Basic Immunology Functions And Disorders Of The Immune System 6th Edition
Niobe Hennigan
This updated 3rd edition of Basic Immunology provides a readable and concise introduction to the workings of the human immune system, with emphasis on clinical relevance. The format makes learning easy with short, easy-to-read chapters, color tables, key point summaries, and review questions in every chapter. You'll get the latest coverage on regulatory T cells, biology of the Th17 subset of CD4+ T cells, and more. The full-color artwork, comprehensive glossary, and clinical cases are just some of the features that reinforce and test your understanding of how the immune system functions. Student Consult online access lets you search the full text online and pursue further study through integration links.
The Lowance Center for Human Immunology, led by Emory Division of Rheumatology Director Ignacio Sanz, MD, cuts across traditional academic divisions in medicine and translates new knowledge in basic immunology to human immune-mediated diseases.
The overall goal of the Lowance Center for Human Immunology is to understand the immunological and molecular mechanisms responsible for human autoimmune, inflammatory and allergic diseases. The Lowance Center studies both the innate and adaptive arms of the immune response and the mutual regulation of the two components.
In the larger picture, the knowledge of immune function derived from the studies pursued at the Lowance Center also provide important insight into multiple other human conditions including transplantation, cancer and the immune response to infections and vaccination. This goal is pursued through the integrated effort of basic, clinical and translational scientists applying state-of-the-art technology and computational biology as well as advanced epidemiology and outcomes research tools.
In addition to providing fundamental insight into disease pathogenesis and treatment, we aim to identify specific immunological defects that can be used to develop biomarkers of disease heterogeneity in order to better segment diseases into discreet subsets. In turn, disease segmentation is used to select treatments targeted to the defective molecular pathways specifically responsible for different disease subsets. This approach should result in more effective and safer treatments for the individual patient (Precision Medicine). The knowledge derived from our studies will also provide better biomarkers of disease progression and response to treatment. Ultimately, we seek to use this knowledge to reverse well-established disease and to prevent disease development in high-risk subjects.
The Lowance Center contributes to improving immunological knowledge and advancing the treatment of human immunological diseases through the coordinated effort of dedicated scientists and physicians working together with clinical coordinators and nurses.
Eliver Ghosn, PhD
The Ghosn Lab combines high-dimensional flow cytometry and multi-OMICs single-cell sequencing technologies as a Systems Immunology approach to study the development and function of tissue-resident immune cells, including tissue-resident macrophages and B lymphocytes that develop early during embryogenesis (fetal life) and persist in tissues throughout adulthood. We use in vivo mouse models of lineage-tracing and fate-mapping, humanized mice, and patient/clinical samples to study the differences between tissue-resident versus circulating immune cells. We expect our studies, from both basic and translational research, to provide new insights into the development and function of the human immune system in infants and adults and shed light on the mechanisms that lead to organ-specific inflammatory disorders (including autoimmunity, infectious diseases, cancers, and immunodeficiencies) that predominant at different developmental ages, and inform the development of new vaccines that are targeted to either children or adults.
Scott A. Jenks, PhD
Jenks has a longing standing interest in the complexity of the immune system. His recent work has focused on understanding alternative pathways of class switched B cell activation that are dramatically expanded and contribute to disease in autoimmune patients. He is also interested in using Vh4.34 antibodies as a model to study the maintenance of serological tolerance and how this breaks down in lupus patients.
Sung Lim, MD
Lim's main interest is outcomes and epidemiology of systemic lupus erythematosus. He is the PI of several grants. He currently has six federally funded grants (CDC, NIH), six pharmaceutical company sponsored clinical trials, one foundation sponsored clinical trial, two foundation grants, one PCORI subaward, and one academic subaward. Lim heads the Lupus Clinic, which was established to treat patients with systemic lupus erythematosus and cutaneous lupus - chronic autoimmune disorders that disproportionately affects African Americans and younger women. As a cutting edge leader, the clinic at Grady uses a multidisciplinary approach of medical care, education, and support groups, along with integrated research projects. Since its opening in 2002, the lupus clinic has been a resource for many epidemiologic, outcomes, quality, and translational studies with national and international visibility. As a result, the Grady Lupus Clinic has led to multiple grants from federal agencies (CDC, NIH), private organizations, foundations, and pharmaceutical companies.
Dmitry Shayakhmetov, PhD
Shayakhmetov's research has been focused on understanding the molecular mechanisms of initiation and maintenance of pathologic inflammation, pathogen-host interactions, and innate immune and inflammatory responses to microbial and viral pathogens.
In this updated edition of Basic Immunology, the authors continue to deliver a clear, modern introduction to immunology, making this the obvious choice for today's busy students. Their experience as teachers, course directors, and lecturers helps them to distill the core information required to understand this complex field. Through the use of high-quality illustrations, relevant clinical cases, and concise, focused text, it's a perfectly accessible introduction to the workings of the human immune system, with an emphasis on clinical relevance.
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Autism is a neurodevelopmental disorder characterized by deficits in communication and social skills as well as repetitive and stereotypical behaviors. While much effort has focused on the identification of genes associated with autism, research emerging within the past two decades suggests that immune dysfunction is a viable risk factor contributing to the neurodevelopmental deficits observed in autism spectrum disorders (ASD). Further, it is the heterogeneity within this disorder that has brought to light much of the current thinking regarding the subphenotypes within ASD and how the immune system is associated with these distinctions. This review will focus on the two main axes of immune involvement in ASD, namely dysfunction in the prenatal and postnatal periods. During gestation, prenatal insults including maternal infection and subsequent immunological activation may increase the risk of autism in the child. Similarly, the presence of maternally derived anti-brain autoantibodies found in 20% of mothers whose children are at risk for developing autism has defined an additional subphenotype of ASD. The postnatal environment, on the other hand, is characterized by related but distinct profiles of immune dysregulation, inflammation, and endogenous autoantibodies that all persist within the affected individual. Further definition of the role of immune dysregulation in ASD thus necessitates a deeper understanding of the interaction between both maternal and child immune systems, and the role they have in diagnosis and treatment.
Nearly 50 years ago, an association of autism with congenital rubella infection was noted, and in the intervening years numerous other infections have been connected to the incidence of ASD. Since that time, mounting evidence for the ability of the immune system and abnormal immune function, including inflammation, cytokine dysregulation, and anti-brain autoantibodies, to act as a significant influence on ASD has prompted researchers to look more closely at the potential role of immune dysregulation and autoimmunity in ASD. This field of research has gained particular traction given that other neurodevelopmental disorders, such as schizophrenia, also present alongside a spectrum of changes in immune function. Here, we review the potential of the immune system to serve as a collective, complex etiology for autism and ASD in at least a subset of cases. A graphic overview of the various neuronal and immune system components involved in the topics under discussion are depicted in Figure 1, indicating the many cells and molecules that may lead from an altered immune system to altered neurodevelopment. We divided this work into two sections, separated into prenatal and postnatal exposures. It begins in the gestational period with an examination of maternal infection, immune activation, and autoantibodies present during pregnancy, followed by the ongoing, postnatal role of dysregulation in the immune system in a child with ASD. We hope that through this comprehensive review, we will provide evidence supporting the notion that immune dysregulation in autism is a viable pathway towards the identification and subsequent treatment of this ASD subpopulation in the future.
Overview of the immune system as a mediator of behavior. Understanding how immune dysfunction in ASD can lead to changes in behavior requires understanding a complex network of interactions between several cell types from both the innate and adaptive arms of the immune system. Several immune factors mediate effects of CNS function. T-cell and NK-cell subpopulations may have altered activity and an impaired reaction to stimulation. Some cytokines can inhibit neurogenesis and promote neuron death, while others can promote the growth and proliferation of neurons and oligodendrocytes. Complement proteins and microglia can participate in synaptic scaling and pruning, while brain-reactive autoantibodies can change the development or function of neurons. When the many components of the immune system are dysregulated, these networks can lead to changes in neurodevelopment and behavior.
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