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PubMed1983

[Immune complex diseases].

Immune complex diseases (ICD) include different diseases of infectious and noninfectious origin in the pathogenesis of which the leading role belongs to immune complexes circulating in the blood stream. Three variants of the ICD course are distinguished: fulminant, acute, and chronic. The main morphological manifestation of ICD is vasculitis (in the fulminant course--microangiothrombopathy) and its consequences in the form of various circulation disorders. Renal glomeruli are frequently involved (glomerulonephritis). Immunopathologic reactions in the form of hypersensitivity reaction or inhibition of immune response are important in ICD.

Arterioles↗
PubMed1989

Intravenous gamma-globulin therapy in systemic lupus erythematosus and immune complex disease.

Immune complexes (ICs) are felt to be of primary pathological importance in the mediation of many human glomerular diseases. This is based on the demonstration of Ig and C' in renal cortex tissue of affected individuals. Systemic lupus erythematosus (SLE) is a prototype IC disease where ICs have been demonstrated in target tissues. Moreover, glomerulonephritis (GN) is a common feature of many autoimmune and infectious diseases associated with IC generation. Current therapeutic alternatives are restricted to immunosuppressive agents. Tomino et al. (Clin. Exp. Immunol. 58, 42, 1984) demonstrated that glomerular IC deposits could be solubilized with HGG. Palla et al. (Clin. Nephrol. 26, 314, 1986) treated four membranous nephritis patients with IVGG and had dramatic resolution of proteinuria in three of them. Gaedlicke et al. (Blut 48, 387, 1984) reported improvement in vasculitis in one of two patients treated with IVGG. We have experienced exacerbation of GN with IVGG therapy in two SLE patients. IVGG is useful in treating the common variable immunodeficiency that occurs in some SLE patients and in treating the immunodeficiency associated with florid nephrotic syndrome. IVGG given to one patient with Henoch-Schönlein purpura resulted in the onset of gross hematuria. In sum, IVGG may be useful in treating specific IC renal diseases by solubilization of circulating or in situ ICs but definitive proof is lacking. In other situations, IVGG may exacerbate the glomerulonephritis, possibly through enhanced IC formation. Furthermore, IVGG may induce modulation of immune responses by induction of auto-anti-idiotypic immunity.

Antibodies, Anti-Idiotypic↗
PubMed1977

Is primary biliary cirrhosis an immune complex disease?

Large immune complexes are present in the circulation of patients with primary biliary cirrhosis and result in the activation of complement by the classical pathway. Such large complexes are capable of producing tissue damage. The granulomatous lesions surrounding the small bile-ducts within the liver of patients with primary biliary cirrhosis and the vasculitis, rheumatoid arthritis, and associated lesions are all compatible with immune complex injury. It is postulated that such large complexes could be formed in the vicinity of the bile-ducts by an antigen absorbed from the bile or biliary epithelium. Complexes reaching the systemic circulation might be responsible for the associated extra-hepatic diseases.

Antibody Formation↗
PubMed1977

Pityriasis lichenoides--an immune complex disease.

Circulating immune complexes have been detected in patients with pityriasis lichenoides during disease activity when IgM and C3 have been observed in dermal vessels on direct immunofluorescence of fresh lesions. This implies that pityriasis lichenoides is an immune complex disorder and that deposited complexes play a part in the pathogenesis of the condition. There is a characteristic pattern of immunofluorescence which may be a diagnostic aid.

Adolescent↗
PubMed1982

Plasma exchange and immune complex diseases: the predictability of immune complexes removal to clinical response.

58 patients were treated by discontinuous flow plasma exchange because of an immune complex (IC) disease. 41 patients who had a high level of circulating IC prior to plasmapheresis showed both clinical and immunochemical evidence of improvement with plasma exchange. Only 2 patients with a high level of IC did not improve after therapy: these patients suffered from multiple sclerosis and idiopathic thrombocytopenic purpura, respectively. Prior to PE therapy the level of circulating IC in 15 patients was within the normal range, when measured according to Manca et al. In this group none of the patients worsened after therapy, whereas 8 patients showed an objective improvement. The positive correlation between IC removal and clinical results suggests that patients with a high level of circulating IC are most likely to benefit from apheretic treatment.

Amyotrophic Lateral Sclerosis↗
PubMed1980

Biochemical aspects of immune complex formation and immune complex diseases.

Formation of immune complexes is a normal part of the immune defence against soluble antigens. Immune complexes may nevertheless play a pathogenic role of their own. The present review discusses antigen antibody interactions with special regard to immune complex formation. A new classification of antigen antibody interactions is proposed, based on the antigenic valence. Oligovalent antigens and bivalent antibodies form genuine immune complexes. Experimental observations and theoretical considerations indicate that although a vast variety of complexes is possible genuine immune complex formation is a self-limiting process, so it is typical that the smallest possible complexes are formed in the largest amounts. Formation of immune complexes differs in mechanism from most other biological ligand binding reactions, and the extent to which immune complex formation follows its own laws is discussed. To explain the mechanism of precipitin reactions, a two-stage model is proposed. The outcome of antigen antibody interactions is further complicated because antibody preparations are typically heterogeneous, and the impact of antibody heterogeneity is also discussed.

Animals↗
PubMed1980

[Immunologic and allergic lung diseases. 2. Endogenous and exogenous immune complex diseases].

For the respiratory tract immunologic reactions of type I and type III according to Coombs and Gell are most important. The classical example for type-I-reaction is extrinsic (= "allergic") asthma. Mechanisms of sensitzation, of mediator release out of mast cells and of immunotherapy by specific hyposensitization are summarized. Immunologic type-III-reactions may lead to immune complex diseases of the lung. There are two different pathways: In the several forms of extrinsic alveolitis the interstitial lung tissue is involved, whereas the intrinsic forms of immune complex diseases mainly result in lung vasculitis. The diagnostic and therapeutical essentials of immunologic and allergic lung disease are discussed in detail.

Adrenal Cortex Hormones↗
PubMed1978

Immune complex mediated diseases.

Immune complexes formed in the circulation are believed to be the principal pathogenetic agents in certain human diseases, notably in various forms of glomerulonephritis and arteritis. Criteria for the recognition of immune complex deposits in tissue are discussed and recently developed sensitive methods that detect circulating immune complexes are reviewed. In addition, the evidence implicating certain antigens and causative agents in human immune complex mediated glomerulonephritis and arteritis is evaluated.

Animals↗
PubMed1985

Human hypersensitivity angiitis, an immune complex disease.

Human hypersensitivity angiitis is an immune complex disease in which patients present with palpable purpuric lesions of the skin and may often have multiple organ involvement. The antigen may be derived from an infectious organism such as the hepatitis virus, streptococcus, or a drug, and complexes with antibody. Under circumstances of vascular turbulence or vessel wall dilatation this complex may become fixed, activating the complement sequence with elaboration of chemotactic factors for neutrophils. These cells release lysosomal enzymes resulting in vessel wall destruction. Red blood cells leak into the tissue producing purpura and the inflammatory infiltrate accounts for the palpability. Although many patients have skin lesions only, others may have involvement of joints, gastrointestinal tract, kidneys, and even the lungs. The central question in the pathogenesis of this disease is why the immune complex is so selective in its site of deposition. Part of the reason must be related to the lattice formation of a particular complex, while other reasons are related to host factors of altered vascular permeability, integrity of clearance mechanisms or even a genetically determined defect of the phagocytic system.

Animals↗
PubMed1984

Pulmonary immune effector cells: II. Antigen-specific blastogenic responsiveness of lymphocyte populations during pulmonary immune complex disease in guinea pigs.

A guinea pig pulmonary immune complex disease was used to evaluate local antigen (ovalbumin)-specific lymphoproliferative responses in lung tissue, bronchoalveolar spaces, and hilar lymph nodes (HLN) at various time intervals after challenge. The responses of lung tissue and bronchoalveolar lymphocytes appear to be mediated by T cells, whereas the response of HLN lymphocytes was mediated by B and/or T cells, depending on the stage of the disease. The blastogenic response of HLN lymphocytes to concanavalin A was much greater than that observed in lung tissue or bronchoalveolar lymphocyte preparations, even after the removal of adherent cells, suggesting a possible inherent difference between these cell populations in their response to mitogen. This study demonstrates that lung tissue, bronchoalveolar, and HLN lymphocytes are not only capable of responding blastogenically to specific antigen, but that this responsiveness varies throughout the course of the disease. The lymphoproliferative responses and concurrent changes in the proportion of pulmonary immune effector cells are discussed in relation to cellular immunoregulation during the in vivo progression of this pulmonary immune complex disease.

Animals↗
PubMed1972

Virus-associated immunopathology: animal models and implications for human disease. 1. Effects of viruses on the immune system, immune-complex diseases, and antibody-mediated immunologic injury.

The tissue damage caused by virus infection has been traditionally explained by the ability of viruses to multiply in cells and thereby injure or destroy them. Recent evidence suggests, however, that lesions may also be caused by the host's immune response to viral antigens and that the immune system itself may be perturbed by some viruses. This memorandum reviews recent developments in viral immunopathology, with special reference to animal model systems, and indicates the possible relevance of the new concepts and techniques for certain diseases of man. Certain viruses, notably the leukaemia viruses and some of those causing persistent infections, depress the host's ability to mount an antibody response to antigens, while other viruses may enhance the antibody response. Cell-mediated immunity may also be depressed. Another immunopathological manifestation of virus infection is immune-complex disease. When viruses or their antigens persist in the circulation they combine with specific antibody, and the resulting complexes lodge in various sites, especially the kidney. Further combination with complement leads to the release of tissue-damaging substances. A third condition associated with virus infection is antibody-mediated immunologic injury. Both oncogenic and non-oncogenic viruses frequently induce new antigens on the surface of the cells they invade. When antibody attaches to these antigens in the presence of complement, the cells are destroyed.

Animals↗
PubMed1982

Development of chronic pulmonary inflammation in immunized guinea pigs by aerosol challenge with antigen: relationship of immune complex disease and cell-mediated hypersensitivity.

Immunized guinea pigs develop immune complex disease (ICD) in the lungs after a single aerosol challenge with specific antigen. In the current study, immunized guinea pigs developed chronic pulmonary inflammation and cellular immunity (CI) in the lungs when aerosol challenged daily with specific antigen for 2 wk. When immune serum was passively transferred to normal recipients that were then aerosol challenged with specific antigen for 2 wk, chronic pulmonary inflammation and CI did not develop. These results suggest that ICD produced by passive transfer of serum and subsequent aerosol exposure to antigen was inadequate to cause chronic pulmonary inflammation and CI. The development of chronic pulmonary inflammation by aerosol challenge with antigen was suppresed with cobra venom factor. However, because of other studies, we attribute this suppression to the diminution of complement (C) factors in the alternative C pathway that affect macrophage mobility rather than to the depletion of C5a, which is important in the development of ICD.

Aerosols↗