Immunity (Lecture Notes) PDF

Immunity Lecturer: Beth Flott, Ed.D, RN  Immunity Definition - The normal physiological response to microorganisms and proteins as well as conditions associated with an inadequate or excessive immune response Antecedents Defining Characteristics Positive Consequences Risk Facto...

Immunity Lecturer: Beth Flott, Ed.D, RN  Immunity Definition - The normal physiological response to microorganisms and proteins as well as conditions associated with an inadequate or excessive immune response Antecedents Defining Characteristics Positive Consequences Risk Factors Negative Consequences Interrelated Concepts Exemplars Immunity Three primary functions: Protects the body from invasion of microorganisms and other antigens Removes dead or damaged tissue and cells Recognizes and removes cell mutations that have demonstrated abnormal cell growth and development  Immunity ▪ Innate Immunity – first & second lines of defense ▪ Skin, reflexes including coughing, barriers such as cilia in lungs, normal flora ▪ Inflammation response – activated rapidly, non- specific, chemical mediators attract many types of cells and activate plasma protein systems to get rid of pathogens Acquired Immunity – third line of defense Passive Immunity Artificial - Introduction of antibodies through transfusions Natural – acquiring antibodies from mother to baby Active Immunity ▪ Artificial – response to an immunization Natural – actually acquiring the disease/pathogen  Immunity Acquired Immunity Develops slowly, specific to pathogens, has a memory Major histocompatibility complexes (MHC) – proteins that help differentiate host cells from foreign proteins. MHC presents antigens to immune cells. Cells Involved B lymphocytes – produce antibodies T lymphocytes – directly kill microorganisms NK cells – directly kill microorganisms Dendritic cells – look for foreign antigens  Immunity B lymphocytes – Two types First type – Plasma B Cells: Secrete antibodies/immunoglobulins Second type – Memory B Cells Interacts with helper T lymphocytes Mainly involved with humoral immunity Immunoglobulins - responsible for the body’s response to invading bacteria and viruses and provide the humoral component of immune response. Antibodies produced include: IgG IgM IgD IgE IgA Immunity Antibody Functions Direct Neutralization – Inactivating or blocking the binding of antigens to receptors Agglutination – Clumping of insoluble particles that are in suspension Precipitation – Making a soluble antigen into an insoluble precipitate Indirect Activate components of innate resistance (including complement and phagocytes)  Immunity Primary response Dominated by IgM Secondary response Dominated by IgG Facilitated by Memory Cells IgE Defends against parasitic infections (allergies) IgA Secretions of the mucous membranes  Immunity T Lymphocytes – Mainly involved in cellular immunity (four major types) Helper T cells (CD4) – regulate most of system’s function via protein mediators and lymphokines Cytotoxic T cells – directly kill foreign antigens, may kill cells of the host Suppressor T cells – suppress function of helper and cytotoxic T cells to prevent hyperimmune response Memory T cells – remember subsequent exposure to same antigen  Immunity Antigen – foreign material Molecules bind to receptors in body First exposure – slower to initiate Second exposure - immune response destroys “remembers” antigen in future; can attack quicker Immunity Primary immune response Latent period – before detection; involves antigen processing Activation – 7-14 days; T helper cells stimulate cytokines which directs immune response Antibodies rise for several weeks; individuals often recover during this time Secondary immune response Memory immune response Subsequent exposure – memory cells release antibodies faster due to recognition of antigen Booster vaccinations  Immunity Exaggerated Immune Response  Immunity – Exaggerated Immune Response Hypersensitivity Reactions Type I reactions are IgE- mediated disorders. Type II reactions are antibody- mediated disorders. Type III reactions are complement-mediated immune disorders. Type IV reactions are T-cell– mediated disorders.  Immunity – Exaggerated Response Type I Hypersensitivity Reactions Allergic reactions Antigen = allergen Can result in anaphylaxis Three types of cells involved – mast cells, basophils, and T-helper cells (CD4) Immunity – Exaggerated Response Type I Hypersensitivity Reaction ▪ Initial/Primary Phase – vasodilation, vascular leakage, smooth muscle contraction; lasts 5-60 minutes; mast cell degranulation with histamine release ▪ Late Phase – more infiltration of tissue with eosinophils; 8 hours-several days; leukotrienes and prostaglandins produce same delayed and prolonged response as histamine Anaphylaxis – systemic, life-threatening type I reaction; antigen is introduced via injection, insect sting, or absorption through skin or GI mucosa. Widespread edema, vascular shock, bronchospasm and respiratory distress  Immunity – Exaggerated Response Type II Hypersensitivity Reactions – Antibody-mediated reactions Complement and antibody receptor–mediated phagocytosis – transfusion reaction Complement and antibody receptor–mediated inflammation – vascular rejection in organ transplants Antibody-mediated cellular dysfunction – Grave’s disease  Immunity – Exaggerated Immune Response Type II Hypersensitivity Reaction - Transfusion Reaction A reaction that occurs with ABO incompatibility The transfused erythrocytes are destroyed by agglutination or complement-mediated lysis ABO Blood Type Consists of two major carbohydrate antigens (A and B) that are expressed on virtually all cells The erythrocytes of persons with type A blood have the type A carbohydrate antigen; those with B blood carry B antigen; those with AB blood carry both A and B antigens; those with type O carry neither Type O individuals are considered to be the universal donor Type AB are considered to be the universal recipients https://www.redcrossblood.org/donate-blood/blood- types.html  Immunity – Exaggerated Immune Response Type III Hypersensitivity Response Immune complex reaction Leads to damage when comes in contact with vessel lining or deposited in tissues Leads to vasculitis in certain autoimmune diseases such as lupus Immunity – Exaggerated Immune Response Type IV Hypersensitivity Reaction – Cell-Mediated Immune Responses Direct – killing of a target cell by an NK or cytotoxic T cell; can end up killing infected target cells even if virus has no bad effects; kills virtually all infected cells (hepatitis) Delayed – takes 24-72 hours to develop, cell-mediated and includes T cells and macrophages (reaction to PPD test; poison ivy) Immunity Autoimmune Response Immunity – Autoimmune Response Self-tolerance – the ability to differentiate self from foreign antigens A loss of self-tolerance can lead to autoimmune conditions Risk factors – genetics and environmental factors such as infectious agents  Immunity – Autoimmune Response Rheumatoid Arthritis Risk factors – women, genetic predisposition, typical onset age 40-60 Infectious agent (especially Epstein-Barr virus) may initiate autoimmune process Immune complexes formed – inflammatory response occurs in synovial and musculoskeletal tissues Membranes form new tissue that produces enzymes and encourages additional tissue damage Periods of exacerbation and remission Manifestations – swelling, stiffness, pain in joints, fatigue, anorexia, weakness Immunity – Autoimmune Response Systemic Lupus Erythematosus Characterized by the production of a large variety of antibodies and immune complexes against self- antigens – multiple organs affected Most characteristic are against nucleic acids, histones, ribonucleoproteins and other nuclear materials Some symptoms are a result of a type III hypersensitivity reaction Risk factors – women, genetic predisposition Clinical Manifestations – butterfly rash, fatigue, photosensitivity arthritis, affects most tissues/organs  Immunity – Autoimmune Response Multiple Sclerosis Chronic inflammatory disease involving the degeneration of CNS myelin and loss of axons More common in women between 20 and 40 Autoreactive T and B cells cross the blood-brain barrier and recognize myelin and oligodendrocyte autoantigens Loss of myelin disrupts nerve conduction with subsequent death of neurons and brain atrophy White matter can be microscopically abnormal and gray matter lesions and atrophy have been documented Manifestations - Paresthesias; weakness; impaired gait; visual disturbances; and/or urinary incontinence Immunity – Autoimmune Response Multiple Sclerosis Types Relapsing-remitting Secondary progressive Primary progressive  Immunity – Autoimmune Response Psoriasis/Psoriatic Arthritis Most common type – plaque psoriasis Skin becomes scaly and inflamed as cells of outer layer of skin reproduce faster than normal Dermis and epidermis thickening d/t hyperproliferation of keratinocytes New dermal vessels form; neutrophils and lymphocytes migrate to area causing inflammation Up to 42% also develop psoriatic arthritis – autoimmune response also affects joints leading to stiffness, pain, and joint damage  Immunity Suppressed Immune Response  Immunity – Suppressed Immune Response Primary Entire immune system is inadequate and missing some components necessary for adequate immune response Secondary – person previously had intact immune response Induced – medications; avoid transplant rejection Illness  Immunity – Suppressed Immune Response HIV/AIDS HIV – retrovirus that infects cells in immune system and leads to defects in cellular and humoral immunity HIV 1 – leads to AIDS, most cases HIV 2 – less pathogenic Ranges from asymptomatic to life-threatening condition: disease progression is highly variable Current anti-retroviral therapy has increased length of life  Immunity – Suppressed Immune Response HIV/AIDS Transmitted through exchange of body fluids Infects cells that express CD4 receptor on surface (MHC) – receptor necessary for T cells to recognize antigens; effects CD4 T helper cells Virus rapidly disseminates before body can elicit an immune response After few weeks, host develops response and partial restoration of T lymphocytes Virus can elude immune clearance resulting in persistent infection Immunity – Suppressed Immune Function HIV/AIDS HIV Primary Infection – 2-4 weeks after infection; fever, fatigue, headache, rash Chronic HIV Infection – often shows no manifestations for up to several years; HIV continues to rapidly replicate; intense reduction of circulating T lymphocytes Symptomatic Disease – condition more severe, night sweats, diarrhea AIDS – characterized by severe immunodeficiency, opportunistic infections/malignancies (tuberculosis, Kaposi’s sarcoma, cytomegalovirus), and/or CD4 count falls below 200 Diagnostics – All Immune Exemplars CRP ESR Allergy testing Antibody testing Immunologic Assay Testing ELISA and Western Blot - HIV Treatments Immunosuppresive medications Biologic agents Phototherapy - psoriasis Questions??