Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1989-3-13
pubmed:abstractText
A syndrome characterized by lymphadenopathy, hypergammaglobulinemia, and immunodeficiency develops in C57BL/6 mice inoculated with LP-BM5 murine leukemia viruses. By studying the number and antigenic specificity of B cells activated in the course of this disease, we found that a series of reproducible changes in the humoral immune system were induced by retroviral infection. The rate of B cell proliferation and the proportion of B cells activated to secrete Ig increased by nearly 10-fold at 4 wk post inoculation. B cells producing antibodies reactive with a panel of three conventional Ag and five autoantigens were stimulated simultaneously and proportionally to secrete, demonstrating that such activation was polyclonal in nature. At 12 wk post infection, the number of Ig-secreting B cells continued to rise and significant hypergammaglobulinemia developed. At 16 wk post infection, immunostimulation gave way to immunosuppression, as evidenced by a slight decline in the number of Ig-secreting lymphocytes and a sharp reduction in the concentration of serum antibody. At this time, the B cell repertoires of infected mice diverged markedly from those of uninfected animals. These changes are comparable to those found in some patients infected with HIV, and provide a useful model to study the association between retroviral infection and regulatory abnormalities of the humoral immune system.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
142
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1144-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Characteristics of B cell proliferation and activation in murine AIDS.
pubmed:affiliation
Infectious Diseases Branch, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, MD 20892.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.