Transplantation immunity to simian virus 40-transformed cells in tumor-bearing mice. II. Evidence for macrophage participation at the effector level of tumor cell rejection.
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Biomedical subjects
J M Zarling
Publications and source records attributed to J M Zarling.
Participation of macrophages in tumor immunity.
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Animals↗
Expression of concanavalin A binding sites in rabbit kidney cells infected with vaccinia virus.
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Agglutination↗
In vitro assessment of cellular immunity to vaccinia virus: contribution of lymphocytes and macrophages.
The possible contributions of lymphocytes and macrophages to immunity to vaccinia virus were examined in vitro by determination of antigen-specific inhibition of migration of macrophages and the replication of the virus in purified macrophages. Lymphocytes from various anatomic sites of vaccinia virus-immune rabbits mixed with macrophages from nonimmune rabbits resulted in antigen-specific inhibition of macrophage migration; purified lymphocytes of peritoneal exudates were found to be the most potent inhibitors. Macrophages from peritoneal exudates of immune rabbits purified to contain less than 1% lymphocytes were sensitive to inhibition of migration by vaccinia antigens. Virus grew in macrophages from nonimmune rabbits, but failed to replicate in macrophages from the peritoneal cavity of immune rabbits. Alveolar maracrophages from immune rabbits were not inhibited from migrating in the presence of the viral antigen, and the virus replicated in these cells. The data suggest, but do not prove, that cellular immunity to vaccinia virus in rabbits may be mediated both by lymphocytes and by macrophages.
Journal Article↗
T-cell responses to human AIDS virus in macaques immunized with recombinant vaccinia viruses.
There is much interest in developing vaccines against acquired immune deficiency syndrome (AIDS), which is caused by a retrovirus termed human immunodeficiency virus (HIV). Isolates of this virus include human T-lymphotropic virus type III (HTLV-III), lymphadenopathy-associated virus (LAV), and AIDS-associated retrovirus (ARV). Several approaches towards the development of an AIDS vaccine result in the production of antibodies in subprimates. These methods involve the use of: antigens isolated from the AIDS virus; viral antigens expressed by transfected cells or by recombinant vaccinia viruses; and particular synthetic peptides of viral antigens. Because T-cell-mediated immunity (in addition to antibodies) is involved in resistance to diseases and death caused by various enveloped viruses, we sought to determine whether potential AIDS vaccines can induce T-cell responses against the AIDS virus. Here we report that immunization of non-human primates, Macaca fascicularis (macaques), with recombinant vaccinia viruses that express LAV envelope glycoproteins gp41 and gp110 results not only in the production of antibodies against the LAV envelope antigens but also in the generation of T-cells that proliferate and produce the lymphokine interleukin-2 (IL-2), in response to stimulation with purified LAV. We believe this is the first report demonstrating T-cell-mediated immunity to the virus that causes AIDS.
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Evaluation of protective efficacy of recombinant subunit vaccines against simian immunodeficiency virus infection of macaques.
Simian immunodeficiency virus (SIV) was used as a model to study the protective efficacy of an immunization regimen currently being evaluated as candidate vaccines against HIV in human subjects. Four Macaca fascicularis were first immunized with recombinant vaccinia virus expressing the envelope glycoprotein gp160 of SIVmne and then boosted with subunit gp160. Both cell-mediated and humoral immune responses against SIV, including neutralizing antibodies, were elicited. The macaques were shown to be protected from a homologous virus infection as determined by serology, lymphocyte cocultivation, polymerase chain reactions and in vivo transmission analyses. Four unimmunized control animals were readily infected. However, viremia in infected control animals could decrease substantially following the initial phase of infection so that persistent infection might not be readily detectable.
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