BIOH 370 1st EditionLecture 18 Outline of Last Lecture Lymphatics and Immunity Day 4I. T Cells Development and MaturationII. ThymusIII. Thymic SelectionIV. Antigen Presenting Cellsa. Professional APCsb. Non-professional APCsV. MHC Synthesis and Antigen Loading in APCsVI. Functions of Secondary Lymphoid OrgansVII. TonsilsOutline of Current Lecture Lymphatics and Immunity Day 5I. Structure of the Lymph NodeII. Spleena. Functionsb. Structurec. SplenomegalyIII. Mucosa Associated Lymphoid TissueThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.IV. Functions of Participating in Adaptive Immune ResponsesV. Ways to Acquire Adaptive ImmunityVI. Immune System’s Role in Organ TransplantsVII. ImmunodeficiencysVIII. Mechanism of Autoimmune Diseases- Multiple SclerosisIX. Hypersensitivities- Immediate Hypersensitivity- Reactionsa. Type I Hypersensitivityb. Type II Hypersensitivityc. Type III Hypersensitivityd. Type IV (delayed-type) Hypersensitivitye. Anaphylactic ShockCurrent LectureLymphatics and Immunity Day 5I. Structure of the Lymph NodeII. Spleen- Largest lymphoid organ- Served by splenic artery and vein, which enter and exit at the hilus- Red Pulp: blood filled venous sinuses and splenic cords (RBCs, macrophages, lymphocytes, plasma cells, and granulocytes)- White Pulp: lymphatic tissue(lymphocytes, macrophages arranged around central arteries)b. Functions:- Site of lymphocyte proliferation and immune surveillance and response- Cleanses the blood of aged cells and platelets and debrisc. Structure:- Two distinct areaso White pulp around central arterieso Mostly lymphocytes on reticular fibers and involved in immune functionso Red pulp in venous sinuses and splenic cords-Rich in macrophages for disposal of worn-out RBCs and bloodborne pathogens- Stores breakdown products of RBCs (e.g., iron) for later reuse - Stores blood platelets- Site of fetal erythrocyte production (normally ceases after birth)- Has a fibrous capsule and trabeculae- Contains lymphocytes, macrophages, and huge numbers of erythrocytesd. Splenomegaly: - Enlarged Spleen- Cells get stuck and backed up spleenbecause RBCs in sickled form- Can be comorbid with lymphomaIII. Mucosa Associated Lymphoid Tissue- Peyer’s patcheso Clusters of lymphoid follicleso In the wall of the distal portion of the small intestineo Similar structures are also found in the appendix- Peyer’s patches and the appendixo Destroy bacteria, preventing them from breaching the intestinal wallo Generate “memory” lymphocytes - MALTs: Mucosa Associated Lymphoid Tissueo GALT- gastroo RALT- respiratoryo VALT- valva vaginalIV. Functions of Participating in Adaptive Immune ResponsesV. Ways to Acquire Adaptive ImmunityVI. Immune System’s Role in Organ Transplants- Four varietieso Autografts: from one body site to another in the same persono Isografts: between identical twinso Allografts: between individuals who are not identical twinso Xenografts: from another animal species- Depends on the similarity of the tissues- Patient is treated with immunosuppressive therapyo Corticosteroid drugs to suppress inflammationo Antiproliferative drugso Immunosuppressant drugs- Many of these have severe side effectsVII. Immunodeficiencys:- Congenital and acquired conditions that cause immune cells, phagocytes, or complement to behave abnormally- Genetic defect- Marked deficit in B and T cells- Abnormalities in interleukin receptors- Defective adenosine deaminase (ADA) enzyme o Metabolites lethal to T cells accumulate- SCID is fatal if untreated; treatment is with bone marrow transplantsVIII. Mechanism of Autoimmune Diseasesa. Foreign antigens may resemble self-antigens- Antibodies against the foreign antigen may cross-react with self-antigenb. New self-antigens may appear, generated by- Gene mutations - Changes in self-antigens by hapten attachment or as a result of infectious damagec. Release of novel self-antigens by trauma of a barrier (e.g., the blood-brain barrier)- Multiple SclerosisIX. Hypersensitivities- Immune responses to a perceived (otherwise harmless) threat - Causes tissue damage- Different types are distinguished byo Their time courseo Whether antibodies or T cells are involved- Antibodies cause immediate and subacute hypersensitivities- T cells cause delayed hypersensitivity - Immediate Hypersensitivityo The mechanism involves IL-4 secreted by TH2 cellso IL-4 stimulates B cells to produce IgEo IgE binds to mast cells and basophils, resulting in a flood of histamine release and inducing the inflammatory responsea. Type I Hypersensitivity: IgE–mediated release of histamine and other mediators from mast cells and basophilso skin (urticaria and eczema)o eyes (conjunctivitis)o nasopharynx (rhinorrhea, rhinitis),o bronchopulmonary tissues (asthma)o gastrointestinal tract (gastroenteritis)o 15 - 30 minutes from the time of exposure to the antigen, although sometimes it may have a delayed onset (10 - 12 hours)o Treatment with anti-histaminesb. Type II Hypersensitivity(cytotoxic): IgG or IgM antibodies bound to cell surface antigens, with subsequent complement fixation.o Usually to endogenous antigenso Sometimes to exogenous antigens o Drug induced hemolytic anemia (mismatched blood transfusions)o Reaction time, minutes to hourso Treated with anti-inflammatoriesc. Type III Hypersensitivity: (ie, immune-complex reactions) circulating antigen-antibody immune complexes that deposit in postcapillary venules, with subsequent complement fixation.o Immune Complex Hypersensitivityo May affect a variety of organs and tissueso i.e. serum sicknesso Guillain-Barre Syndrome– motor weakness, areflexia, CSF albuminocytological dissociation, and diminished deep tendon reflexeso Treatment: anti-inflammatoriesd. Type IV (delayed-type) Hypersensitivity: (ie, delayed hypersensitivity reactions, cell-mediated immunity) are mediated by T cellso Mediated by T cellso involved in the pathogenesis of many autoimmune and infectious diseaseso tuberculin (Montoux) reactiono Treatment: anti-inflammatoriese. Anaphylactic Shock:o Systemic response to allergen that directly enters the bloodo Basophils and mast cells are enlisted throughout the bodyo Systemic histamine releases may causeConstriction of bronchioles Sudden vasodilation and fluid loss from the bloodstreamHypotensive shock and deatho Treatment: