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Results for “Immune Complex Diseases”

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At least 37 records · Page 2Linked to original sources
PubMed1998

The immune system can affect learning: chronic immune complex disease in a rat model.

Evidence is presented that the immune system can affect central nervous system functioning, leading to changes in learning. Immune complex disease is induced in rats and their behavior tested using a Lashley maze. Significant differences in behavior were found between the animals with high disease activity and those with low disease activity and the non-disease controls. These changes were not due to uremia and are most likely due to the immune response. There is some evidence immune complex deposits in the choroid plexus may play some role, but not the sole or major role in the behavioral changes. This provides a model by which immunologic processes can cause neuropsychiatric manifestations in autoimmune diseases like lupus, as well as showing that immune processes can affect behavioral functioning.

Animals↗
PubMed1992

The Seventh K Prathap Memorial Lecture. The pathogenesis of autoimmune immune complex disease.

It has been proposed that autoimmune immune complex disease, of which SLE is the type example, is caused essentially by a failure to properly metabolise immune complexes and that this allows the establishment of feedback cycles which cause more immune complexes to be formed. The essential genetic predisposition to this disease is complement deficiency of the components of the early classical pathway and some degree of genetic complement deficiency, particularly of C4a, is found in more than half the patients. It seems likely that acquired complement deficiencies, possibly present at the time of initiation of the disease, may be important in many of the other cases.

Autoimmune Diseases↗
PubMedDate not supplied

Immune deposits and immune complex disease.

Presence in tissues of immune deposits containing antigens, antibodies and complement is the hallmark of immune complex disease. In the Review the present concepts concerning the pathogenesis of inflammatory injury associated with immune deposits resulting from a local deposition of circulating immune complexes or formed 'in situ' are discussed.

Animals↗
PubMed1984

Antigen feeding modifies the course of antigen-induced immune complex disease.

Low affinity mice, prone to chronic immune complex disease (ICD) induced by daily injection of antigen, were fed 0.05% HSA in their drinking water for 7 days before the start of daily injections of HSA. Antigen feeding resulted in a marked decrease in the incidence of ICD despite the presence of high levels of circulating immune complexes. These complexes, which persisted in the circulation for long periods, were of low molecular weight and did not localize in the glomeruli. Antigen fed mice had lower levels of free antibody in their sera compared with control mice which may have favoured the formation of small latticed complexes in antigen excess. Antibody affinity was not apparently affected by prior feeding with antigen.

Administration, Oral↗
PubMed1980

Disseminated vasculomyelinopathy: an immune complex disease.

The numerous nervous system abnormalities which follow antecedent infections and immunization appear to share a common pathogenesis involving the immune system. Pathologically, a small vessel vasculopathy involving arterioles and capillaries as well as venules in both gray and white matter is the earliest and most consistent change. Perivascular demyelination appears to develop subsequently. Delayed hypersensitivity to myelin basic protein may not adequately account for these changes. Humoral immunity may be involved instead. I postulate that antigen-antibody complexes, formed following the introduction of foreign antigen by infection or inoculation, cause vascular injury with secondary damage to myelin. There is considerable evidence that circulating immune complexes are present in some postinfectious nervous system disorders, as are associated systemic features which suggest immune complex disease. Similar clinical and pathological nervous system changes occur in a variety of disorders in which circulating immune complexes are thought to cause vascular injury.

Antigen-Antibody Complex↗
PubMed1983

Autoimmunity and immune complex disease after neonatal induction of transplantation tolerance in mice.

Mice made neonatally tolerant to alloantigens were found to develop an immunologic disease resembling systemic lupus erythematosus. In BALB/c mice neonatally injected with C57BL/6 X BALB/c F1 hybrid spleen cells, features of autoimmunity were observed first. After 5-24 wk, antinuclear, anti-SS DNA, thymocytotoxic, and rheumatoid factor-like antibodies were detected in association with hypergammaglobulinemia and with the occurrence of circulating immune complexes and cryoglobulins. Some of the antinuclear antibodies were found to be produced by F1 donor B cells persisting in the host. Second, immunopathologic changes were detected in tolerant mice. In the kidneys, an immune complex glomerulonephritis of the membranous type was observed. Immunoglobulin deposits were also found in the choroid plexus and at the dermoepidermal junction. In addition, thrombocytopenia was a common finding, and a positive direct Coomb's test occasionally was detected. Features of autoimmune disease were closely associated with the effective induction of transplantation tolerance, as revealed by the inability of spleen cells to generate in vitro cytolytic responses against C57BL/6 alloantigens. It is suggested that, although transplantation tolerance is associated with a lack of cytolytic reaction of the host against F1 hybrid donor alloantigens, other types of allogeneic interactions could lead in this model to the development of autoimmunity and immunopathology.

Animals↗
PubMed1978

Hereditary C2 deficiency associated with immune complex disease.

A patient presenting with a syndrome probably due to immune complex deposition was investigated and found to possess an inherited C2 complement deficiency. Family studies indicated that the deficiency was transmitted as an autosomal recessive trait. HLA typing for the HLA-A and HLA-B specificities and HLA-D specificities indicated a close linkage between the HLA and C2 genes, as has been described elsewhere. The HLA-A and B locus specificities HLA-AW25 and HLA-B18 were coded for by each of the two chromosomes carrying the C2(0) gene. However, the two chromosomes differed at the HLA-D locus, as one coded for HLA-DW2 whilst the other did not. This case, therefore, provides a unique haplotype and may be of importance in mapping the C2(0) locus, as it suggests that the gene order on chromosome 6 is HLA-D, C2(0), HLA-B, HLA-A. Extensive complement component assays indicated that utilization of complement in the patient was occurring via the alternate complement pathway. It is suggested that, as a result of the C2 deficiency, infections with viruses and other agents could lead to an immune complex disease due to an impaired capacity to effectively eliminate circulating complexes.

Adult↗
PubMed1979

Soluble immune complex disease associated with antigen heterogeneity an HLA related disorder.

It is suggested that soluble immune complex diseases arising after infections may result from the liberation of partially synthesized bacterial polypeptide or viral nucleic acid antigens. These disrupted antigens will have heterogeneous molecular weights due to antigenic material which is incomplete as a result of premature termination of synthesis. Antigens of this type have been shown to result in significant soluble complex formation in vitro when reacted with antisera from many individuals. Interestingly, this was demonstrated using an antigen which has been instrumental in defining, in the mouse, immune response genes. These genes are known to be linked to genes which code for lymphocyte antigens. If particular immune response genes are linked to HLA types in humans, as is thought to be the case, there may be a large number of soluble immune complex diseases caused by infectious agents which may be HLA type associated.

Antigen-Antibody Complex↗
PubMed1979

Idiopathic neutropenia with normocellular bone marrow: an immune-complex disease.

The presence of circulating immune-complexes (IC) and their in vivo interaction with polymorphonuclear neutrophils (PMN) have been detected in two cases of idiopathic neutropenia with normocellular bone marrow. The injection of patients' sera into New Zealand White rabbits caused a striking neutropenia due to sequestration of PMN in the vascular bed of kidneys and lungs. The kinetics of PMN disappearance from peripheral blood and the pattern of sequestration overlapped that induced by the injection of pre-formed soluble IC. Treatment with plasmapheresis caused an early and lasting increase of PMN; rabbit PMN were almost unaffected by the injection of patient serum after the course of plasmapheresis. These data are consistent with the possibility that idiopathic neutropenia with normocellular bone marrow may be caused by persistent in vivo interaction between IC and circulating PMN.

Adult↗