheimu ◽  
...  
Keyword(s):  
Immune Deficiency ◽  
T Lymphocytes ◽  
Severe Combined Immune Deficiency ◽  
Peripheral Tissues ◽  
Human T Lymphocytes ◽  
Combined Immune Deficiency

Development of Autologous T Lymphocytes in Two Males with X-Linked Severe Combined Immune Deficiency: Molecular and Cellular Characterization

2000 ◽  
Vol 95 (1) ◽  
pp. 39-50 ◽  
Author(s):  
Patrizia Mella ◽  
Luisa Imberti ◽  
Duilio Brugnoni ◽  
Silvia Pirovano ◽  
Fabio Candotti ◽  
...  
Keyword(s):  
Immune Deficiency ◽  
T Lymphocytes ◽  
Severe Combined Immune Deficiency ◽  
Combined Immune Deficiency

scholarly journals Identification of astrovirus serotypes from children treated at the Hospitals for Sick Children, London 1981–93

1994 ◽  
Vol 113 (1) ◽  
pp. 153-159 ◽  
Author(s):  
J. Noel ◽  
D. Cubitt
Keyword(s):  
Immune Deficiency ◽  
Aqueous Suspension ◽  
Deficiency Disease ◽  
Severe Combined Immune Deficiency ◽  
Virus Particles ◽  
Combined Immune Deficiency ◽  
Sick Children ◽  
Type 3

SUMMARYAn enzyme immunoassay (EIA) for astrovirus type 1 together with immune electronmicroscopy (IBM) was used to type a collection of 162 astroviruses obtained from 1981–93 from children with diarrhoea. The EIA was found to be specific for astrovirus type 1. Astrovirus types 2–4 were typed by IEM.Astrovirus type 1 was the prevalent serotype 107/125 (86%), followed by type 3 (8%), type 4 (6%) and type 2 (1 %). Six samples containing astrovirus could not be typed or detected by EIA because they were coated with coproantibodies; 11 others were not identified. Virus particles could no longer be detected in 15/162 (9%) samples following storage for≥2 years.Selected samples containing astrovirus types 1–4 were passaged in CaCO2cells and their identity confirmed by one or both assays. One sample was shown to have remained viable for 10 years when stored as an aqueous suspension at −20 °C.Two patients with severe combined immune deficiency disease (SCID) were shown to be excreting astrovirus type 1 for 32 and 102 days respectively. One child was simultaneously shedding rotavirus and the other child was excreting adenovirus.

Identical mutations in RAG1 or RAG2 genes leading to defective V(D)J recombinase activity can cause either T-B–severe combined immune deficiency or Omenn syndrome

Blood ◽  
2001 ◽  
Vol 97 (9) ◽  
pp. 2772-2776 ◽  
Author(s):  
Barbara Corneo ◽  
Despina Moshous ◽  
Tayfun Güngör ◽  
Nicolas Wulffraat ◽  
Pierre Philippet ◽  
...  
Keyword(s):  
Immune Deficiency ◽  
T Lymphocytes ◽  
Gene Mutations ◽  
Omenn Syndrome ◽  
Severe Combined Immune Deficiency ◽  
Recombination Activating Genes ◽  
Developmental Program ◽  
Combined Immune Deficiency ◽  
Inherited Mutations

Abstract Omenn syndrome (OS) is an inherited disorder characterized by an absence of circulating B cells and an infiltration of the skin and the intestine by activated oligoclonal T lymphocytes, indicating that a profound defect in the lymphoid developmental program could be accountable for this condition. Inherited mutations in either the recombination activating genes RAG1 orRAG2, resulting in partial V(D)J recombinase activity, were shown to be responsible for OS. This study reports on the characterization of new RAG1/2 gene mutations in a series of 9 patients with OS. Given the occurrence of the same mutations in patients with T-B–severe combined immune deficiency or OS on 3 separate occasions, the proposal is made that an additional factor may be required in certain circumstances for the development of the Omenn phenotype. The nature of this factor is discussed.

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