Localization of Preformed, Circulating Immune Complexes in Murine Skin

Joselow, Steve A.; Mannik, Mart

doi:10.1111/1523-1747.ep12260644

Cited by 23 publications

(13 citation statements)

References 18 publications

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“…In contrast, immune complexes that contain only one or two antibody molecules, collectively called small-latticed immune complexes, do not deposit in glomeruli (6). Small-latticed immune complexes with the same antigen-antibody systems in mice also failed to deposit in blood vessels of skin, heart and extraglomerular vessels in kidneys (7). A difference, however, was observed in the persistence of immune deposits in glomeruli and other vascular beds in this model.…”

Section: Deposition Of Circulating Immune Complexesmentioning

confidence: 68%

“…The extraglomerular immune deposits were more extensive, most likely owing to the higher concentration of circulating large-latticed immune complexes since the uptake by Kupffer cells was decreased by the reduction was alkylation of antibody molecules. Glomerular immune deposits reached the maximum 12 h after injected and persisted beyond 96 h (6,7). These results idicate a clear difference in the mechanisms of deposition of immune complexes in glomeruli and in other vascular beds.…”

Section: (B) Small Blood Vessels In the Heart (C) Extraglomerular Renmentioning

confidence: 87%

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Experimental Models for Immune Complex‐mediated Vascular Inflammation

Mannik

1987

Journal of Internal Medicine

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Several clinical syndromes of vasculitis exist. The etiology of most inflammatory conditions of blood vessels are not known, but immune mechanisms appear to account for many forms of vasculitis. The reasons for suggesting that immune mechanisms are involved in these disorders are multiple. Inflammatory vascular lesions are common and reproducible in experimental models of acute serum sickness, chronic serum sickness, spontaneous models of autoimmune diseases, and certain chronic viral diseases in animals. Vasculitis is a common manifestation of human serum sickness, and vasculitis is part of known immunologically mediated diseases such as systemic lupus erythematosus and rheumatoid arthritis.Similar to other target organs, immunologically mediated inflammation of blood vessels may arise by involvement of only cellular immunity, by involvement of humoral immunity, or potentially a combination of both. The purpose of this article is to consider the involvement of immune complexes in the pathogenesis of vascular inflammation. Clinical aspects of vasculitides will be considered by P. A. Bacon in this volume and have been reviewed in a monography by Cupps and Fauci (1).In human diseases the size of blood vessels involved vanes among the categories of vasculitides. In small vessel vasculitis or leukocytoclastic vasculitis inflammation and immune deposits affect venules, capillaries and arterioles. In periarteritis nodosa the lesions and immune deposits involve in segmental fashion small and medium size arteries. In some patients with systemic, necrotizing vasculitis both large and small vessels are involved. It is not clear what leads to involvement of blood vessels with varying size. A single etiologic agent, for example hepatitis virus B, can cause immune complex-mediated vascular inflammation ranging from small vessel vasculitis to involvement of medium size vessels in periarteritis nodosa. General considerations of immune complex-mediated vascular inflammationThe development of vasculitis in acute and chronic serum sickness in experimental animals was appreciated by many workers. How immune complexes localized in blood vessel walls, however, was not understood. The work of Cochrane and colleagues in the mid-nineteen sixties provided substantial new information on the mechanisms of localization of immune complexes in blood vessels of experimental animals, as reviewed by Cochrane and Koffler (2).A key feature was that circulating immune complexes localized in blood vessels only after an increase of permeability. In rabbits with serum sickness, this was caused by release of vasoactive amines from aggregated platelets, which was brought about by platelet activating factor that was released by interaction of antigen with IgE class of antibodies. For guinea pigs, in contrast, the vasoactive amines were released from basophils. Furthermore, the necessary increased permeability could be induced by administration of vasoactive amines while appropriate immune complexes were present in circulation. Immune complexes that posse...

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Section: Deposition Of Circulating Immune Complexesmentioning

confidence: 68%

Section: (B) Small Blood Vessels In the Heart (C) Extraglomerular Renmentioning

confidence: 87%

Experimental Models for Immune Complex‐mediated Vascular Inflammation

Mannik

1987

Journal of Internal Medicine

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“…In contrast, in glomeruli with open fenestrations the deposition was immediate. Of interest is that the antiHSAEQ injected alone persisted longer at the DEJ than in glomeruli [34]. The fixed anionic sites at the DEJ are present at the dermal and epidermal sides of the lamina densa of the basement membrane, as demonstrated with a polycationic probe [37].…”

Section: Deposition Of Circulating Immune Complexes Iu Dermalmentioning

confidence: 98%

“…A few years ago we examined in normal mice the localization in dermal vessels of preformed immune complexes, injected as a single large dose, containing 5 mg of antibodies [34]. The disappearance kinetics and glomerular localization of similar preparations had been examined previously [10,33].…”

Section: Deposition Of Circulating Immune Complexes Iu Dermalmentioning

confidence: 99%

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Development of Immune Complexes In the Skin.

Mannik¹

1989

J Invest Dermatol

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Complement activation by immune complexes induces inflammation, but during this process the nature of the complexes is altered. Once immune complexes have attained sufficient lattice to activate complement, further increase of the lattice and immune precipitation are limited by the incorporation of complement components. The presence of complement components in immune complexes facilitates their disposal from circulation by complement receptors on red cells in humans. Without complement activation the disposal of immune complexes of sufficient lattice is mediated by Fc receptors. The development of immune deposits in tissues can arise by several mechanisms. Circulating immune complexes may be deposited in a number of vascular beds. Immune deposits in tissues may also arise by local formation. This process may involve structural antigens in tissues, cell surface antigens that are shed after interaction with specific antibodies or antigens that have become planted in tissues and then combine with antibodies. Charge-charge interactions enhance deposition of immune complexes in several organs, involving fixed negative charges in tissues and positive charges on antigens or antibodies in immune complexes. Successful detection of immune deposits in dermal vessels requires the examination of fresh lesions. Local vascular changes contribute significantly to deposition of immune complexes in dermal vessels. Charge-charge interactions enhance this deposition and contribute to the development of deposits at the dermal-epidermal junction in experimental animals.

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Neurological manifestation of vasculitis: Update on immunopathogenic mechanisms and clinical features

Moore

1995

Ann Neurol.

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Study of the vasculitides illustrates a spectrum of interactions from physiological to pathological between the immune system and the blood-vessel wall. Endothelial cells demonstrably recruit leukocytes by both antigen-specific and antigen-nonspecific mechanisms in the systemic vasculitides. A cascade of cytokine and factors can initiate, perpetuate, and regulate the close interactions of leukocytes and the endothelium. Specific types of leukocytes (neutrophils, T lymphocytes, eosinophils) predominate in the vascular infiltrates of specific diseases. Other mural cells potentially initiate the inflammatory process; this may be particularly important in the central nervous system where regulatory systems may diminish a primary role of the endothelium in vascular inflammation. Neurological abnormalities are a prominent feature of some vasculitides and rare in others. In polyarteritis nodosa, Wegener's granulomatosis, and lymphomatoid granulomatosis neurological features may be prominent and early. The cutaneous vasculitides, hypersensitivity vasculitis, are seldom associated with neurological abnormalities. Isolated angiitis of the central nervous system is notable because it invariably targets the central nervous system and because it must be distinguished from other causes of central nervous system vasculitis, including infections and toxins. In this article we review some of the recent information adding to our knowledge of the immunopathogenic and clinical features in the vasculitides affecting the nervous system.

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Localization of Preformed, Circulating Immune Complexes in Murine Skin

Cited by 23 publications

References 18 publications

Experimental Models for Immune Complex‐mediated Vascular Inflammation

Experimental Models for Immune Complex‐mediated Vascular Inflammation

Development of Immune Complexes In the Skin.

Neurological manifestation of vasculitis: Update on immunopathogenic mechanisms and clinical features

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