I propose a T‐cell receptor (TcR)‐based mechanism by which immunity mediates both “genetic self” and “microbial self” thereby, connecting microbiome disease with autoimmunity. The hypothesis is based on simple principles. First, TcR are selected to avoid strong cross‐reactivity with “self,” resulting in selection for a TcR repertoire mimicking “genetic self.” Second, evolution has selected for a “microbial self” that mimics “genetic self” so as to share tolerance. In consequence, our TcR repertoire also mimics microbiome antigenicity, providing a novel mechanism (...) for modulating tolerance to it. Also, the microbiome mimics the TcR repertoire, acting as a secondary immune system. I call this TcR‐microbiome mimicry “holoimmunity” to denote immune tolerance to the “holobiont self.” Logically, microbiome‐host mimicry means that autoimmunity directed at host antigens will also attack components of the microbiome, and conversely, an immunological attack on the microbiome may cross‐react with host antigens producing “holoautoimmunity.”. (shrink)

I argue that a distinction between three autoimmunities is implied in Derrida’s _Rogues_. These are the autoimmunities of democracy as a regime of power, of democracy to come and of sovereignty. I extrapolate the relations between three different autoimmunities using the figure of the internal enemy in order to argue for an agonistic conception of democracy.

As I previously argued, the concept of autoimmunity refers to the partial incapability of the human agent to distinguish between her knowledge and her ignorance, due to an involuntary mechanism which underlies the fixation and revision of beliefs. In this chapter I will contend that the new concept of “cognitive autoimmunity” can be usefully employed beyond the epistemological and logical fieldwork, in order to describe the cognitive mechanism supporting what the philosophical literature calls “epistemic feelings” (Muñoz 2013, 2014; (...) Michaelian and Muñoz 2014). The cognitive autoimmunity of the agents will justify both the fact that a lot of instantiations of ignorance are bound not to be recognized by their owners, and the fact that philosophers have had an hard time trying to describe ignorance as a concept. Moreover, the cognitive autoimmunity will explain how the fugitive state of ignorance has an impact on the metacognitive capacity of the human cognition. (shrink)

Autoimmune diseases such as multiple sclerosis (MS) and rheumatoid arthritis (RA) involve complex interactions between local tissues and the immune system. Here, we highlight the immunological parallels between the central nervous system (CNS) meninges and the synovial joint, two sites traditionally considered immune‐privileged. Both harbor resident immune cells and lymphatic vessels and support the formation of tertiary lymphoid organs (TLO) during chronic inflammation. In MS, meningeal TLO contributes to cortical grey matter damage, while in RA, synovial TLO drives joint destruction. (...) T peripheral helper (Tph) cells, a subset of CD4+ T cells, are key players in both conditions by supporting B cell activation and autoantibody production. Epstein–Barr virus (EBV) infection, particularly in B cells within TLO, is implicated in the pathogenesis of both diseases. Targeting EBV‐infected B cells, depleting Tph cells, or disrupting TLO represent promising therapeutic strategies for controlling disease progression and severity in MS and RA. (shrink)

Shortly before his death in 2004, Jacques Derrida provocatively suggested that the greatest problem confronting contemporary democracy is that ‘the alternative to democracy can always be represented as a democratic alternative ’. This article analyses the manner in which certain manifestly anti-democratic practices, like terror and torture, come to be taken up in defense of democracies as a result of what Derrida calls democracy’s ‘autoimmune’ tendencies.

Our paper is a comparative analysis of Alexander Dugin's The Fourth Way and Karl Popper's The Open Society. Both works of the two thinkers are viewed as completely concrete (and real) conceptual frameworks, offering two radically different models of perception of the world, the individual and community relations, of the international relations. Our analysis takes into consideration both the internal, that is the “intimate enemies of democracy”, and the new (old) enemies of the open society that “relapse” through the Fourth (...) Way. Our theoretical research is focused on the parallel between the negative starting premises for the functioning of the Open Society – historicism, utopian social engineering, collectivism and chieftainism – studied in relation to the same principles, which, respectively, are the foundation of the Fourth Political Theory. The article also considers another important problem: the thesis, that the internal, autoimmune diseases of the Open Society, are in fact the preconditions, on which the doctrines of its external opponents are based. (shrink)

The aim of this article is to read Rogues, in order to show that Derrida is neither a philosopher of democracy nor a critic of sovereignty, but rather a thinker of democratic sovereignty. Taking my cue from his Aporias, I argue that democratic sovereignty is aporetically in excess over itself, for it is based on articulating the path through the im-possible passage from the unconditional injunction of the ‘promise’ to the exigency of sovereignty. That is why it can neither be (...) absorbed into the conditions of any existing democracy nor abstracted into any pure identity of sovereignty. Political trends today fail in enduring the aprioricity of aporia, as neoliberals valorize the posited conditions of existing democracy and populists the objective pregivenness of the ‘people’. (shrink)

I begin by examining the logic of autoimmunity as characterized by Jacques Derrida, ‘that strange behaviour where a living being, in quasi-suicidal fashion, ‘‘itself’’ works to destroy its own protection, to immunize itself against its own immunity’ (Borradori, 2003: 94). According to Derrida, religion, democracy, terrorism and recent responses to the trauma of terrorism can be understood in terms of this logic. Responses to terrorism are ‘autoimmune’ and increase the trauma of terrorism as well as risking democratic values. I (...) argue that the risks of autoimmunity can be negotiated in better ways if we see how autoimmunity relates to another important Derridean concept, hospitality. (shrink)

This essay uses Derrida's concept of autoimmunity to critique Homeland, a television show that deals with an American prisoner of war who has been ‘turned’ into an operative for an al Queda-like movement. Autoimmunity is critical to thinking the ways in which the existence of a turned POW within the state, who belongs visibly to the state, presents a particularly heteronomic challenge to how the distinction between Self and Other operates. This Self who has taken up the cause (...) of the Other presents, this essay argues, an infinitely greater threat to the state precisely because it cannot be identified as Other, precisely because bears no ostensible traces of the Other. (shrink)

In this essay, I argue that a comparison of Derrida’s “Faith and Knowledge” to the texts and thought of classical rabbinic Judaism can illuminate new conceptual connections among the different elements of Derrida’s thought. Both Derrida and the rabbinic texts can be viewed as affirming a type of “holding back” and “allowing the other to be,” stances which Derrida links to “religiosity” and to “messianicity beyond all messianism.” Moreover, the rabbinic texts appear to avoid the “autoimmune” reaction that Derrida sees (...) as stemming from many sacrificial and self-sacrificial logics in which the self is problematically sacrificed in order to preserve the “unscathed” other. In addition, the rabbinic texts’ stance concerning divine authorization for war and capital punishment help to illuminate Derrida’s claim that the ostensibly “secular” wars of modern states are in fact better understood as “wars of religion.”. (shrink)

A pathogenic connection between autoreactive T cells, fungal infection, and carcinogenesis has been demonstrated in studies of human autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy as well as in a mouse model in which kinase-dead Ikkα knock-in mice develop impaired central tolerance, autoreactive T cell–mediated autoimmunity, chronic fungal infection, and esophageal squamous cell carcinoma, which recapitulates APECED. IκB kinase α is one subunit of the IKK complex required for NF-κB activation. IKK/NF-κB is essential for central tolerance establishment by regulating the development of medullary (...) thymic epithelial cells that facilitate the deletion of autoreactive T cells in the thymus. In this review, we extensively discuss the pathogenic roles of inborn errors in the IKK/NF-κB loci in the phenotypically related diseases APECED, immune deficiency syndrome, and severe combined immunodeficiency; differentiate how IKK/NF-κB components, through mTEC, T cells/leukocytes, or epithelial cells, contribute to the pathogenesis of infectious diseases, autoimmunity, and cancer; and highlight the medical significance of IKK/NF-κB in these diseases. IKK/NF-κB regulates the expression of many genes that encode proteins involved in many crucial biological functions, such as immunity, tissue homeostasis, and fungal/bacterial/viral infections. Also, IKKα plays anti-tumor activities in many organs independently of NF-κB pathways. Thus, an inborn error in one of these gene loci can cause severe human diseases through these complicated mechanisms. (shrink)

Here we discuss the hypothesis that the RNA components of the Ro ribonucleoproteins (RNPs), the Y RNAs, can be processed into microRNAs (miRNAs). Although Ro RNPs, whose main protein components Ro60 and La are targeted by the immune system in several autoimmune diseases, were discovered many years ago, their function is still poorly understood. Indeed, recent data show that miRNA-sized small RNAs can be generated from Y RNAs. This hypothesis leads also to a model in which Ro60 acts as a (...) modulator in the Y RNA-derived miRNA biogenesis pathway. The implications of these Y RNA-derived miRNAs, which may be specifically produced under pathological circumstances such as in autoimmunity or during viral infections, for the enigmatic function of Ro RNPs are discussed. (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)

Systemic autoimmune diseases are characterized by the production of antibodies against a broad range of self-antigens. Recent evidence indicates that the majority of these autoantigens are modified in various ways during cell death. This has led to the hypothesis that the primary immune response in the development of autoimmunity is directed to components of the dying cell. In this article, we summarize data on the modification of autoantigens during cell death and the possible consequences of this for autoimmunity. (...) BioEssays 22:627–636, 2000. © 2000 John Wiley & Sons, Inc. (shrink)

This paper elaborates some of the conceptual implications of Derrida’s call for “another thinking of life” in Voyous: Deux essais sur la raison. The paper first argues that Derrida’s deconstruction of the opposition between metaphorical and literal uses of the discourse of life in La vie la mort is radicalized in Voyous when he argues that democracy’s “autoimmunitary suicide” should be the point of departure for rethinking life in general. To understand further these autoimmune-suicidal tendencies, the paper turns to Derrida’s (...) engagement with Aristotle’s conceptual figure of the prime mover in Voyous. The paper argues that Derrida turns to Aristotle because the prime mover illustrates the ways in which the concept of life remains historically and structurally informed by the philosophical value of ipseitocratic sovereignty, which is allergic to the disseminatory, proliferating, and improper qualities that the philosophical tradition has always ascribed to democracy. Autoimmunity thus provides a way for thinking of a democratic life that is not entirely determined by the teleological power of any divinely good life. (shrink)

Political activists can cheer when Jacques Derrida says that his idea of “democracy to come” is “a call for militant and interminable political critique.” Our acclamations grow louder when he adds that this idea is “a weapon aimed at the enemies of democracy.” He identifies these “enemies” as people who use the discourse of democracy as an “obscene alibi” for “tolerating the plight” of people “deprived of bread and water” and “equality or freedom.”1 He accuses the United States of committing (...) this sort of hypocrisy when it denounces other states for practicing the very roguery in which it indulges.2We can also praise Derrida for what he offers us as well as rejects. He comments that there is a need for a “European... (shrink)

During the final decade of his life, Jacques Derrida came to use the trope of autoimmunity with greater and greater frequency. Indeed it today appears that autoimmunity was to have been the last iteration of what for more than forty years Derrida called deconstruction. This essay looks at the consequences of this terminological shift for our understanding not only of Derrida's final works (such as Rogues) but of his entire corpus. By taking up a term from the biological (...) sciences that describes the process by which an organism turns in quasi-suicidal fashion against its own self-protection, Derrida was able to rethink the very notion of life otherwise and demonstrate the way in which every sovereign identity, from the self to the nation-state to, most provocatively, God, is open to a process that both threatens to destroy it and gives it its only chance of living on. (shrink)

Introduction. Toward a hermeneutics of skepticism -- Montaignean meditations -- Ideology, critique, and the event of literature -- Irony, power, and the death drive -- Queering difference, or the feminine logic of the "non-all" -- Immunizing ontology : the speculative turn -- Conclusion. Desire of the theorist.

This essay explores the treatment of violence in Derrida's ethico-political work, stressing the underlying continuity of Derrida's thinking of politics, from his first reading of Levinas to one of the last notions he developed, autoimmunity. Haddad analyzes the use to which the idea of a “lesser violence” has been put, arguing that it is incompatible with Derrida's other claims.

ExcerptIn this essay, I analyze the modern institution of liberal democracy in the context of the historical development of “biopolitics,” as conceptualized seminally by Michel Foucault in the mid-1970s. I will argue that the principal virtue of liberal democracy is its social stability, and that the principal danger to it—and by extension the stability of Western societies—is its underlying tendency toward “autoimmunity,” as classically theorized by Jacques Derrida, which is to say, toward destroying itself in an attempt to safeguard (...) itself against misidentified threats. (shrink)

The pregnancy compensation hypothesis provides a mechanistic explanation for the evolution of sex differences in immune system functioning, the excess of women experiencing autoimmune disease, and why this is observed only in industrialized nations; none of which can be explained by the staying alive theory, as proposed by the authors of the target article.

This article analyses the biochemical object of tnf inhibitors from the perspective of living with an autoimmune disease. The author tries to tease out how the concept of immune inhibition is used in tandem with the biochemical object of tnf inhibitors to dominate in defining and narrating what health and disease, normal and pathological, cure and healing can mean in the context of autoimmune bodies. Specifically, and within the ‘pathological’ framework of autoimmune diseases, the pharmacological treatment of tnf inhibition is (...) designed to suppress the ‘overly’ active immune system, thus acting as a negative or suppressing biochemical agent aimed at putting the ‘malfunctioning’ immune system back in balance. As can be seen in the current conjuncture, tnf inhibitors officially —and governmentally— place those taking them in a risk group, as they 'lower' their overall bodily immunity and make them more vulnerable to infectious diseases, while stabilizing their patho-logical, ‘over’-immune uninhibited condition. Part personal narrative of being diagnosed with an autoimmune condition, part speculative autoimmune theory inspired by such a diagnosis, the article ultimately calls for a different form of embodiment that is neither negative nor affirmative, and yet is resistant even to itself. (shrink)

The molecular components of complement are a major part of the armoury of the mammalian immune system, being required for the lysis of antibody‐targeted cells. Several of the complement proteins are known to be encoded by genes within the major histocompatibility complex (MHC). Molecular analysis of these genes is providing new information on the basis of complement action and the possible roles of this system in autoimmune disease.

The nonobese diabetic (NOD) mouse spontaneously develops an autoimmune diabetes that shares many immunogenetic features with human insulin-dependent diabetes mellitus (IDDM), type 1 diabetes. The mononuclear cell infiltrates in the islet, which results in the development of insulitis (a prerequisite step for the development of diabetes) are primarily composed of T cells. It is now well accepted that these T cells play important roles in initiating and propagating an autoimmune process, which in turn destroys insulin-producing islet β cells in the (...) pancreas. T cells are subdivided into CD4+ helper T cells and CD8+ cytotoxic T cells. CD4+ T cells are further subdivided into Th1 and Th2 cells based on profiles of cytokine production, and these two T-cell populations counterregulate each other. Because many autoimmune diseases are Th1 T-cell mediated, current studies have focused on manipulating the Th1/Th2 imbalance to suppress the autoimmune process in the NOD model. Furthermore, the incidence of disease is much higher in females than that in males, suggesting an involvement of sex-steroid hormones in the development of diabetes. Understanding insights of the mechanism of immune-mediated islet cell destruction and the interaction between the immune and the neuroendocrine system may, therefore, provide new therapeutic means of preventing this chronic debilitating disease. BioEssays 20:750–757, 1998. © 1998 John Wiley & Sons, Inc. (shrink)

This chapter traces the historical and conceptual evolution of schizophrenia as a diagnostic category and examines its persistent complexity and contested status. This evolution is a product of overlapping clinical characterisations, shifting theoretical frameworks, and multiple research agendas. Two competing perspectives on its ontological status are entertained with the goal of finding a productive synthesis: the continuity hypothesis, which treats schizophrenia as a stable brain disorder recognisable across time, and the discontinuity thesis, which frames it as a culturally and historically (...) situated construct without essential unity. Although the term ‘schizophrenia’ has endured for over a century, its referents have varied, and its boundaries remain diffuse. Clinical presentations are heterogeneous, outcomes are variable, and underlying mechanisms are diverse—ranging from neurodevelopmental disruptions to immune-mediated processes. These complexities challenge attempts to define schizophrenia as a natural kind or unitary disease entity. At the clinical level, it remains a disorder marked by persistent disturbances in selfhood, perception, cognition, affect, and social functioning. Contemporary advances in neuroscience, genetics, and immunology have refined our understanding of these disturbances, generating new explanatory models while also exposing the limitations of traditional nosologies. The recognition of autoimmune psychosis and other neurologically identifiable causes of schizophrenia-like syndromes illustrates that neuropsychiatric disorders remain relevant to schizophrenia. Schizophrenia is not a discrete disease entity; it is a historically contingent and evolving set of clinical concepts. (shrink)

Severe COVID‐19 is often accompanied by coagulopathies such as thrombocytopenia and abnormal clotting. Rarely, such complications follow SARS‐CoV‐2 vaccination. The cause of these coagulopathies is unknown. It is hypothesized that coagulopathies accompanying SARS‐CoV‐2 infections and vaccinations result from bacterial co‐infections that synergize with virus‐induced autoimmunity due to antigenic mimicry of blood proteins by both bacterial and viral antigens. Coagulopathies occur mainly in severe COVID‐19 characterized by bacterial co‐infections with Streptococci, Staphylococci, Klebsiella, Escherichia coli, and Acinetobacter baumannii. These bacteria express (...) unusually large numbers of antigens mimicking human blood antigens, as do both SARS‐CoV‐2 and adenoviruses. Bacteria mimic cardiolipin, prothrombin, albumin, and platelet factor 4 (PF4). SARS‐CoV‐2 mimics complement factors, Rh antigens, platelet phosphodiesterases, Factors IX and X, von Willebrand Factor (VWF), and VWF protease ADAMTS13. Adenoviruses mimic prothrombin and platelet factor 4. Bacterial prophylaxis, avoidance of vaccinating bacterially infected individuals, and antigen deletion for vaccines may reduce coagulopathy risk. Also see the video abstract here: https://youtu.be/zWDOsghrPg8. (shrink)

Few topics in contemporary science hold the wide interest commanded by immunology, so this graceful and timely account of the development of this science is a welcomed addition to the literature. Succinct, well-written, and informed, Intolerant Bodies narrates the history of immunology through the lens of autoimmune disease. In what the authors call “a biography” , they have focused on four central illnesses: multiple sclerosis, systemic lupus erythematosus, rheumatoid arthritis, and type 1 diabetes mellitus. However, the story told here extends (...) far beyond the topic of “attack against self” to provide perhaps the best overview of immunity available for the general reader. The specialist will also appreciate the rich anecdotal material and benefit from the historical insights scattered throughout the text. So the book is, in fact, more than a history of autoimmunity and offers a compact history for those who need not consult more comprehensive accounts (e .. (shrink)

Certain steroids can react with proteins to form stable, covalent addition products. 16α‐hydroxyestrone and the glucocorticoids, for example, contain ketol moieties which permit them to react non‐enzymatically with proteins by forming Schiffbase rearrangement products with lysine residues. The oral contraceptive agent, 17α‐ethinylestradiol, can add to proteins after being enzymatically activated by microsomal oxidation. Elevated plasma levels of these steroids result in an increased amount of protein modification in vivo. Recent investigations have linked the occurrence of steroid‐modified proteins with pathological sequelae (...) associated with high steroid levels. (shrink)

(2009). “Twenty Paragraphs of Written Instructions”. Angelaki: Vol. 14, shadows of cruelty sadism, masochism and the philosophical muse – part one, pp. 59-68.

자크 데리다는 순수하고 신성하게 보이는 곳에, 혹은 그렇게 보지 않으면 안 된다는 명령이 자리하고 있는 곳에, 자신의 해체론을 개입시킨다. 데리다의 해체는 ‘…처럼’ 보이는 곳과 ‘반드시 그처럼!’의 강박이 도사리는 곳의 균열점을 내파한다. 정확히 말하면, 그 균열점이 참조하는 의미 체계의 울타리를 해체한 곳에서, 데리다는 진정한 새로움 그 자체를 도래하도록 울타리를 개방하고 의미를 해방한다. 데리다는 의미에 예속된 인간의 모습 중에서, 특히 자기편(in­)에 득이 되는 울타리의 조건을 설정한 후, 그 바깥을 불가능(im­)의 그 무엇으로 설정하는 모습을 비판한다. 자기·내부·울타리 안이 구축될 때, 동시동연(同時同延)적으로 금기와 위반이 함께 (...) 구성될 수밖에 없는 상황을 자가면역(自家免疫)으로 설정한 데리다는, 선물·정의·종교·용서·환대 등의 강박적 의미지평이 태생적으로 자가면역의 장(場)임을 밝힌다. 이는 그 의미들이 해체될 수밖에 없는 내재적 필연성을 지님을 뜻한다. 우리의 일반 사유를 관할하는 의미의 울타리를 해체한 자리에서 데리다는, 과장된·궁극의 윤리성을 완전히 새로운 시간과 함께 도래하게 한다. 이에 대한 구체적 논의를, 데리다는 인간 심리에서 예민한 부분이라 볼 수 있는 용서의 논의로 다룬다. 통상의 용서를 해체한 자리에 광기어린 용서의 흔적을 발굴하는 데리다의 시선을 따라가면, 무한을 그저 가능한 것 이상의 그 어떤 상태로 막연하고 신비롭게 다루던 수학계의 관성을 난폭하게 절단시킨 실무한(實無限)의 위상과 동형인 부분이 짚어진다. 실무한은 기성의 가무한(假無限)에 정향된 수학 풍토와 완벽한 단절을 이룬다. 두 무한 개념의 차이는 결코 좁혀지지 않는다. 실무한은 전혀 새로운 문제­틀을 강제한다. 이러한 강제는 부정적 폭력이 아니라, 수학적 난제를 해결한 건설적 폭력이다. 이러한 실무한의 위상이 데리다식 용서의 위상과 동형임을 밝히는 것이 본고의 논점이다. (shrink)