In 1910, Charles Richet suggested that studying individual variations in anaphylactic responses might both open a way to experimental investigation of the biological basis of individuality and help unify the immunological and physiological approaches to biological phenomena. The very opposite would happen however. In the next two decades, physiologists and immunologists interested in anaphylaxis and allergy experienced more and more difficulties in communicating. This divergence between the physiopathological and immunological approaches derived from discrepancies between the experimental systems used by each (...) of these scientific communities. Trying to develop a point of view that took into account all bodily reactions to stimuli, physiologists thought that individual variations between the laboratory animals they used (mainly dogs and cats) constituted important experimental data. Seeking to develop reproducible studies of infection, immunity and 'sensitisation', bacteriologists and immunologists considered that individual variations between the laboratory animals they used (mainly small rodents) constituted 'noise' and not a 'signal'. Each group's loyalty to the experimental models used in their discipline widened the gap between immunological and physiological explanations of allergies and led to the abandonment of studies on the biological basis of individuality. (shrink)

Traditionally, autoimmune disease has been considered to be a case of false recognition; the immune system mistakenly identifies 'self' tissues as foreign, attacking them thus causing damage and malady. Accordingly, the history of autoimmunity is usually told as part ot the history of immunology, that is, of theories and experiments relating to the ability of the immune system to discriminate between self and nonself. This paper challenges this view, claiming that the emergence of the notion of autoimmunity in the 1950s (...) must be considered as part of a long develolpment in thought about pathology throughout the twentieth century, namely the conceptualisaiton of disease as a reactive and self-destructive process. During the first part of the twentieth century this notion became one of the cornerstones of pathology and was increasingly employed for the explanation of the non-infections, slow-burning diseases. Thus, the category of chronic disease had been defined anew, now encompassing all those diseases characterised by a persistent inflammatory process. Inflammation, in turn, was conceived as double-eged physiological mechanism, which was usually the direct mediator of damage, of the essence of disease. The paper also shows how this kind of analysis could emable a unified historical discussion of autoimmunity and allergy, hitherto considered to have distinct conceptual origins. (shrink)

In the inter-war period physicians elaborated numerous ‘biotherapies’ grounded in the complex interactions between physiology, bacteriology and immunology. The elaboration of these non-specific biological treatments was stimulated by the theory of generalized anaphylaxis that linked the violent reaction to a foreign protein to a broad array of chronic diseases, from asthma and urticaria to rheumatism or chronic colitis. Such diseases were perceived as the result of an ‘abnormal reactivity’ to a sensitisation of tissues and organs by bacteria and by foreign (...) proteins, a view that provided an effective bridge between new concepts derived from bacteriology and immunology and the long-standing pathological tradition. Accordingly, physicians attempted to treat these conditions through specific desensitisation and non-specific biological therapies: peptone treatment, protein therapy, haemotherapy, ‘antivirus’ or ‘opotherapy’. Therapies that attempted to neutralise the harmful effects of chronic infections through ‘desensitisation’ were not seen as marginal medical practices, but were promoted by leading advocates of the ‘Pasteurian sciences’, such as Richet, Widal, Vallery-Radot, Wright and Fleming. They also led to development of new products by the pharmaceutical industry. (shrink)

An allergy is commonly understood to be an overreaction of the immune system to harmless substances that are misrecognised as foreign. This concept of allergy as an abnormal, misdirected immune response—a biological fault—stems from the idea that the immune system is an inherently defensive operation designed to protect the individual through an innate capacity to discriminate between the benign and toxic, or self and nonself. However, this definition of allergy represents a radical departure from its original formulation. Literally meaning ‘altered (...) reactivity’, the term was coined in 1906 by Austrian paediatrician Clemens von Pirquet, to describe the fundamentally mutable nature of the immune response.This paper argues that the conventional interpretation of allergy-as-pathology derives from specific concepts of ‘organism’, ‘response’, and ‘normal’ immune function that have—for over a century—governed the perception and study of immune phenomena within immunology. Through an examination of Louis Pasteur’s conceptualisation of the host body/microorganism relationship, I argue that immunology is founded on a view of the organism as a discrete, autonomous entity, and on a concomitant notion of the immune response as essentially reactive. Revisiting the concept of ‘altered reactivity’, this paper points to the fact that allergy was initially posited as a general theory of immune responsiveness and, importantly, one that poses a significant challenge to orthodox notions of immunopathology. It suggests that Pirquet’s unique view of immune responsiveness presents an account of organismic or biological identity that encapsulates, rather than reduces, its ecological complexity. (shrink)