Front Cover; Advances in Immunology; Copyright; Contents; Contributors; Chapter 1: NOD. H-2h4 Mice: An Important and Underutilized Animal Model of Autoimmune Thyroiditis and Sjogrenś Syndrome; 1. Introduction; 2. Spontaneous Autoimmune Thyroiditis; 2.1. SAT in WT NOD. H-2h4 mice/importance of iodine; 2.2. B cells and autoantibodies in SAT; 2.3. T cells as effector cells in SAT; 2.4. Regulatory T cells in SAT; 2.5. IFN-< U+00de> is required for development of SAT; 2.6. CD40 and CD40/CD154 interactions in SAT; 3. TEC Hyperplasia/Proliferation; 3.1. TEC H/P develops only if IFN-< U+00de> is absent. 3.2. TEC H/P histology, incidence, and kinetics of development3.3. Mice with severe TEC H/P have reduced thyroid function and thyroid fibrosis; 3.4. TEC H/P is a T cell-dependent autoimmune disease; 3.4.1. CD4+ versus CD8+ T cells; 3.4.2. B cells in TEC H/P; 3.5. TGF-< U+00dd> and TNF-< U+00dc> are effector cytokines for TEC H/P; 3.6. Use of the adoptive transfer model to examine kinetics of TEC H/P development and assess therapeutic protocols; 3.7. Agonistic anti-CD40 induces proliferation of thyrocytes in IFN-< U+00de> -/- NOD. H-2h4 mice promotes development of severe TE ... 3.8. Some IFN-< U+00de> -/- NOD. H-2h4 mutants develop early and severe TEC H/P3.8.1. CD28-/- mice; 3.8.2. PD-1-/-IFN-< U+00de> -/- NOD. H-2h4 mice; 4. NOD. H-2h4 Mice Can Be Used as a Model of Experimentally Induced Autoimmune Thyroiditis; 5. SS in NOD. H-2h4 Mice and NOD. H-2h4 Mutants; 6. Concluding Remarks; Acknowledgments; References; Chapter 2: Approaches for Analyzing the Roles of Mast Cells and Their Proteases In Vivo; 1. Mast Cell Biology; 1.1. Origin and tissue distribution of mast cells; 1.2. The spectrum of mast cell-derived mediators; 1.3. Phenotypic heterogeneity and functional plasticity. 1.4. Mast cell-associated proteases and their cellular distribution2. Nongenetic Approaches for Analyzing the Functions of Mast Cells and Mast Cell-Associated Proteases In Vivo; 2.1. Pharmacological approaches; 2.1.1. Mast cell stabilizers; 2.1.2. Mast cell activators; 2.1.3. Purified or recombinant mast cell proteases; 2.1.4. Tryptase and chymase inhibitors; 2.1.5. Tyrosine kinase inhibitors; 2.2. Antibody-based approaches; 3. Genetic Approaches for Analyzing the Functions of Mast Cells In Vivo; 3.1. Mice with mutations affecting c-kit structure or expression and M̀̀C knockin micé́. 3.2. MC-deficient mice with normal c-kit3.2.1. Mcpt5-Cre; R-DTA mice; 3.2.2. Cpa3Cre/+-C̀̀re-Master ́́mice; 3.2.3. Cpa3-Cre; Mcl-1fl/fl-H̀̀ello Kitty ́́mice; 3.3. Inducible models of mast cell deficiency; 3.3.1. Mcpt5-Cre; iDTR mice; 3.3.2. M̀̀as-TRECK ́́mice; 3.3.3. Cpa3-Cre; iDTR mice; 3.3.4. KitCreERT2 and KitCreERT2/+R26-GFPStopFDTA mice; 3.4. Specific deletion of mast cell-associated products by Cre-lox approaches; 4. Genetic Approaches for Analyzing the Functions of Mast Cell-Associated Proteases In Vivo.
Advances in Immunology, a long-established and highly respected publication, presents current developments as well as comprehensive reviews in immunology. Articles address the wide range of topics that comprise immunology, including molecular and cellular activation mechanisms, phylogeny and molecular evolution, and clinical modalities. Edited and authored by the foremost scientists in the field, each volume provides up-to-date information and directions for the future. Key features: * Contributions from leading authorities * Informs and updates on all the latest developments.