Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1981-11-22
pubmed:abstractText
Previous studies demonstrated that BALB/c mice with the IgA-secreting plasmacytomas MOPC-315 (alpha lambda 2), MOPC-167 (alpha kappa), McPC-603 (alpha kappa) and TEPC-15 (alpha kappa) developed large numbers of T cells with surface membrane receptors for IgA (T alpha cells). The lack of T alpha cell expansion in mice with variant plasmacytomas that were nonsecretors or low secretors of IgA implied that elevated serum IgA contributed to the increase in T alpha cells. The present studies show that normal BALB/c mice that were given daily injections of 30 mg of IgA (M315 protein) develop a marked increase in the number of T alpha cells. These studies also show that the T alpha cells induced by injection of IgA are Lyt1-2+ T cells. In addition, the data presented demonstrate that nylon wool nonadherent T cells, treated with purified polymeric IgA (M315 protein) in vitro, develop a marked increase in the number of T alpha cells. The in vitro induction of T alpha cells by IgA requires DNA and protein synthesis. These findings indicate that the T alpha cell expansion observed in mice with IgA myeloma is related to the high serum level of IgA and not to the myeloma tumor per se. In addition, these observations have a more general relevance to the issue of B cell regulation because they demonstrate that secreted immunoglobulin can directly induce expansion of immunoregulatory T cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:volume
127
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1560-3
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
T cells with Fc receptors for IgA: induction of T alpha cells in vivo and in vitro by purified IgA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't