摘要:

ABSTRACTSeveral syngeneic monoclonal anti-idiotypic antibodies were obtained against PY206, a monoclonal antibody specific for X-31 (H3N2) influenza virus hemagglutinin. This idiotype was found in the sera of BALB/c mice immunized with various influenza viruses. Adsorption experiments indicated that the PY206 Id was borne by antibodies specific for viral hemagglutinin (HA) and/or neuraminidase (NA). This idiotype was identified on other monoclonal antibodies specific for various influenza HAs (H3and H1). Study of the variable-region (V) genes of these monoclonal antibodies showed that its expression is independent of variable kappa (Vk)21 light-chains and that the heavy-chains of the strongly idiotype-positive hybridomas derive from either the variable heavy (VH) J558 or VH7183 family. Finally, Western blot analysis demonstrated that PY206 idiotypic determinants are located exclusively on the heavy chain.

ISSN:0882-8245    

DOI:10.1089/vim.1987.1.1

年代:1987

数据来源: MAL

摘要:

ABSTRACTA monoclonal antibody specific for glycoprotein C (gC) of herpes simplex virus type 1 (HSV-1) was used to prepare a heterologous anti-idiotypic antibody in rabbits. After absorption with normal mouse immunoglobulin (NMS) the anti-idiotypic (anti-id) antibody retained binding activity for MoAb D4.1, the immunogen. The anti-id (anti-id C) also demonstrated a cross-reactive binding activity, as shown by ELISA, for MoAb D4.2 and MoAb D4.8 which was specific for glycoprotein D (gD) and glycoprotein B (gB) of HSV-1, respectively. Also, anti-id C bound to and eluted from MoAb D4.2 and MoAb D4.8 affinity columns retained the ability to bind all three monoclonal antibodies. This crossreactive anti-id could inhibit the binding of each of the three monoclonal antibodies to their respective proteins, suggesting an antigen combining site specificity. Subsequently, the idiotope on MoAb D4.8 was shown to be outside the antigen combining site, since anti-id C recognized MoAb D4.8 complexed with gB. The anti-id, however, did not bind MoAb D4.1 or MoAb D4.2, if these monoclonals were bound to gC or gD, respectively, suggesting the cross-reactive determinant was paratopic on those two monoclonals. Immunization of mice with anti-id C could prime splenocytesinvivoto proliferate in response to HSV antigen stimulationinvitro. Thus, spleen cells involved in the HSV immune responseinvitro recognized the anti-idiotypic antibody in vivo.

ISSN:0882-8245    

DOI:10.1089/vim.1987.1.13

年代:1987

数据来源: MAL

摘要:

ABSTRACTA neutralizing monoclonal antibody (C26-15) against the haemagglutinin (H protein) of measles virus was generated which caused cell-cell fusion inhibition in cultures of measles virus-infected cells. It was shown that this phenomenon coincided with a down-regulation of the expression of both the H protein and the fusion (F) protein. We also showed cell-cell fusion inhibition with a polyclonal rabbit serum directed against Tween-ether inactivated measles virus, which did not contain biologically active antibodies against the F protein. Cell-cell fusion inhibition caused by anti-H antibodies is distinct from cell-cell fusion inhibition induced by a direct interaction of anti-F antibody with the F protein in the membrane of infected cells. Since both mechanisms may also be involved in theinvivosituation, the exclusive role for the generation of anti-F antibody to prevent virus spread by cell-cell fusioninvivois questioned. It is speculated that the observed down-regulation of both glycoproteins may lead to a less efficient killing of infected cells by cytotoxic T-lymphocytes, which may constitute an alternative explanation for the insufficient protection after vaccination with an inactivated measles vaccine.

ISSN:0882-8245    

DOI:10.1089/vim.1987.1.25

年代:1987

数据来源: MAL

摘要:

ABSTRACTThe properties of two morphologically distinct L3T4+, Lyt2−"helper" T-cell clones specific for herpes simplex virus were investigated. Both of the clones produced IL-3 and interferon, but neither produced IL-2. Clone D6.6 produced macrophage agglutinating factor, a fibronectin-like lymphokine, and also a delayed hypersensitivity (DH) response when injected locally into syngeneic mice. Despite the presence of a DH producing clone and a non-DH producing clone, both were able to reduce the local virus titre to an equivalent degree. It is suggested that this protective activity is associated with the production of interferon-γ. The significance of these results to mechanisms of protection against herpes simplex virusinvivois discuss

ISSN:0882-8245    

DOI:10.1089/vim.1987.1.35

年代:1987

数据来源: MAL

摘要:

ABSTRACTWe describe the antibody responses to three strains of canine distemper virus (CDV) isolated from dogs with chronic neurological disease in the Los Angeles area using the naturally occurring sera and cerebrospinal fluids (CSFs) of these animals as probes for comparison. CDV/CDE-2 was derived from a dog with chronic distemper encephalitis, and CDV/ODE-8 and CDV/ODE-10 were derived from dogs with old dog encephalitis. Sera and CSFs were used in autologous (same dog) and allogeneic (different dog) combinations to immune precipitate the [35S]-methionine-labelled H, P, NP, F1, and M polypeptides of the virus-infected cell cultures. The polypeptides were separated by SDS-PAGE and detected by fluorography. There was decreased recognition by the CSF and sera of the polypeptides of the viral isolates in several autologous as well as allogeneic combinations. It is concluded that the immune responses to the CDV strains are not identical, and it is likely that viral mutations occurred after the animals were infected. Some mutations may have contributed to the pathogenesis of distemper encephalitis in these animals and some may have occurred during subsequent passage of the viruses in cell culture. This may explain the decreased recognition of the polypeptides of the viral isolates by the CSF and sera.

ISSN:0882-8245    

DOI:10.1089/vim.1987.1.45

年代:1987

数据来源: MAL

摘要:

ABSTRACTThe incubation of herpes simplex virus (HSV) immune murine splenocytes with HSV antigens induced suppressor cells which inhibited HSV-specific cytotoxic T lymphocyte (CTL) induction. The cell mediating the suppression was identified as a Thy 1+Lyt 2+I-J+cell. The induction of this suppressor cell required the participation of at least three leukocyte populations. That is, depleting the cultures of either Lyt l+or Lyt 2+splenocytes resulted in a failure to induce suppressor cell activity. Likewise the removal of raacrophage-1ike antigen-presenting cells (APC), in particular I-A−I-J+APC, abolished suppressor-cell induction. Though the Lyt 2+I-J+cells had to be provided by HSV-immune mice, both the APC and the Lyt 1+cells could be provided by HSV-naive mice. Though the induction of the suppressor cell was virus specific, its action was nonspecific as evidenced by the suppression of influenza-specific CTL induction. The implication of our results for the understanding and manipulation of herpesvirus disease is briefly discusse

ISSN:0882-8245    

DOI:10.1089/vim.1987.1.55

年代:1987

数据来源: MAL

ISSN:0882-8245    

DOI:10.1089/vim.1987.1.69

年代:1987

数据来源: MAL