Virus-specific proliferative T-cell responses: parameters and specificity
Autor: | R.M. Zinkernagel, G. Kreeb |
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Rok vydání: | 1980 |
Předmět: |
Time Factors
viruses T cell T-Lymphocytes Immunology Spleen Stimulation Vaccinia virus Major histocompatibility complex Antibodies Viral Virus chemistry.chemical_compound Mice In vivo medicine Animals Mice Inbred BALB C Mice Inbred C3H biology Macrophages H-2 Antigens Chromosome Mapping Molecular biology In vitro Mice Inbred C57BL medicine.anatomical_structure chemistry biology.protein Vaccinia Cell Division |
Zdroj: | Cellular immunology. 53(2) |
ISSN: | 0008-8749 |
Popis: | The genetic requirements for inducing virus-specific T-cell proliferation were investigated by taking spleen cells from animals primed with vaccinia virus in vivo , then culturing the cells in vitro with vaccinia virus-infected syngeneic peritoneal macrophages, and finally restimulating these cells a second time in vitro with vaccinia virus-infected macrophages from several strains of mice. Under these conditions, T cells proliferated in the tertiary response to virus-specific stimulation, whereas background proliferation caused by allogeneic differences between stimulator and responder cells was minimal. Compatibility between T cells and infected stimulator cells at the K or I regions alone or at I - A or I - A + I - B regions of the major histocompatibility complex (MHC) produced strong proliferative responses, whereas compatibility at D alone often resulted in somewhat weaker responses. However, these responses were rarely as great as in combinations of completely syngeneic stimulator and responder cells. Homology between responding and virus-infected stimulating cells in more than one of the H -2 K , D , or I regions resulted in an additive, but not potentiating, effect. Genes coded outside the H-2 region did not seem to play a role in this system. In some rare cases, a weak response occurred across allogeneic barriers, but in general, virus-specific T-cell proliferation was strongly H-2 restricted. |
Databáze: | OpenAIRE |
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