Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1989-7-24
pubmed:abstractText
Elimination of CD4+ helper T cells by treatment with monoclonal antibodies (mcAb) in vivo has been used as a new mode of immunosuppression in organ transplantation and autoimmune diseases. To explore the potential risks of this therapeutic approach we have studied antiviral responses in mice depleted of CD4+ T cells. Depletion of CD4+ T cells in vivo completely suppressed the generation of a primary virus-specific cytotoxic response. Injection of high doses of recombinant interleukin-2 (rIL-2) given after virus immunization restored the responsiveness of helper cell-depleted mice to virus-expressing target cells, suggesting a crucial role of IL-2 in antiviral defense mechanisms. In contrast to primary responses, memory cytolytic responses to viral antigens persisted despite depletion of greater than 90% of CD4+ helper T cells. The generation of such memory cytotoxic responses was dependent upon help provided by CD4+ lymphocytes surviving the antibody therapy. After antibody treatment, frequencies of virus-specific helper cells were minimal in primed mice, excluding insufficient helper cell elimination as the reason for the persistence of memory responses. Data presented here suggest that there exist distinct helper pathways in primary and secondary cytolytic antiviral responses that might represent several subsets of helper T cells as well as differences in helper signals required by distinct effector cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0041-1337
pubmed:author
pubmed:issnType
Print
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1034-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:2472023-Animals, pubmed-meshheading:2472023-Antibodies, Monoclonal, pubmed-meshheading:2472023-Antibodies, Viral, pubmed-meshheading:2472023-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:2472023-Cell Line, pubmed-meshheading:2472023-Epitopes, pubmed-meshheading:2472023-Immunization, Secondary, pubmed-meshheading:2472023-Immunosuppressive Agents, pubmed-meshheading:2472023-Interleukin-2, pubmed-meshheading:2472023-Lymphocyte Activation, pubmed-meshheading:2472023-Lymphocyte Depletion, pubmed-meshheading:2472023-Mice, pubmed-meshheading:2472023-Mice, Inbred BALB C, pubmed-meshheading:2472023-Mice, Inbred C57BL, pubmed-meshheading:2472023-Moloney murine sarcoma virus, pubmed-meshheading:2472023-Neoplasm Transplantation, pubmed-meshheading:2472023-Recombinant Proteins, pubmed-meshheading:2472023-Sarcoma, Experimental, pubmed-meshheading:2472023-Stem Cells, pubmed-meshheading:2472023-T-Lymphocytes, Cytotoxic
pubmed:year
1989
pubmed:articleTitle
Immunosuppression by anti-CD4 treatment in vivo. Persistence of secondary antiviral immune responses.
pubmed:affiliation
Department of Medicine, Heidelberg University Medical School, Federal Republic of Germany.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't