Biomedical subjects
Publications and source records attributed to F Shakib.
The quantitative measurement of the IgG subclass composition of the sera from sixteen patients with cystic fibrosis has revealed grossly elevated levels of IgG4 in seven patients. The possible significance of this observation is discussed in relation to recent reports of a high incidence of immediate-type hypersensitivity in such patients.
The IgG subclass composition of 24 matched pairs of synovial fluids and sera, from 24 patients with rheumatoid arthritis, was determined. The subclass composition of rheumatoid synovial fluid IgG was found to be qualitatively the same as that of the corresponding serum, differing only in certain quantitative aspects. A 7-8% increase in IgG1 level found in the sera of rheumatoid arthritis patients relative to that in the sera of normal individuals was accompanied by 6-8, 0-7, and 0-3% decreases in IgG2, IgG3, and IgG4, respectively.
The radial immunodiffusion method of Mancini has been applied to quantitative study of IgG subclasses in a normal population. The method was assessed in terms of both reproducibility and antiserum consumption. The distribution of IgG subclasses in a group of normal individuals was studied, and compared with their incidence in a series of monoclonal proteins investigated by previous workers and particularly with other quantitative studies on groups of normal individual's sera.
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Although milk-specific IgG4 is frequently detectable in sera of apparently healthy individuals, the presence of alpha-casein (AC IgG4-specific) in high concentration (i.e. greater than 9.98 micrograms/ml) appears to be diagnostic of milk intolerance causing eczema in adults. The detection of egg-specific IgG4, on the other hand, has no similar diagnostic potential in egg-intolerant cases.
Although IgG4 (or at least one of its variants) does have receptors on basophils, this IgG subclass apparently cannot mediate an allergen-triggered release of mediators. Evidence is now available to suggest that IgG4-bearing basophils can be "fired off" to release histamine with an IgM anti-IgG which is frequently found in atopic patients. If an autoimmune process of the kind described here can contribute to the pathological changes in atopic disorder, then a whole new approach to the diagnosis and treatment of allergic disease must be considered.
In this paper we hypothesise that circulating autoanti-IgE antibodies, which are found in allergic asthma patients, could potentially enhance IgE synthesis by blocking its binding to CD23 on B lymphocytes, thereby potentiating the release of soluble fragments of CD23 which have B cell growth-promoting activity. We have investigated this possibility indirectly by measuring soluble (s) CD23 and IgG subclass anti-IgE antibody levels in asthmatic patients' sera, to find out if the two parameters are related. However, we were unable to show any significant correlations between serum IgG subclass anti-IgE activities and sCD23 levels. This may have been due, at least in part, to the heterogeneous epitope specificity of the autoanti-IgE being detected. Interestingly, there was a significant inverse correlation (p = 0.0178) between serum IgE and sCD23 levels in asthma; an observation which underlines the notion that binding of IgE to membrane CD23 abrogates the release of sCD23. The present study confirms and extends previous reports of significantly raised circulating levels of IgG anti-IgE in asthma patients (p = 0.0004), by further demonstrating that IgG anti-IgE is mostly restricted to IgG1. Given that IgG1 binds very efficiently to C1q and Fc gamma Rs, our observation lends further support to the notion that IgG anti-IgE may facilitate the removal of IgE-allergen complexes by triggering IgG effector function pathways.
We have compared hookworm infection intensity, as determined by fecal egg count, and circulating levels of IgE and autoantibodies to IgE in atopic and nonatopic parasitized (predominantly hookworm-infected) patients from Kebasob village on Karkar Island, Papua New Guinea. Our study has clearly established that parasitized atopic individuals have significantly higher levels of IgE and autoanti-IgE than their nonatopic counterparts, and that atopy does not appear to influence accumulated levels of hookworm infection. These data, therefore, do not support an earlier report that suggested that the atopic state may confer increased resistance to hookworm infestation in a parasitized community in Papua New Guinea.