Low frequency of HLA-B27 and scarcity of ankylosing spondylitis in a Zairean Bantu population.

Ankylosing spondylitis (AS) is an inflammatory rheumatic disease which is thought to be rarely seen in African Blacks. Its genetic predisposition has been stressed in Caucasians where the HLA-B27 antigen is firmly linked to the disease. In the present study, HLA-B27 antigen was determined in 146 individuals of Bantu root. Only one of these subjects was found to possess HLA-B27 antigen. This study correlates the low frequency of HLA-B27 with the observed scarcity of AS in patients attending a clinic in Kinshasa for osteoarticular diseases.

Evidence for HTLV-III/LAV expression by primary cultures of T8 cells.

The selective targets for HTLV-III/LAV, the causal infectious agent of AIDS and AIDS-related complex (ARC), are T4 cells, apparently because the virus receptor is associated with T4 antigen determinants. This accounts for T4 cell depletion in AIDS and for a decrease of IL-2 production by AIDS peripheral blood lymphocytes (PBL) after in vitro PHA activation. By contrast, T8 cells are not targets for HTLV-III/LAV, since T8 cells from PBL and from long-term cultured T cells (CTC) could not be infected by the virus. We describe 2 samples of PBL from Zairian patients with HTLV-III infection in which HTLV-III was expressed by T8 cells. Evidence that T8 cells were expressing virus was obtained by complement cytotoxicity experiments performed in the presence of OKT8 monoclonal antibody (MAb), which removed HTLV-III-positive cells from cultured T cells producing the virus, and by double labelling experiments, in which some cells exhibit both T8 antigens detected either by IFA (rhodamine) or by rosetting in presence of OKT8 MAbs and HTLV-III antigens detected by IFA (fluorescein) with of anti-HTLV-III p24 and p15 MAbs. Since normal T cells have previously been shown to undergo antigenic diversity, we think these results can be explained by HTLV-III infection of T4 cells which later lost T4 antigens and acquired the T8 phenotype.

[Treatment of idiopathic thrombopenic purpura with immunoglobulins]. / Le traitement du purpura thrombopénique idiopathique par les immunoglobulines.

Twelve patients presenting with idiopathic thrombocytopenic purpura were treated with injections of immunoglobulins. A lasting improvement was observed in 1 and a transient improvement in 8. Intramuscular injections appeared to be more effective than intravenous injections. The increase in the number of platelets was accompanied by a decrease of circulating immune complexes. The antigen-antibody reaction observed between the doses of immunoglobulins injected and the patients' sera suggests that immunoglobulins might act by enhancing the elimination of some antigens of infectious origin.

Circulating immune complexes and disease activity in Crohn's disease.

Circulating immune complexes were determined in 59 consecutive patients with Crohn's disease and 100 blood donors by a double method based on the inhibition of the agglutinating activity of CIq and/or rheumatoid factor on the IgG-coated polystyrene particles. In patients, the incidence of positive immune complexes was 63% and 61% at first testing, 85% and 78% at subsequent determinations; there was a good correlation between the inhibition titres of CIq and those of rheumatoid factor (p less than 0.001). In blood donors, the incidence was 22% and 14% at low titre. The incidence of immune complexes was the lowest (36%) in the group of resected patients without signs of relapse; repeat determinations showed absence of immune complexes three months postoperatively. In patients medically treated for primary disease or relapse, rheumatoid factor titre higher than 1/1 was less frequent than in medically untreated patients with active disease (p less than 0.01). A significantly higher concentration of serum alpha-1-antitrypsin and orosomucoid, and a significantly lower level of serum iron were found in patients with an IC titre exceeding 1/1; longitudinal studies showed in most cases a concordance between the evolution of immune complex titres, inflammatory parameters and clinical status.

The occurrence of circulating immune complexes and viral antigens in idiopathic thrombocytopenic purpura.

The sera of seventy-two patients with ITP were tested for their inhibitory activity on the agglutination of IgG-coated particles by RF or C1q. The majority (83%) displayed an inhibitory effect toward both agglutinators, whereas 17% were found to contain endogenous RF. A negative correlation was observed between the number of platelets and the titres of inhibitory factors. Some sera were fractionated by gel filtration. The inhibitory factors and sometimes trace amounts of IgG were distributed over several peaks eluted before monomeric 7S IgG. The IgG detected in the heavy fractions of two ITP sera corresponded to antigen-antibody complexes as shown by dissociation experiments at acid pH. In all ITP sera analysed by chromatography, DNA has been detected in the heavy fractions and appears to be the antigen of certain complexes. The sera from forty-two patients with ITP were analysed by counter-electrophoresis for the presence of viral antigens. HBs antigen was detected in twenty sera, EBV antigen in five, and adenovirus antigen in six.

Detection of circulating antigen-antibody complexes by their inhibitory effect on the agglutination of IgG-coated particles by rheumatioid factor of Clq.

The agglutination of Ig-coated particles by human RF or Clq can be inhibited by Ig aggregates or AgAb complexes. The effect of Ig class was studied by means of agarose-linked human monoclonal Igs. RF was inhibited by all subclasses of IgG and IgA but not by IgM, whereas Clq reacted with IgM, IgG3 and IgG1. Heat-aggregated IgG3 was fractionated by gel-filtration on Ultrogel. Inhibition was restricted to certain fractions of aggregates, viz (IgG3) approximately 7 and (IgG3) approximately 21 for RF, and (IgG3) approximately 10, (IgG3) approximately 14 and (IgG3) approximately 27 for Clq. In a precipitin curve experiment, it was found that RF was inhibited by soluble complexes over an extended range of AgAb ratios, the inactivation of Clq being limited to complexes with 2-5 times antigen excess. Inhibiting factors were found in patients with various diseases and, at low titres, in 22% of healthy people. In 27% of patients' sera, the inhibitors were demonstrable by Clq only after removal of endogenous RF by adsorption on insolubilized IgG. In several patients endogenous agglutinating activity and direct inhibitory activity tended to alternate during the course of the disease. Sera from various patients were also filtrated on Ultrogel and the elution was monitored by immunoassay of IgA, IgM and IgG, as well as by the two inhibition tests. The inhibiting factors were distributed over several peaks which only partially coincided with the elution profiles of IgG and IgM.