Monoclonal antibodies putatively identifying porcine B cells.

Comparison was made of the binding of 38 test and three standard monoclonal antibodies (mAbs) to B cells from various pig lymphoid tissues by flow cytometry (FCM) and immunohistochemistry. Some mAbs were also tested on B cells from foetal pig tissues. Twenty of the new mAbs bound, though to variable degrees, to porcine B cells but only three were given cluster assignations: C35 (#147) and BB6-11C9 (#167) were assigned to wCD21 and 2F6/8 (#057) was assigned to SWC7.

Changes in swine macrophage phenotype after infection with African swine fever virus: cytokine production and responsiveness to interferon-gamma and lipopolysaccharide.

Cytokines produced by cells of the immune system, including macrophages, can influence inflammatory responses to viral infection. This has been exploited by viruses, which have developed strategies to direct the immune response towards ineffective responses. African swine fever virus (ASFV) is a double-stranded DNA virus that infects macrophages of domestic swine. In this study, primary cells of monocyte macrophage lineage were obtained from the lungs, peritoneum or blood of domestic swine and, after infection with ASFV, supernatants were tested for cytokines using biological assays. The cytokine transforming growth factor-beta (TGF-beta) was detected after infection of macrophage preparations, but tumour necrosis factor (TNF) and interleukin-1 (IL-1) were not detected. ASFV-infected and uninfected macrophage populations were also tested to assess their ability to respond to cytokines by enhancing production of superoxide in the respiratory burst mechanism. Responses to interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS) were suppressed in macrophage populations infected with virus, even at low multiplicities of infection. Addition of TGF-beta to uninfected macrophages resulted in a similar suppression of response, but antibody to TGF-beta did not prevent suppression induced by virus. These results are discussed in relation to the pathology of African swine fever.

Monoclonal antibodies defining differentiation antigens of swine lymphoid and myeloid cells.

Monoclonal antibodies recognising swine leucocyte antigens were identified and the corresponding antigens were characterised by determining their tissue distribution and molecular weight as well as immunohistochemical staining. On the basis of these data, we suggest that two antibodies are specific for a molecules within a porcine orthologue of one of the human CDII/CD18 complexes. We suggest that two others recognise swine wCD21, that one may recognise swine wCD6 and that another recognises an antigen designated by the International Swine CD Workshop cluster SWC9. Other antibodies were obtained which are specific for swine macrophages or B cells, but CD or cluster assignments for these antigens have not been made. Detailed analysis of the antibodies is presented. It is proposed that these antibodies will be useful in studies of the pig immune system and of virus infection.

Secretion of a macrophage-activating factor distinct from interferon-gamma by human T cell clones.

Supernatants from clones of human T lymphocytes that were responding to a purified Mycobacterium tuberculosis antigen were able to activate macrophages and macrophage-like myeloma cells (U937) to release increased amounts of the microbicidal agent hydrogen peroxide. The activity was not neutralized by monoclonal antibody against interferon-gamma (IFN-gamma), was greater than could be accounted for by the IFN-gamma activity in the supernatants, and was separated from IFN-gamma by high performance liquid chromatography. It is evident that IFN-gamma is not the only macrophage activator released by T lymphocytes responding to microbial antigen, and may not even be the main one to enhance antimicrobial activity in infections such as tuberculosis.

The reaction of the anti-interferon-alpha monoclonal antibody, NK2, with different interferons.

Analysis of the neutralization of human interferon-alpha by the monoclonal antibody NK2 showed, by three different methods, that the avidity constant was about 10(10)M-1. A small decrease in the avidity constant (and in the antibody titre) with increasing interferon concentrations was observed, suggesting that the antibody-interferon complex had a little biological activity. The antibody neutralizes the interferon by preventing the binding of interferon to susceptible cells. It does not react with human-gamma, mouse-alpha, monkey, bovine or rabbit interferons.