Cutaneous Deposition of Immune Complexes in Chronic Serum Sickness of Mice Induced with Cationized or Unaltered Antigen

Joselow, Steve A.; Gown, Allen M.; Mannik, Mart

doi:10.1111/1523-1747.ep12277404

Cited by 9 publications

(3 citation statements)

References 13 publications

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“…Antigen and antibody charge also affect IC lattice formation, complement activation, and tissue deposition (Gauthier and Mannik 1990; Michelin et al 2002; Theofilopoulos and Dixon 1979; Wener 2007). Cationic antigens bind to anionic sites in glomerular basement membrane, knee joint, or dermoepidermal junction as shown by injection of antigen or preformed ICs into mice, rats, or rabbits (Adler et al 1983; Border et al 1981; Gallo, Caulin-Glaser, and Lamm 1981; Gauthier and Mannik 1990; Isaacs and Miller 1982; Joselow, Gown, and Mannik 1985; Theofilopoulos and Dixon 1979; van den Berg and van de Putte 1985; Wener 2007). Preformed ICs containing cationic antibodies may deposit in glomerular and/or small myocardial blood vessel walls with ICs containing neutrally charged antibodies remaining in circulation (Krant, Gauthier, and Mannik 1989).…”

Section: Formation Of Ics and Complement Activationmentioning

confidence: 99%

Formation, Clearance, Deposition, Pathogenicity, and Identification of Biopharmaceutical-related Immune Complexes

et al. 2014

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Vascular inflammation, infusion reactions, glomerulopathies, and other potentially adverse effects may be observed in laboratory animals, including monkeys, on toxicity studies of therapeutic monoclonal antibodies and recombinant human protein drugs. Histopathologic and immunohistochemical (IHC) evaluation suggests these effects may be mediated by deposition of immune complexes (ICs) containing the drug, endogenous immunoglobulin, and/or complement components in the affected tissues. ICs may be observed in glomerulus, blood vessels, synovium, lung, liver, skin, eye, choroid plexus, or other tissues or bound to neutrophils, monocytes/macrophages, or platelets. IC deposition may activate complement, kinin, and/or coagulation/fibrinolytic pathways and result in a systemic proinflammatory response. IC clearance is biphasic in humans and monkeys (first from plasma to liver and/or spleen, second from liver or spleen). IC deposition/clearance is affected by IC composition, immunomodulation, and/or complement activation. Case studies are presented from toxicity study monkeys or rats and indicate IHC-IC deposition patterns similar to those predicted by experimental studies of IC-mediated reactions to heterologous protein administration to monkeys and other species. The IHC-staining patterns are consistent with findings associated with generalized and localized IC-associated pathology in humans. However, manifestations of immunogenicity in preclinical species are generally not considered predictive to humans.

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Section: Formation Of Ics and Complement Activationmentioning

confidence: 99%

Formation, Clearance, Deposition, Pathogenicity, and Identification of Biopharmaceutical-related Immune Complexes

et al. 2014

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“…Mice given the chronic antigen injections developed mild perivascular inflammation in the dermis. Immune deposits were seen in these vessels when examined at 4 h after the last antigen dose, but not when examined 16 h after the last antigen injection [38].…”

Section: Deposition Of Circulating Immune Complexes Iu Dermalmentioning

confidence: 77%

“…Chronic adniinistration of a cationic antigen to immunized mice leads to immune deposits at the dermal-epidermal junction [38]. For this purpose, mice were immunized with rabbit IgG and then injected intravenously three times per week for four weeks with either cationized rahhit IgG (IgG^o) or unaltered rabbit IgG.…”

Section: Deposition Of Circulating Immune Complexes Iu Dermalmentioning

confidence: 99%

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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Charge‐charge interactions between articular cartilage and cationic antibodies, antigens, and immune complexes

Zatarain-Rios

Mannik

1987

Arthritis & Rheumatism

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Bovine articular cartilage was used to examine the binding of cationized antibodies, antigens, and immune complexes to articular cartilage by charge-charge interactions. Rabbit antibodies to human serum albumin (anti-HSA) and HSA were cationized to various degrees by the addition of amino groups. When approximately 20 or more new amino groups were added to HSA and approximately 25 or more amino groups were added to anti-HSA, the proteins readily bound to cartilage and penetrated into the matrix. Soluble immune complexes made with the cationic antibodies, including small-latticed complexes, bound only to the surface of the cartilage. When cationic HSA was bound to the matrix of the cartilage, unaltered antibodies bound only to thie antigen at the surface and did not penetrate the matrix. This model system defines the manner in which cationic antigens and antibodies bind to and penetrate into the articular cartilage.In antigen-induced synovitis in experimental animals, immune complexes and complement components are present in the superficial layers of articular Presented in part at the 6th International Congress of Immunology,

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Cutaneous Deposition of Immune Complexes in Chronic Serum Sickness of Mice Induced with Cationized or Unaltered Antigen

Cited by 9 publications

References 13 publications

Formation, Clearance, Deposition, Pathogenicity, and Identification of Biopharmaceutical-related Immune Complexes

Formation, Clearance, Deposition, Pathogenicity, and Identification of Biopharmaceutical-related Immune Complexes

Development of Immune Complexes In the Skin.

Charge‐charge interactions between articular cartilage and cationic antibodies, antigens, and immune complexes

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