Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1979-9-25
pubmed:abstractText
The peripheral blood lymphocytes of nine patients with hyper immunoglobulin (Ig)M immunodeficiency were studied in an attempt to define the cellular basis of this disorder. B cells were normal in number but qualitatively abnormal in all patients. Approximately one-half of the B cell consisted of small lymphocytes (7-9 mum in diameter) bearing surface IgM and IgD, as well as C3 receptors. These cells were driven to secrete IgM but not IgG after in vitro stimulation by pokeweed mitogen. In the blood there were also large lymphocytes (10-14 mum in diameter) that possessed surface as well as intracytoplasmic IgM but lacked C3 receptors. These cells spontaneously secreted large amounts of IgM in vitro and on electron microscopy were found to be rich in rough endoplasmic reticulum. Such a subpopulation of lymphoid cells was not detected in normal peripheral blood and was unique for all patients with hyper IgM immunodeficiency studied.T cells from all patients were normal in number and in function both in vivo and in vitro and were able to generate adequate T-cell help to support IgG synthesis by normal B cells. No evidence was obtained for T cells capable of suppressing normal IgG synthesis in any of the patients after coculture with normal peripheral blood lymphocytes. The defect in hyper IgM immunodeficiency is intrinsic to B cells, which fail to switch from IgM to IgG synthesis.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-1083069, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-1085328, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-13882451, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-14064315, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-14248725, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-4137918, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-4168878, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-4170578, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-4200776, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-4332899, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-4551216, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-4578158, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-4605055, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-4610075, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-5331313, http://linkedlifedata.com/resource/pubmed/commentcorrection/313404-6016801
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
385-91
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1979
pubmed:articleTitle
Hyper immunoglobulin M immunodeficiency. (Dysgammaglobulinemia). Presence of immunoglobulin M-secreting plasmacytoid cells in peripheral blood and failure of immunoglobulin M-immunoglobulin G switch in B-cell differentiation.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.