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Arthus reaction

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Arthus reaction
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In immunology, the Arthus reaction (/ˌɑːrˈtjuːs/) is a type of local type III hypersensitivity reaction. Type III hypersensitivity reactions are immune complex-mediated, and involve the deposition of antigen/antibody complexes mainly in the vascular walls, serosa (pleura, pericardium, synovium), and glomeruli. This reaction is usually encountered in experimental settings following the injection of antigens.

History

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The Arthus reaction was discovered by Nicolas Maurice Arthus in 1903.[1] Arthus repeatedly injected horse serum subcutaneously into rabbits. After four injections, he found that there was edema and that the serum was absorbed slowly. Further injections eventually led to gangrene.[citation needed]

Process

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The Arthus reaction involves the in situ formation of antigen/antibody complexes after the intradermal injection of an antigen. If the individual has circulating antibody either from passive immunity or because of prior encounter with the antigen, an Arthus reaction may occur. Typical of most mechanisms of the type III hypersensitivity, Arthus manifests as local vasculitis due to deposition of IgG-based immune complexes in dermal blood vessels. The pathogenesis of the Arthus reaction is often erroneously described to be the result of complement activation, which subsequently results in neutrophil infiltration along with the other hallmarks of inflammation. However, complement in and of itself likely has a minor role in the actual process of the Arthus reaction and other type III hypersensitivities. Specifically, mice lacking the common gamma chain subunit of the Fc receptors that is required for signaling by CD64 (FcγがんまRI) and CD16A (FcγがんまRIIIA) as well as FcεいぷしろんRI have a drastic reduction in their Arthus reaction severity.[2] Furthermore, mice with intact Fc signaling whose complement is depleted through the use of cobra venom have only a minor reduction in their Arthus reaction scores. The reaction as a whole is driven by mast cell degranulation.[3] Subsequent investigation demonstrated that complement, specifically the anaphylatoxin C5a, can drive the Arthus reaction indirectly because the resultant signaling alters the ratio of activating to inhibitory Fc receptors on effector cells.[4][5] Further aggregation of immune complex-related processes induce a local fibrinoid necrosis with ischemia-aggravating thrombosis in the tissue vessel walls.[6] The end result is a localized area of redness and induration that typically lasts a day or so.

Arthus reactions have been infrequently reported after vaccinations containing diphtheria and tetanus toxoid. The CDC's description:

Arthus reactions (type III hypersensitivity reactions) are rarely reported after vaccination and can occur after tetanus toxoid–containing or diphtheria toxoid–containing vaccines. An Arthus reaction is a local vasculitis associated with deposition of immune complexes and activation of complement. Immune complexes form in the setting of high local concentration of vaccine antigens and high circulating antibody concentration. Arthus reactions are characterized by severe pain, swelling, induration, edema, hemorrhage, and occasionally by necrosis. These symptoms and signs usually occur 4–12 hours after vaccination. ACIP has recommended that persons who experienced an Arthus reaction after a dose of tetanus toxoid–containing vaccine should not receive Td more frequently than every 10 years, even for tetanus prophylaxis as part of wound management.[7]

See also

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References

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  1. ^ Injections répétées de serum du cheval chez le lapin, Comptes rendus des séances de la Société de biologie et de ses filiales, Paris, 55 (1903), 817–820.
  2. ^ Sylvestre, D. L.; Ravetch, J. V. (1994-08-19). "Fc receptors initiate the Arthus reaction: redefining the inflammatory cascade". Science. 265 (5175): 1095–1098. Bibcode:1994Sci...265.1095S. doi:10.1126/science.8066448. ISSN 0036-8075. PMID 8066448.
  3. ^ Ramos, B. F.; Zhang, Y.; Jakschik, B. A. (1994-02-01). "Neutrophil elicitation in the reverse passive Arthus reaction. Complement-dependent and -independent mast cell involvement". Journal of Immunology. 152 (3): 1380–1384. doi:10.4049/jimmunol.152.3.1380. ISSN 0022-1767. PMID 8301139. S2CID 5552121.
  4. ^ Shushakova, Nelli; Skokowa, Julia; Schulman, Jurriaan; Baumann, Ulrich; Zwirner, Jörg; Schmidt, Reinhold E.; Gessner, J. Engelbert (2002-12-15). "C5a anaphylatoxin is a major regulator of activating versus inhibitory FcγがんまRs in immune complex–induced lung disease". The Journal of Clinical Investigation. 110 (12): 1823–1830. doi:10.1172/JCI16577. ISSN 0021-9738. PMC 151656. PMID 12488432.
  5. ^ Ravetch, Jeffrey V. (2002-12-15). "A full complement of receptors in immune complex diseases". Journal of Clinical Investigation. 110 (12): 1759–1761. doi:10.1172/JCI17349. ISSN 0021-9738. PMC 151658. PMID 12488423.
  6. ^ Kumar, Vinay; Abbas, A.K.; Fausto, N.; Aster, J.C. (2010). "6". In William Schmitt (ed.). Robbins and Cotran Pathologic Basis of Disease (8th ed.). Philadelphia: Saunders Elsevier. p. 205.
  7. ^ Preventing Tetanus, Diphtheria, and Pertussis Among Adolescents: Use of Tetanus Toxoid, Reduced Diphtheria Toxoid and Acellular Pertussis Vaccines, K. R. Broder et al., MMWR Recommendations and Reports, March 24, 2006 / 55(RR03), 1–34, page 18.
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