Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
|
pubmed:dateCreated |
1990-9-27
|
pubmed:abstractText |
Lymphocyte function and cell surface phenotype were examined in fifteen patients with late onset hypogammaglobulinaemia. The percentage of surface immunoglobulin-positive B cells in fourteen of the fifteen patients was in the normal range. Patients' B cells expressed MHC class II antigens at normal levels. For one patient, there was relatively high sIgD and low sIgM expression on B cells; the rest of the patients did not differ from controls in surface immunoglobulin density. The proportion of B cells positive for CD5 in patients was comparable to normal controls, and considerably less than in cord blood. However, the pattern of immunoglobulin isotype secretion in vitro by patients' B cells closely paralleled responses of cord blood B cells. Spontaneous secretion of IgM and IgG by patients' B cells was very low. Following polyclonal activation in the presence of autologous T cells, cells from thirteen patients secreted IgM within the normal range in response to at least one activator. The response of patients' purified B cells to IL-2 and gamma-IFN was variable. For four of six tested, B cells cultured with IL-2 and gamma-IFN together with polyclonal activators secreted normal levels of IgM. B cells from the other two patients secreted little or no IgM in response to these cytokines. For fourteen patients, IgG secretion following polyclonal activation remained low both when B cells were cultured with T cells or with a combination of IL-2 and gamma-IFN. IgG subclass imbalance was seen in one patient, whose cells secreted an unusually high proportion of IgG3, and undetectable IgG2 and IgG4; this pattern was consistent whether T cell help was provided by autologous or allogeneic T cells. Similarly purified B cells from this patient showed deficient IgG2 and IgG4 production in response to IL-2 and gamma-IFN.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD5,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-DR Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin M,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
|
pubmed:status |
MEDLINE
|
pubmed:issn |
0278-0240
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
8
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
69-83
|
pubmed:dateRevised |
2011-11-17
|
pubmed:meshHeading |
pubmed-meshheading:1696871-Adult,
pubmed-meshheading:1696871-Agammaglobulinemia,
pubmed-meshheading:1696871-Aged,
pubmed-meshheading:1696871-Antigens, CD,
pubmed-meshheading:1696871-Antigens, CD5,
pubmed-meshheading:1696871-Antigens, Differentiation,
pubmed-meshheading:1696871-B-Lymphocytes,
pubmed-meshheading:1696871-Cell Membrane,
pubmed-meshheading:1696871-Female,
pubmed-meshheading:1696871-HLA-DR Antigens,
pubmed-meshheading:1696871-Histocompatibility Antigens Class II,
pubmed-meshheading:1696871-Humans,
pubmed-meshheading:1696871-Immunoglobulin G,
pubmed-meshheading:1696871-Immunoglobulin M,
pubmed-meshheading:1696871-Interferon-gamma,
pubmed-meshheading:1696871-Interleukin-2,
pubmed-meshheading:1696871-Lymphocyte Activation,
pubmed-meshheading:1696871-Male,
pubmed-meshheading:1696871-Middle Aged,
pubmed-meshheading:1696871-Phenotype,
pubmed-meshheading:1696871-Recombinant Proteins,
pubmed-meshheading:1696871-T-Lymphocytes
|
pubmed:articleTitle |
B cell differentiation and lymphocyte surface phenotype in late onset hypogammaglobulinaemia.
|
pubmed:affiliation |
Division of Immunology, School of Pathological Sciences, University of Newcastle upon Tyne.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|