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Stiehm's Immune Deficiencies: Inborn Errors in Immunity, Second Edition, is ideal for physicians and other caregivers who specialize in immunology, allergies, infectious diseases and pulmonary medicine.

This book enters into the many worlds of expression brought forth across Africa by the ravaging presence of HIV/AIDS. Africans and non-Africans, physicians and social scientists, journalists and documentarians share here a common and essential interest in understanding creative expression in crushing and uncertain times. Chapters investigate and engage the social networks, power relationships, and cultural structures that enable the arts to convey messages of hope and healing, and of knowledge and good counsel to the wider community. And from Africa to the wider world, the text here brings intimate, inspiring portraits of the performers, artists, communities, and organizations that have shared here their insights and the sense they have made of their lives and actions from deep within this devastating epidemic. Covering the wide expanse of the African continent, the chapters include explorations of, for example, the use of music to cope with AIDS; the relationship between music, HIV/AIDS, and social change; visual approaches to HIV literacy; radio and television as tools for “edutainment”; several individual artists’ confrontations with HIV/AIDS; various performance groups’ response to the epidemic; combating HIV/AIDS with local cultural performance; and more. Source material, such as song lyrics and interviews, weaves throughout the collection, which is a nuanced and profoundly affective portrayal of the intricate relationship between HIV/AIDS and the arts in Africa.

The politics and science of health and disease remain contested terrain among scientists, health practitioners, policy makers, industry, communities, and the public. Stakeholders in disputes about illnesses or conditions disagree over their fundamental causes as well as how they should be treated and prevented. This thought-provoking book crosses disciplinary boundaries by engaging with both public health policy and social science, asserting that science, activism, and policy are not separate issues and showing how the contribution of environmental factors in disease is often overlooked.

Recent studies have reported the pathological effect of ICOS + T cells, but ICOS signals also widely participate in anti-inflammatory responses, particularly ICOS + regulatory T (Treg) cells. The ICOS signaling pathway endows Tregs with increased generation, proliferation, and survival abilities. Furthermore, there is enough evidence to suggest a superior capacity of ICOS + Tregs, which is partly attributable to IL-10 induced by ICOS, yet the associated mechanism needs further investigation. In this review, we discuss the complicated role of ICOS + Tregs in several classical autoimmune diseases, allergic diseases, and cancers and investigate the related therapeutic applications in these diseases. Moreover, we identify ICOS as a potential biomarker for disease treatment and prognostic prediction. In addition, we believe that anti-ICOS/ICOSL monoclonal antibodies exhibit excellent clinical application potential. A thorough understanding of the effect of ICOS + Tregs and the holistic role of ICOS toward the immune system will help to improve the therapeutic schedule of diseases.

Protein S-palmitoylation is a covalent and reversible lipid modification that specifically targets cysteine residues within many eukaryotic proteins. In mammalian cells, the ubiquitous palmitoyltransferases (PATs) and serine hydrolases, including acyl protein thioesterases (APTs), catalyze the addition and removal of palmitate, respectively. The attachment of palmitoyl groups alters the membrane affinity of the substrate protein changing its subcellular localization, stability, and protein-protein interactions. Forty years of research has led to the understanding of the role of protein palmitoylation in significantly regulating protein function in a variety of biological processes. Recent global profiling of immune cells has identified a large body of S-palmitoylated immunity-associated proteins. Localization of many immune molecules to the cellular membrane is required for the proper activation of innate and adaptive immune signaling. Emerging evidence has unveiled the crucial roles that palmitoylation plays to immune function, especially in partitioning immune signaling proteins to the membrane as well as to lipid rafts. More importantly, aberrant PAT activity and fluctuations in palmitoylation levels are strongly correlated with human immunologic diseases, such as sensory incompetence or over-response to pathogens. Therefore, targeting palmitoylation is a novel therapeutic approach for treating human immunologic diseases. In this review, we discuss the role that palmitoylation plays in both immunity and immunologic diseases as well as the significant potential of targeting palmitoylation in disease treatment.

Dendritic cells (DC) are antigen-presenting cells that can communicate with T cells both directly and indirectly, regulating our adaptive immune responses against environmental and self-antigens. Under some microenvironmental conditions DC develop into anti-inflammatory cells which can induce immunologic tolerance. A substantial body of literature has confirmed that in such settings regulatory DC (DCreg) induce T cell tolerance by suppression of effector T cells as well as by induction of regulatory T cells (Treg). Many  in vitro  studies have been undertaken with human DCreg which, as a surrogate marker of antigen-specific tolerogenic potential, only poorly activate allogeneic T cell responses. Fewer studies have addressed the abilities of, or mechanisms by which these human DCreg suppress autologous effector T cell responses and induce infectious tolerance-promoting Treg responses. Moreover, the agents and properties that render DC as tolerogenic are many and varied, as are the cells’ relative regulatory activities and mechanisms of action. Herein we review the most current human and, where gaps exist, murine DCreg literature that addresses the cellular and molecular biology of these cells. We also address the clinical relevance of human DCreg, highlighting the outcomes of pre-clinical mouse and non-human primate studies and early phase clinical trials that have been undertaken, as well as the impact of innate immune receptors and symbiotic microbial signaling on the immunobiology of DCreg.

Dietary carbohydrate fibers are known to prevent immunological diseases common in Western countries such as allergy and asthma but the underlying mechanisms are largely unknown. Until now beneficial effects of dietary fibers are mainly attributed to fermentation products of the fibers such as anti-inflammatory short-chain fatty acids (SCFAs). Here, we found and present a new mechanism by which dietary fibers can be anti-inflammatory: a commonly consumed fiber, pectin, blocks innate immune receptors. We show that pectin binds and inhibits, toll-like receptor 2 (TLR2) and specifically inhibits the proinflammatory TLR2-TLR1 pathway while the tolerogenic TLR2-TLR6 pathway remains unaltered. This effect is most pronounced with pectins having a low degree of methyl esterification (DM). Low-DM pectin interacts with TLR2 through electrostatic forces between non-esterified galacturonic acids on the pectin and positive charges on the TLR2 ectodomain, as confirmed by testing pectin binding on mutated TLR2. The anti-inflammatory effect of low-DM pectins was first studied in human dendritic cells and mouse macrophages and was subsequently tested in TLR2-dependent ileitis in a mouse model. In these mice, ileitis was prevented by pectin administration. Protective effects were shown to be TLR2-TLR1 dependent and independent of the SCFAs produced by the gut microbiota. These data suggest that low-DM pectins as a source of dietary fiber can reduce inflammation through direct interaction with TLR2-TLR1 receptors.

As of July 2023, 209 monoclonal antibody drugs have been approved by the FDA for marketing use, which are widely distributed in the fight against immune diseases, infectious diseases, and neurological and metabolic diseases. In this book, we introduce current monoclonal drug development techniques, delivery and therapeutic application of neutralizing antibodies, development and application of anti-inflammatory factor monoclonal antibodies, research progress and prospect of monoclonal antibodies against human infectious diseases (including SARS-CoV-2, Enterovirus, Herpesvirus, Hepatitis Virus, and Orthopoxvirus), and the research and applications of nanobodies in human infectious diseases. Most of the content of this book is aimed at viral infectious diseases that are widespread and seriously endanger human health. For example, SARS-CoV-2 continues to circulate the world. Enteroviral infections continue to cause morbidity and mortality in susceptible individuals worldwide. Hepatitis viruses continue to constitute a significant global health threat that results in substantial morbidity and mortality; Herpesviruses lead to significant health challenges, notably through conditions like herpes, varicella, zoster, mononucleosis, and various cancers including Kaposi's sarcoma, nasopharyngeal carcinoma, and lymphoma. This book provides valuable insights for designing next-generation monoclonal antibodies.

This seventh edition of Medical Immunology, now in a full-color presentation, continues to provide a succinct clinical review of the human response to infection while being firmly grounded in science. The authors, distinguished and experienced educators, have been able to anticipate readers' conceptual challenges and use illustrations, diagrams, and algorithms throughout to simplify complex concepts. With an emphasis on clinical applications, methodological advances, immunological diseases, and innovative interventions, this tried and true guide navigates readers through state-of-the-sciences technologies and demonstrates their implementation in the day-to-day clinical practice of immunology.

Background Immune thrombocytopenia (ITP) is an immune-mediated disorder marked by impaired self-tolerance, leading to accelerated platelet destruction, reduced platelet production, and a range of bleeding manifestations. This study aimed to evaluate the role of TIM-3 in children with newly diagnosed ITP. Methods This cross-sectional study included 80 children, comprising two equal groups. Group I consisted of children with newly diagnosed primary ITP, from whom samples were collected at diagnosis before treatment and again at remission (platelet count ≥ 100 × 10⁹/L with resolution of bleeding symptoms after treatment). Group II included age, and sex matched healthy children serving as controls. Results TIM-3 levels were significantly and positively correlated with platelet counts at both diagnosis and remission ( P  < 0.05), while showing a significant negative correlation with bleeding scores ( P  ≤ 0.001). Hemoglobin levels increased markedly after remission compared with diagnosis. White blood cell counts at diagnosis differed highly significantly between patients and controls ( P  ≤ 0.001), and TIM-3 levels at diagnosis were significantly lower in the ITP group than in healthy controls. Conclusions This study assessed TIM-3 role in newly diagnosed children with ITP. According to the results, TIM-3 could affect the immune response and platelet destruction in individuals with ITP, suggesting a key function for this protein in the disease’s pathophysiology. Trial registration Not applicable.