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The Inducible System: Antigens
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Superantigens bind very tightly to the MHC of the antigen presenting cell. The binding site for superantigens, unlike a processed antigen fragment, is outside the antigen-binding site of the MHC. Superantigens, therefore, are not processed and are not presented by the APC in standard fashion.
Antigens
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Superantigens are a class of macromolecules which stimulate T cells via a recently discovered mechanism which is very different from that of most T cell immunogens. In order to interact with T cell antigen receptors, most proteins must be processed (partially degraded) and presented with MHC molecules. Superantigens sidestep this mechanism and in their native state bind directly to T cell receptors and cross-link them with MHC molecules on other cells. This results in widespread activation of T cells with many different specificities. The staphylococcal exotoxins are examples of a superantigen family (see Chapter 6 for further discussion).
Evidence for a Role of Infections in the Activation of Autoreactive T Cells and the Pathogenesis of Autoimmunity
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
J. Ludovic Croxford, Stephen D. Miller
Superantigens are immunostimulatory molecules, which can stimulate T cells displaying particular TCR Vβ subsets, independent of antigen recognition. They bind outside of the TCR cleft and therefore are capable of activating a wide range of T cell clones.14 Although studies have not confirmed the ability of superantigens to induce autoimmunity, they can play a role in the exacerbation and induction of relapse, once clinical disease has been induced.15 Superantigens have been shown to play an important role in animal models of MS and arthritis, and in human Crohn’s disease.15-17
The Immunologic Profiles of Kawasaki Disease Triggered by Mycoplasma pneumoniae Infection
Published in Fetal and Pediatric Pathology, 2023
Hong-bo Hu, Xiao-peng Shang, Jian-gang Wu, Ya-ling Cai
Children with KD often experience the abnormal activation of T cells during the disease period, resulting in the abnormal activation of the immune system and causing clinical syndromes. This is the key step and initial link of the activation of the immune system in KD [19,20]. It has been demonstrated that the number of CD4+T cells and the CD4/CD8 ratio were increased, while the number of CD8+T lymphocytes was reduced in patients with KD [10,21]. In the present study, the CD4/CD8 ratio of MP-KD was higher than that of KD. It is hypothesized that the presence of vasculitis in KD may be triggered by an immune response to a superantigen from an infectious pathogen in those who are genetically susceptible [5, 7]. Mycoplasma arthritidis has been shown to produce a superantigen, implying that other Mycoplasma species, such as MP, may do the same [22,23]. Superantigens are polyclonal CD4+ T lymphocyte stimulators that cause massive cytokine production [24]. There is also some evidence that both Th1 and Th2 cytokines may be activated during the acute state of KD [25]. As a result, interacting directly with class II major histocompatibility complex molecules, MP superantigens activate polyclonal CD4+ T lymphocytes, resulting in a massive release of cytokines that cause vascular inflammation [5,7,26].
Pathophysiological Considerations in Periorbital Necrotizing Fasciitis: A Case Report
Published in Ocular Immunology and Inflammation, 2023
Yalda Hadizamani, Stefano Anastasi, Anouk Schori, Rudolf Lucas, Justus G. Garweg, Jürg Hamacher
Risk factors increasing susceptibility to develop NF include diabetes mellitus, chronic renal failure, cardiovascular disease, drug abuse and alcoholism.2,3,8,43,44 The patient’s general condition, risk factors and underlying comorbidities as well as pathogenic virulence factors determine the outcome of NF. Around 45% of patients with arterial hypotension and streptococcal-induced toxic shock syndrome develop acute respiratory distress syndrome.45 Morbidity and mortality of the Streptococcus-induced toxic shock syndrome are higher than for the Staphylococcus-induced toxic shock syndrome and are in a range of 30–80%.45,46 Patients who have neutralizing antibodies against superantigens are less likely to develop NF.37 If superantigens however enter the bloodstream of patients devoid of neutralizing antibodies from previous exposures, they can trigger a sudden, significant and non-specific T cell stimulation and consequently a cytokine storm,37 resulting in systemic toxicity, multi-organ failure and septic shock.38,47 The Streptococcus-induced toxic shock syndrome can present with locally invasive Streptococcal infections such as pharyngitis or more violent diffuse disorders like arthritis, bacteremia, endocarditis, meningitis, pneumonia, sinusitis, cellulitis, myositis and necrotizing fasciitis.48
Symbiotic microorganisms: prospects for treating atopic dermatitis
Published in Expert Opinion on Biological Therapy, 2022
Rongrong Chai, Zongguang Tai, Yunjie Zhu, Chaochao Chai, Zhongjian Chen, Quangang Zhu
Superantigens allow cell interactions unconstrained by antigenic peptides presented by major histocompatibility class II molecules on antigen-presenting cells and T-cell receptors on T cells, leading to excessive cytokine production and resulting in cytotoxicity [90,91]. Superantigens are types of allergens that stimulate IgE responses [104]. For example, exfoliative toxin A derived from S. aureus digests the epithelial barrier, thereby releasing enterotoxins and inducing proinflammatory cytokines, such as IL-4, IL-12, and IL-22 [105]. The alpha-toxin secreted by S. aureus forms heterodimer complexes at the cell membrane, which create porous channels that lead to cell lysis [106]. Figure 2 shows the effect of different bacteria on AD skin. In a study by Nakatsuji et al. [105], S. aureus penetrated the epidermis of human skin equivalents and mouse skin. The abundance of S. aureus increased in the skin of cathelicidin knockout and ovalbumin-sensitized filaggrin mutant mice. Although this penetration did not show the characteristics of infection, it altered cytokine and adenylate responses. This inflammatory trigger may further alter the surface microbiota and make the disease ‘chronic’ by increasing barrier destruction. The proteases and phenol-soluble modulins secreted by S. aureus bind to the induced keratinocyte proteases, destroy the skin barrier, activate the local immune response, and initiate an AD-like phenotype [107]. These findings suggest that the colonization of S. aureus is strongly associated with AD.