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A. E. Wold - One of the best experts on this subject based on the ideXlab platform.
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Superantigens and adhesins of infant gut commensal Staphylococcus aureus strains and association with subsequent development of atopic eczema
British Journal of Dermatology, 2017Co-Authors: F. L. Nowrouzian, Gérard Lina, Elisabeth Hodille, E. Lindberg, B. Hesselmar, R. Saalman, I. Adlerberth, A. E. WoldAbstract:BACKGROUND: According to the hygiene hypothesis, insufficient immune activation by microbes increases the risk of allergy development. Staphylococcus aureus, which is part of the skin and gut microbiota of infants in Western countries, produces a variety of T-cell-activating enterotoxins, called Superantigens. OBJECTIVES: To investigate whether early (0-2 months of age) gut colonization by S. aureus strains that carry specific Superantigens and adhesins was related to subsequent development of atopic eczema in a Swedish birth cohort. METHODS: Staphylococcus aureus was isolated from rectal swabs and cultured quantitatively from faecal samples, with individual strains being tested for carriage of genes for Superantigens and adhesins. Atopic eczema was diagnosed at onset of symptoms and at 18 months of age. RESULTS: Although the frequency of early gut colonization by S. aureus was not related to subsequent eczema development, the S. aureus strains that were found to colonize those infants who developed atopic eczema were less likely to carry the gene encoding the Superantigen SElM (P = 0\textperiodcentered008) and the gene for elastin-binding protein (P = 0\textperiodcentered03), compared with strains that were isolated from infants who had not developed atopic eczema by 18 months of age. CONCLUSIONS: Gut colonization by S. aureus strains carrying a certain combination of Superantigen and adhesin genes was negatively associated with subsequent development of atopic eczema. Such strains may provide stimulation and promote maturation of the infant immune system.
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Superantigens and adhesins of infant gut commensal staphylococcus aureus strains and association with subsequent development of atopic eczema
British Journal of Dermatology, 2017Co-Authors: F. L. Nowrouzian, Gérard Lina, Elisabeth Hodille, E. Lindberg, B. Hesselmar, R. Saalman, I. Adlerberth, A. E. WoldAbstract:SummaryBackground According to the hygiene hypothesis, insufficient immune activation by microbes increases the risk of allergy development. Staphylococcus aureus, which is part of the skin and gut microbiota of infants in Western countries, produces a variety of T-cell-activating enterotoxins, called Superantigens. Objectives To investigate whether early (0–2 months of age) gut colonization by S. aureus strains that carry specific Superantigens and adhesins was related to subsequent development of atopic eczema in a Swedish birth cohort. Methods Staphylococcus aureus was isolated from rectal swabs and cultured quantitatively from faecal samples, with individual strains being tested for carriage of genes for Superantigens and adhesins. Atopic eczema was diagnosed at onset of symptoms and at 18 months of age. Results Although the frequency of early gut colonization by S. aureus was not related to subsequent eczema development, the S. aureus strains that were found to colonize those infants who developed atopic eczema were less likely to carry the gene encoding the Superantigen SElM (P = 0·008) and the gene for elastin-binding protein (P = 0·03), compared with strains that were isolated from infants who had not developed atopic eczema by 18 months of age. Conclusions Gut colonization by S. aureus strains carrying a certain combination of Superantigen and adhesin genes was negatively associated with subsequent development of atopic eczema. Such strains may provide stimulation and promote maturation of the infant immune system.
Patrick M. Schlievert - One of the best experts on this subject based on the ideXlab platform.
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Staphylococcal and Streptococcal Superantigen Exotoxins
Clinical microbiology reviews, 2013Co-Authors: Adam R. Spaulding, Donald Y M Leung, Wilmara Salgado-pabón, Petra L. Kohler, Alexander R. Horswill, Patrick M. SchlievertAbstract:SUMMARY This review begins with a discussion of the large family of Staphylococcus aureus and beta-hemolytic streptococcal pyrogenic toxin T lymphocyte Superantigens from structural and immunobiological perspectives. With this as background, the review then discusses the major known and possible human disease associations with Superantigens, including associations with toxic shock syndromes, atopic dermatitis, pneumonia, infective endocarditis, and autoimmune sequelae to streptococcal illnesses. Finally, the review addresses current and possible novel strategies to prevent Superantigen production and passive and active immunization strategies.
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Staphylococcal Superantigens Cause Lethal Pulmonary Disease in Rabbits
The Journal of infectious diseases, 2010Co-Authors: Kristi L. Strandberg, Jessica H. Rotschafer, Sara M. Vetter, Rebecca A. Buonpane, David M. Kranz, Patrick M. SchlievertAbstract:Background The Centers for Disease Control and Prevention (CDC) and others reported that methicillin-resistant S. aureus (MRSA) are significant causes of serious human infections, including pulmonary illnesses. We investigated the role played by Superantigens in lung-associated lethal illness in rabbits. Methods A rabbit model was established to investigate the potential role played by Superantigens, staphylococcal enterotoxin B (SEB), staphylococcal enterotoxin C (SEC), and toxic shock syndrome toxin-1 (TSST-1). Rabbits received intrabronchial community-associated (CA) MRSA strains USA200 (TSST-1(+)), MW2 (SEC(+)), c99-529 (SEB(+)), or purified Superantigens. Some rabbits were preimmunized against Superantigens or treated with soluble high-affinity T cell receptors (Vβ-TCR) to neutralize SEB and then challenged intrabronchially with CA-MRSA or Superantigens. Results Rabbits challenged with CA-MRSA or Superantigens developed fatal, pulmonary illnesses. Animals preimmunized against purified Superantigens, or treated passively with Vβ-TCRs and then challenged with CA-MRSA or Superantigens, survived. Lung histological analysis indicated that nonimmune animals developed lesions consistent with necrotizing pneumonia after challenge with CA-MRSA or purified Superantigens. Superantigen-immune animals or animals treated with soluble Vβ-TCRs did not develop pulmonary lesions. Conclusions Superantigens contribute to lethal pulmonary illnesses due to CA-MRSA; preexisting immunity to Superantigens prevents lethality. Administration of high-affinity Vβ-TCR with specificity for SEB to nonimmune animals protects from lethal pulmonary illness resulting from SEB(+) CA-MRSA and SEB.
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Cytolysins augment Superantigen penetration of stratified mucosa
Journal of immunology (Baltimore Md. : 1950), 2009Co-Authors: Amanda J. Brosnahan, Mary J. Mantz, Christopher A. Squier, Marnie L. Peterson, Patrick M. SchlievertAbstract:Staphylococcus aureus and Streptococcus pyogenes colonize mucosal surfaces of the human body to cause disease. A group of virulence factors known as Superantigens are produced by both of these organisms that allows them to cause serious diseases from the vaginal (staphylococci) or oral mucosa (streptococci) of the body. Superantigens interact with T cells and APCs to cause massive cytokine release to mediate the symptoms collectively known as toxic shock syndrome. In this study we demonstrate that another group of virulence factors, cytolysins, aid in the penetration of Superantigens across vaginal mucosa as a representative nonkeratinized stratified squamous epithelial surface. The staphylococcal cytolysin α-toxin and the streptococcal cytolysin streptolysin O enhanced penetration of toxic shock syndrome toxin-1 and streptococcal pyrogenic exotoxin A, respectively, across porcine vaginal mucosa in an ex vivo model of Superantigen penetration. Upon histological examination, both cytolysins caused damage to the uppermost layers of the vaginal tissue. In vitro evidence using immortalized human vaginal epithelial cells demonstrated that although both Superantigens were proinflammatory, only the staphylococcal cytolysin α-toxin induced a strong immune response from the cells. Streptolysin O damaged and killed the cells quickly, allowing only a small release of IL-1β. Two separate models of Superantigen penetration are proposed: staphylococcal α-toxin induces a strong proinflammatory response from epithelial cells to disrupt the mucosa enough to allow for enhanced penetration of toxic shock syndrome toxin-1, whereas streptolysin O directly damages the mucosa to allow for penetration of streptococcal pyrogenic exotoxin A and possibly viable streptococci.
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prevalence of Superantigen secreting bacteria in patients with kawasaki disease
The Journal of Pediatrics, 2002Co-Authors: Donald Y M Leung, Cody H Meissner, Stanford T Shulman, Wilbert H Mason, Michael A Gerber, Mary P Glode, Barry L Myones, Gary J Wheeler, Robin Ruthazer, Patrick M. SchlievertAbstract:Abstract Objectives: To assess the prevalence of Superantigen secreting bacteria in children with acute Kawasaki disease (KD) relative to control patients. Study design: Bacterial cultures were obtained in a blinded fashion from the throat, rectum, and groin of 45 patients with untreated acute KD and 37 febrile control patients from 6 centers in the United States. Cultures were processed for the presence of Superantigen-producing bacteria at a central laboratory. Results: Staphylococci or streptococci that produced Superantigens (TSST-1, SEB, SEC, SPEB, SPEC) were isolated from 25 of 45 patients with KD (56%) as compared with 13 of 37 (35%) control patients ( P =.078). Because SEB- and SEC-producing Staphylococcus aureus have not been associated with KD and because they do not induce a Vβ2+ T-lymphocyte response, we analyzed the difference between groups relative to Superantigens TSST-1 or SPEB/SPEC production. TSST-1 secreting S aureus or SPEB/SPEC producing group A streptococci were isolated from 20 of 45 (44%) patients with KD compared with 7 of 37 (19%) control patients ( P =.019). Conclusions: The overall isolation rates of Superantigen (TSST-1, SPEB, SPEC, SEB, SEC) producing bacteria between patients with KD and febrile control patients were not statistically significant. However, future studies should further examine the potential role of Vβ2-stimulatory Superantigens (TSST-1 and SPEB/SPEC) in KD. (J Pediatr 2002;140:742-6)
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evidence for the involvement of bacterial Superantigens in psoriasis atopic dermatitis and kawasaki syndrome
Fems Microbiology Letters, 2000Co-Authors: Jeremy M Yarwood, Donald Y M Leung, Patrick M. SchlievertAbstract:A growing body of evidence implicates streptococcal and staphylococcal Superantigens in the development of psoriasis, atopic dermatitis and Kawasaki syndrome. In each of these illnesses, an abnormal state of immunologic activity is observed. Superantigens, which have a unique ability to activate large numbers of lymphocytes, are likely to contribute to these disorders in a number of ways. The demonstrated activities of bacterial Superantigens include increasing the number of circulating lymphocytes, with activation of autoreactive subsets, upregulation of tissue homing receptors on circulating lymphocytes, and local activation of immune cells within affected tissues. Through these and other mechanisms, Superantigens have a proven ability to induce high levels of inflammatory cytokines and/or initiate autoimmune responses that contribute to the development of skin and vascular disorders. Though development of the illnesses discussed in this review are highly complex processes, Superantigens may well play a critical role in their onset or maintenance. Understanding Superantigen function may elucidate potential therapeutic strategies for these disorders.
F. L. Nowrouzian - One of the best experts on this subject based on the ideXlab platform.
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Superantigens and adhesins of infant gut commensal Staphylococcus aureus strains and association with subsequent development of atopic eczema
British Journal of Dermatology, 2017Co-Authors: F. L. Nowrouzian, Gérard Lina, Elisabeth Hodille, E. Lindberg, B. Hesselmar, R. Saalman, I. Adlerberth, A. E. WoldAbstract:BACKGROUND: According to the hygiene hypothesis, insufficient immune activation by microbes increases the risk of allergy development. Staphylococcus aureus, which is part of the skin and gut microbiota of infants in Western countries, produces a variety of T-cell-activating enterotoxins, called Superantigens. OBJECTIVES: To investigate whether early (0-2 months of age) gut colonization by S. aureus strains that carry specific Superantigens and adhesins was related to subsequent development of atopic eczema in a Swedish birth cohort. METHODS: Staphylococcus aureus was isolated from rectal swabs and cultured quantitatively from faecal samples, with individual strains being tested for carriage of genes for Superantigens and adhesins. Atopic eczema was diagnosed at onset of symptoms and at 18 months of age. RESULTS: Although the frequency of early gut colonization by S. aureus was not related to subsequent eczema development, the S. aureus strains that were found to colonize those infants who developed atopic eczema were less likely to carry the gene encoding the Superantigen SElM (P = 0\textperiodcentered008) and the gene for elastin-binding protein (P = 0\textperiodcentered03), compared with strains that were isolated from infants who had not developed atopic eczema by 18 months of age. CONCLUSIONS: Gut colonization by S. aureus strains carrying a certain combination of Superantigen and adhesin genes was negatively associated with subsequent development of atopic eczema. Such strains may provide stimulation and promote maturation of the infant immune system.
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Superantigens and adhesins of infant gut commensal staphylococcus aureus strains and association with subsequent development of atopic eczema
British Journal of Dermatology, 2017Co-Authors: F. L. Nowrouzian, Gérard Lina, Elisabeth Hodille, E. Lindberg, B. Hesselmar, R. Saalman, I. Adlerberth, A. E. WoldAbstract:SummaryBackground According to the hygiene hypothesis, insufficient immune activation by microbes increases the risk of allergy development. Staphylococcus aureus, which is part of the skin and gut microbiota of infants in Western countries, produces a variety of T-cell-activating enterotoxins, called Superantigens. Objectives To investigate whether early (0–2 months of age) gut colonization by S. aureus strains that carry specific Superantigens and adhesins was related to subsequent development of atopic eczema in a Swedish birth cohort. Methods Staphylococcus aureus was isolated from rectal swabs and cultured quantitatively from faecal samples, with individual strains being tested for carriage of genes for Superantigens and adhesins. Atopic eczema was diagnosed at onset of symptoms and at 18 months of age. Results Although the frequency of early gut colonization by S. aureus was not related to subsequent eczema development, the S. aureus strains that were found to colonize those infants who developed atopic eczema were less likely to carry the gene encoding the Superantigen SElM (P = 0·008) and the gene for elastin-binding protein (P = 0·03), compared with strains that were isolated from infants who had not developed atopic eczema by 18 months of age. Conclusions Gut colonization by S. aureus strains carrying a certain combination of Superantigen and adhesin genes was negatively associated with subsequent development of atopic eczema. Such strains may provide stimulation and promote maturation of the infant immune system.
Lone Skov - One of the best experts on this subject based on the ideXlab platform.
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Bacterial Superantigens and inflammatory skin diseases.
Clinical and experimental dermatology, 2000Co-Authors: Lone Skov, Ole BaadsgaardAbstract:Bacteria seem to play an important role in the induction and maintenance of inflammatory skin diseases such as psoriasis and atopic dermatitis. Toxins from bacteria including Streptococcus and Staphylococcus aureus, have been shown to function as a new type of allergen termed ‘Superantigen’. Superantigens bypass the normal control of T-cell activation and activate all T-cell clones bearing certain types of variable chain on the T-cell receptor: this leads to vigorous T-cell activation and cytokine release. These bacterial Superantigens may be involved in induction and aggravation of inflammatory skin diseases. Guttate psoriasis is often preceded by a streptococcal throat infection and T cells specific for streptococcal Superantigens have been identified in the skin of patients. The skin of patients with atopic dermatitis is often colonized with Superantigen-releasing Staph. aureus, and application of a staphylococcal Superantigen to human skin induces an eczematoid reaction.
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Superantigens and their importance for inflammatory skin diseases
Ugeskrift for laeger, 1999Co-Authors: Lone Skov, Baadsgaard OAbstract:Superantigens are a group of bacterial and viral proteins that are characterized by their capacity to stimulate a large number of T-cells simultaneously. Superantigens bind directly to the MHC class II molecule on the antigen-presenting cell and crosslink the cell with T-cells expressing certain V beta-chains on their T-cell receptor which leads to a vigorous polyclonal T-cell activation. Staphylococcal Superantigens seem to be involved in the pathogenesis of systemic diseases such as toxic shock syndrome and Kawasaki syndrome. Furthermore, Superantigens seem to play an important role in the induction and maintenance of inflammatory skin diseases such as atopic dermatitis and psoriasis. The skin of patients with atopic dermatitis is often colonized with Superantigen-releasing Staphylococcus aureus, and application of staphylococcal Superantigen on intact human skin induces a local dermatitis reaction. Guttate psoriasis is often preceded by a streptococcal throat infection, and T-cells specific for streptococcal Superantigens have been identified in fresh guttate psoriasis lesions.
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Superantigens. Do they have a role in skin diseases
Archives of dermatology, 1995Co-Authors: Lone Skov, Ole BaadsgaardAbstract:Superantigens are a group of bacterial and viral proteins that are characterized by their capacity to stimulate a large number of T cells. They bind directly to the major histocompatibility complex class II molecule on the antigen-presenting cell and cross-link the antigen-presenting cell with T cells expressing certain T-cell receptors, leading to polyclonal T-cell activation. They have been shown to play a role in toxic shock syndrome and mucocutaneous lymph node syndrome and are postulated to play a role in other systemic diseases. Because inflammatory skin diseases such as atopic dermatitis and psoriasis are often known to be colonized with Superantigen-releasing Staphylococcus aureus , the role of Superantigens in skin diseases is of major importance. Recent studies have demonstrated that if a staphylococcal Superantigen is applied on intact human skin, a clinical picture of dermatitis evolves. Furthermore, in the presence of Superantigens, epidermal cells potently activate T cells. Thus, Superantigens may play a role in the induction and exacerbation of inflammatory skin diseases. (Arch Dermatol. 1995;131:829-832)
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The potential role of Staphylococcus aureus Superantigens in atopic eczema
Journal of the European Academy of Dermatology and Venereology, 1995Co-Authors: Lone SkovAbstract:Abstract Aim To study the effect of skin testing with Staphylococcus aureus Superantigen. Subject Atopic dermatitis and Superantigens. Methods Patch testing. Results Atopic eczema is a multifactorial genetic skin disorder. Staphylococcus aureus is often present on the skin of patients with atopic eczema and recently it has been shown that the majority of these staphylococci secrete Superantigens. Superantigens are bacterial and viral proteins characterized by their capacity to stimulate a large number of T cells. Superantigens bind directly to the major histocompatibility complex class II molecule on the antigen presenting cell and cross-link the antigen presenting cell with T cells expressing certain T cell receptors leading to polyclonal T cell activation. Both Langerhans cells and major histocompatibility complex class II positive keratinocytes contain the capacity to activate T cells in the presence of Superantigens. Conclusion Superantigen applied on intact human skin or on uninvolved atopic skin induces eczema. Thus, Superantigens may play a role in the exacerbation of atopic eczema.
Raymond Kaempfer - One of the best experts on this subject based on the ideXlab platform.
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Broad-Spectrum Peptide Antagonists of Superantigen Toxins
Superantigens, 2014Co-Authors: Revital Levy, Gila Arad, Iris Nasie, Dalia Hillman, Raymond KaempferAbstract:Bacterial Superantigens are among the most lethal of toxins. These stable proteins bind directly to most major histocompatibility (MHC) class II molecules and stimulate virtually all T cells bearing particular domains in the variable portion of the β-chain of the αβ T cell receptor (TCR), without need for processing by antigen-presenting cells. The peptides are capable of protecting mice from the lethal effects of Superantigen toxins as widely different as staphylococcal enterotoxins (SE) SEB and toxic shock syndrome toxin 1 (TSST-1), and they can rescue animals already deeply into toxic shock. The Superantigen antagonist peptides described in this chapter protect or rescue mice from lethal shock in a molar excess of as low as 20 fold over the toxin, implying that they bind tightly to a cellular target that is critical for Superantigen action. The antagonist peptides described in the chapter provide a new molecular tool for understanding the mechanism of excessive human immune response activation by Superantigens that occurs during toxic shock and for the identification of a novel target ligand that may interact with this Superantigen domain. Removal of two amino acids from the dodecamer motif led to a significant decline in antagonist activity; this truncation may affect conformational stability or appropriate folding onto this putative receptor and reduce its affinity for the target.
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CD28: Direct and Critical Receptor for Superantigen Toxins
Toxins, 2013Co-Authors: Raymond Kaempfer, Gila Arad, Revital Levy, Iris Nasie, Dalia Hillman, Ziv RotfogelAbstract:Every adaptive immune response requires costimulation through the B7/CD28 axis, with CD28 on T-cells functioning as principal costimulatory receptor. Staphylococcal and streptococcal Superantigen toxins hyperstimulate the T-cell-mediated immune response by orders of magnitude, inducing a lethal cytokine storm. We show that to elicit an inflammatory cytokine storm and lethality, Superantigens must bind directly to CD28. Blocking access of the Superantigen to its CD28 receptor with peptides mimicking the contact domains in either toxin or CD28 suffices to protect mice effectively from lethal shock. Our finding that CD28 is a direct receptor of Superantigen toxins broadens the scope of microbial pathogen recognition mechanisms.
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binding of Superantigen toxins into the cd28 homodimer interface is essential for induction of cytokine genes that mediate lethal shock
PLOS Biology, 2011Co-Authors: Gila Arad, Revital Levy, Iris Nasie, Dalia Hillman, Ziv Rotfogel, Uri Barash, Emmanuelle Supper, Tomer Shpilka, Adi Minis, Raymond KaempferAbstract:Bacterial Superantigens, a diverse family of toxins, induce an inflammatory cytokine storm that can lead to lethal shock. CD28 is a homodimer expressed on T cells that functions as the principal costimulatory ligand in the immune response through an interaction with its B7 coligands, yet we show here that to elicit inflammatory cytokine gene expression and toxicity, Superantigens must bind directly into the dimer interface of CD28. Preventing access of the Superantigen to CD28 suffices to block its lethality. Mice were protected from lethal Superantigen challenge by short peptide mimetics of the CD28 dimer interface and by peptides selected to compete with the Superantigen for its binding site in CD28. Superantigens use a conserved β-strand/hinge/α-helix domain of hitherto unknown function to engage CD28. Mutation of this Superantigen domain abolished inflammatory cytokine gene induction and lethality. Structural analysis showed that when a Superantigen binds to the T cell receptor on the T cell and major histocompatibility class II molecule on the antigen-presenting cell, CD28 can be accommodated readily as third Superantigen receptor in the quaternary complex, with the CD28 dimer interface oriented towards the β-strand/hinge/α-helix domain in the Superantigen. Our findings identify the CD28 homodimer interface as a critical receptor target for Superantigens. The novel role of CD28 as receptor for a class of microbial pathogens, the Superantigen toxins, broadens the scope of pathogen recognition mechanisms.
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Peptide antagonists of Superantigen toxins
Molecular Diversity, 2004Co-Authors: Raymond KaempferAbstract:Superantigens produced by Staphylococcus aureus and Streptococcus pyogenes are among the most lethal of toxins. Toxins in this large family trigger an excessive cellular immune response leading to toxic shock. Superantigens are secreted by the bacteria as diverse natural mixtures, a complexity that demands development of broad-spectrum countermeasures. We used a rational approach to design short peptides with homology to various domains in a typical Superantigen (staphylococcal enterotoxin B) and screened each peptide for its ability to antagonize, in human peripheral blood mononuclear cells, Superantigen-mediated induction of the genes encoding T helper 1 cytokines that mediate shock: interleukin-2, interferon-gamma and tumor necrosis factor. A dodecamer peptide proved a potent antagonist against widely different Superantigens. This peptide protected mice from killing by Superantigens and it was able to rescue mice undergoing toxic shock. The antagonist peptide shows homology to a β-strand-hinge-α-helix domain that is structurally conserved among Superantigens, yet currently of unknown function and remote from the binding sites for the known ligands essential for T cell activation, the major histocompatibility complex class II molecule and T cell receptor. The antagonist activity of this peptide thus identifies a novel domain in Superantigens that is critical for their toxic action. The antagonist peptide provides a new tool for understanding the mechanism of excessive human immune response activation by Superantigens that occurs during toxic shock and for identification of a novel target ligand that may interact with this Superantigen domain.
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Broad-spectrum immunity against Superantigens is elicited in mice protected from lethal shock by a Superantigen antagonist peptide.
Immunology letters, 2004Co-Authors: Gila Arad, Revital Levy, Dalia Hillman, Raymond KaempferAbstract:Bypassing the restricted presentation of conventional antigens, Superantigens trigger an excessive cellular immune response leading to toxic shock. Antagonist peptides that inhibit the induction of human Th1 cytokine gene expression by a variety of bacterial Superantigens protect mice from lethal toxic shock. We show that the surviving mice rapidly develop a broad-spectrum, protective immunity against further lethal toxin challenges with the same Superantigen and even with Superantigen toxins that they have not encountered before. By blocking the induction of a cellular immune response leading to toxic shock, the antagonist peptide allows the Superantigen to induce a vigorous humoral immune response directed against itself, resulting in anti-toxin IgM and IgG that are broadly protective. Adoptive transfer of these antibodies to naïve mice rendered them resistant to lethal Superantigen challenge. The appearance of these antibodies does not require immunization with an adjuvant and is not elicited by the antagonist peptide. Our results show that Superantigens are potent immunogens when given the opportunity to induce a B cell response, in conditions where a deleterious Th1 response is prevented by the Superantigen antagonist peptide.
