Serum immunoglobulin (Ig) levels were measured in 788 coalworkers and 121 nonmining controls for comparison with the radiological category of pneumoconiosis after taking into account age and smoking habit. In addition a simple assessment of humoral immune competence was made by estimating the titre of serum antibody against the common gut commensal Escherichia coli. Smoking was found to depress serum IgA and IgM whilst levels of IgG and IgA increased slightly with age. Men with radiological signs of coalworkers pneumoconiosis (CWP) had significantly raised levels of IgA and IgG with increasing pneumoconiosis category. Even coalworkers with less than category 1 simple pneumoconiosis had raised levels of IgA, suggesting that increased production of this immunoglobulin occurs before radiologically identifiable pathological changes have occurred in the lung tissue. No association between reduced humoral immune competence and radiological category of pneumoconiosis was found. Whether high Ig levels in men exposed to coal dust are merely a passive response to dusted lung tissue or whether they indicate that an immunological process is important in the development of pneumoconiotic lesions remains uncertain.

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Sera from 2421 coalminers, representing all the radiological categories of pneumoconiosis, and from 260 healthy blood donors, as controls, were examined for antinuclear factor and rheumatoid factor. Antinuclear factors were present in 21.5% of sera from the controls and in 23.1 % from the coalminers' group. Rheumatoid factor was present in 5.3% of coalminers and as expected occurred particularly in the few men with progressive massive fibrosis who also had rheumatoid disease. The combined prevalence of both factors showed an increase with age at all disease levels and a significant association with pneumoconiosis category only in men older than 60 years. This study provides no evidence that autoantibodies are likely to be of value in detecting men predisposed to the development of massive fibrosis other than those with rheumatoid disease.

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SUMMARYIn this review B cell responses in HIV-infected individuals are summarized together with the techniques used to date to produce human monoclonals to HIV and the properties of these antibodies. Profound disturbances in B cell responses are apparent both in vivo and in vitro. While there is evidence in vivo of marked polyclonal B cell activation, primary and secondary antibody responses are impaired. Similarly these cells exhibit spontaneous immunoglobulin secretion upon in vitro culture but do not readily respond to B cell mitogens and recall antigens including HIV. Furthermore, certain of these defects can be reproduced in normal B cells in vitro by incubation with HIV or HIV coded peptides. Individuals infected with HIV develop antibodies to HIV structural proteins (e.g. pl7, p24, gp41 and gpl20) and regulatory proteins (e.g. vif, nef, RT). Autoantibodies against a number of immunologically important molecules are also frequently observed. The anti-HIV antibodies are predominantly ofthe IgGl isotype and exhibit a variety of effects on the virus in vitro. To date, using conventional immortalization strategies, an appreciable number of human monoclonals to HIV have been developed. These have been specific for gp41, gpl20 and gag with antibodies ofthe former specificity predominating. The majority of these antibodies have been ofthe IgGl isotype. Only a small number ofthe antibodies neutralize virus in vitro and most of these react with gpl20. The neutralizing antibodies recognize conformational and carbohydrate epitopes or epitopes in amino acid positions 306-322. The predominant epitopes recognized by the anti-gp41 antibodies were in amino acid positions 579-620 and 644-662. A high percentage (=^ 25%) of these antibodies enhance viral growth in vitro. The problems relating to the production of human monoclonals to HIV are discussed together with strategies that could be used in the future.