Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-12-23
pubmed:abstractText
Herpes simplex virus type 2 (HSV-2) infection is the most common cause of genital ulcerative disease in the developed world. Keratinocytes are the primary cells involved in clinical lesions caused by HSV-2. In our study, we intensively examined cytokine expression in the HSV-2-infected keratinocytes. We observed upregulation of a series of cytokines including early-induced antiviral cytokines as interferons ?, ? (IFN-?, ?), tumor necrosis factor ? (TNF-?), colony stimulating factors (CSFs) as G-CSF, GM-CSF, interleukin 3 (IL-3), growth factors (EGF, KGF, and IGF-?1), defensins, selectins, leukocyte function-associated antigens (LFAs,) and toll-like receptors (TLR-2, 3, 4, and 9). More importantly, we found that HSV-2-infected keratinocytes stimulated the proliferation of lymphocytes in co-cultivation system. These data suggest that keratinocytes participate in the immune response to HSV-2 infection in two ways. They secrete inflammatory cytokines to resist the HSV-2 infection directly and recruit the immune cells to eliminate the primary infection indirectly and enhance the adaptive immunity to prevent subsequent infections.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0001-723X
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
261-7
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Keratinocytes play a role in the immunity to Herpes simplex virus type 2 infection.
pubmed:affiliation
Shenzhen Key Lab for Translational Medicine of Dermatology, Guangdong Province, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't