Anti-antibodies and anti-idiotype immunoregulation, 1899–1904: The inexorable logic of paul ehrlich

Silverstein, Arthur M.

doi:10.1016/0008-8749(86)90258-3

Cited by 10 publications

(1 citation statement)

References 45 publications

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“…To describe such a calamity, he coined the term 'horror autotoxicus'. 8,9 This proscription of autoimmunity persisted for decades despite the emergence of evidence of autoreactivity in many forms. [10][11][12][13] The explicit recognition of autoimmunity did not occur until the studies described herein in 1957, when a new generation of immunologists and new technologies were in place.…”

mentioning

confidence: 99%

The discovery of autoantibody to deoxyribonucleic acid

Holman

2011

Lupus

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mentioning

confidence: 99%

The discovery of autoantibody to deoxyribonucleic acid

Holman

2011

Lupus

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The Horror Autotoxicus and Multiple-Organ Failure

Baue

1992

Arch Surg

116

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An injury or operation with tissue injury, ischemia, and sepsis provokes a neuroendocrine, immune, and inflammatory response to promote survival and heal the wound. If the injury is massive or complicated by infection, the inflammatory response may become generalized and excessive, producing organ and tissue damage and multiple-organ failure, a modern "horror autotoxicus." Many inflammatory mediators have been identified. In isolated organs, the use of blocking mediators to prevent combined ischemia-reperfusion injury is feasible. With regional ischemia, activator attenuation may be possible. It is unclear whether blockade or modulation of all or part of an excessive inflammatory response will be possible, helpful, and without hazard in patients with multisystem injuries or sepsis. Feedback loops and control mechanisms of these systems will better define such possibilities. Employment of growth factors and other protective agents to stimulate wound healing, infection control, and host resistance may be more helpful. Ultimately, prevention of multiple-organ failure requires sound surgical judgment, techniques, and organ support.

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Thought barriers to understanding rheumatic diseases

Holman

1994

Arthritis & Rheumatism

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The thought barriersAutoimmunity was rediscovered in the 1950s. Rediscovered is the appropriate term because evidence for autoimmunity emerged around the turn of the last century. For reasons that I shall comment upon ldter, it was not recognized for a half century. The rediscovery, together with the simultaneous development of transplantation biology, stimulated the emergence of contemporary immunology. Thus was initiated a period of great expectations. Now, almost another half century later, much has become known about immunologic processes, but, at least as concerns the origin and control of rheumatic diseases, the great expectations have not been fulfilled. This paper explores possible reasons why the expectations are unfulfilled. I will argue that a fundamental reason is that the prevailing conceptual base of our investigation is incommensurate with the rheumatic disease problems which we confront. Rheumatic diseases are chronic biological aberrations unfolding over years, whereas, by and large, our investigative approaches are cross-sectional analyses sometimes repeated over a limited time span. It is intuitively obvious that one would have difficulty understanding a chronic evolving multivariate process from crosssectional observations alone, no matter how penetrating those analyses might be. But, the issue cannot be characterized so simply.

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Anti-antibodies and anti-idiotype immunoregulation, 1899–1904: The inexorable logic of paul ehrlich

Cited by 10 publications

References 45 publications

The discovery of autoantibody to deoxyribonucleic acid

The discovery of autoantibody to deoxyribonucleic acid

The Horror Autotoxicus and Multiple-Organ Failure

Thought barriers to understanding rheumatic diseases

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