Figure 3 Hypothetical mechanisms of smoking-associated

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CHAPTER 43 IMMUNE SYSTEM TOPICS. Use your book to answer the below questions.

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Table 3 Limb-girdle muscular dystrophy standardized data collection form and HPO mapping Thompson, R. & Straub, V. et al. (2016) Limb-girdle muscular dystrophies.

Nat. Rev. Neurol. doi:10/1038/nrneurol

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Autoimmune diseases Ch. 4 p (99 – 159) March 7 /2016 March

Figure 3 Life expectancy at birth in all countries included

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Figure 2 The US Centers for Disease Control and

Immunological Tolerance

Figure 3 Example of how a noncoding regulatory rheumatoid

Figure 4 Host damage from infection-related inflammatory

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Figure 2 Proinflammatory mechanisms in CKD

Figure 1 Factors underlying metabolic alterations in osteoarthritis

Figure 2 Risk factors for sarcopenia

Figure 4 Simplified T cell and antigen presenting

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Figure 2 Peptide vaccination using TAA-derived long peptides

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Figure 3 Proportion of patients for whom NEDA

Figure 5 Number of AHSCT procedures for

Figure 2 Shared genetic loci in systemic autoimmune diseases

Figure 1 Location of HLA variants known to be associated

Figure 1 CAR-T-cell design

Figure 2 Co-stimulatory receptors as immunomodulatory targets

Figure 2 Proposed model of therapeutic mechanisms of AHSCT

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Figure 1 Allele frequency and effect size for ALS-associated genes

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Figure 2 Type 3 immunity and AS

Figure 2 Precision medicine based on a network approach

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Figure 2 Interaction effects between heterozygous HLA‑DRB1

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Figure 6 Lack of IRF5 causes a reduction in neutrophil influx

Figure 3 Differentiation and functional control of T-cell subsets

Figure 1 Clinical correlates of neurodegeneration in MS

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Figure 3 Genetic pleiotropy in ALS

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Figure 4 Lifestyle and environmental factors affect

Figure 1 Evolution of multiple sclerosis

Figure 1 The trajectory of cognitive ageing

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Figure 2 Emerging hallmarks of T cells in rheumatoid arthritis

Figure 3 Stroke-related deaths and DALYs by country development status

Figure 2 Age-specific prevalence of common comorbidities

during the alloimmune response

Maternal allo-recognition of the fetus

Figure 6 Combining population-wide and high-risk strategies

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Figure 2 Logistical requirements for autologous

Figure 3 Potential interplay between physiological

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Figure 1 The VEGF family of growth factors

Figure 2 Cellular pathways implicated in CIPN

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Figure 2 Pathophysiological mechanisms in LGMD

Figure 1 Timing of the effects of deep brain stimulation

Figure 1 A large number of genes are potentially associated with CIPN

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Schematic illustration of the concepts in the pathogenesis of rheumatoid arthritis associated-interstitial lung disease (RA-ILD). Schematic illustration.

Figure 2 Correlation between wGRS and age at onset The figure shows the correlation between weighted genetic risk score (wGRS) and age at onset in all.

Figure 1 The role of macrophages in RA

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Figure 3 Hypothetical mechanisms of smoking-associated processes that contribute to risk of multiple sclerosis Figure 3 | Hypothetical mechanisms of smoking-associated processes that contribute to risk of multiple sclerosis. Smoking promotes activation of proinflammatory pathways, and alters post-translational modification of peptides. Both events can lead to activation of resident CD4+ CNS-antigen-specific autoimmune T cells through recognition peptides presented by HLA-DRB1*15:01 molecules, a hypothesis supported by the fact that smoking increases the risk of rheumatoid arthritis in conjunction with HLA-DRB1*04. The less well understood protective role of class I HLA-A*02 might involve CD8+ cells. Olsson, T. et al. (2016) Interactions between genetic, lifestyle and environmental risk factors for multiple sclerosis Nat. Rev. Neurol. doi:10.1038/nrneurol.2016.187