Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1993-11-9
pubmed:abstractText
Mycoplasma arthritidis produces a potent superantigen (MAM) that activates specific murine and human T lymphocytes to proliferate and secrete lymphokines. We show here that MAM also influences both T- and B-cell functions in vivo. Lymphocytes from mice injected with MAM exhibit a suppression of proliferative responses to MAM in vitro but only a partial suppression of responses to other mitogens. This T-cell anergy not only decreased contact sensitivity to dinitrofluorobenzene but also prolonged survival of skin transplants. In contrast, B-cell reactivity is increased following in vivo injection of MAM, as evidenced by enhanced antibody responses to sheep red blood cells and ovalbumin. Also, there is a marked decrease in the ability of splenocytes from MAM-injected mice to produce interleukin-2 (IL-2) but a marked increase in their ability to produce IL-4 and IL-6. The combined results suggest that MAM induces a lymphokine profile that favors activation of B-cell functions, with a resulting potential for triggering of autoimmune disease.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1058-4838
pubmed:author
pubmed:issnType
Print
pubmed:volume
17 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S163-9
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Immunomodulation in vivo by the Mycoplasma arthritidis superantigen, MAM.
pubmed:affiliation
Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City 84132.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't