Adaptive/Acquired Immunity PDF

Adaptive / Acquired Immunity NUR 219 Professor Mark A. Ailor MSN, RN, CNE Adaptive/Acquired Immunity Mobilized after external barriers have been compromised and inflammation activated Promotes processes against reinfection Differences from infl...

Adaptive / Acquired Immunity NUR 219 Professor Mark A. Ailor MSN, RN, CNE Adaptive/Acquired Immunity Mobilized after external barriers have been compromised and inflammation activated Promotes processes against reinfection Differences from inflammation Inducible Specific Long-lived Has memory Adaptive Immunity - TERMS Elements Antigens Molecules on surface of microbes, infected cells, or abnormal tissues Molecular targets of antibodies Antibodies a blood protein produced in response to and counteracting a specific antigen. Lymphocytes T cells—thymus derived B cells—bone marrow derived The adaptive immune system is comprised of two interrelated immune pathways – humoral and cell- mediated immunity Mark A. Ailor MSN,BA,RN Adaptive Immunity - TERMS Humoral immunity pathway by which antibodies are produced by B lymphocytes to target exogenous antigens Antibodies circulating in blood Bind to antigens on bacteria and viruses Cellular immunity pathway that does not result in antibody production but instead targets antigens T cells in blood and tissues Defend against intracellular pathogens and abnormal cells Humoral Immunity Primary B-Lymphocytes (B-cells) Slow to act Must be exposed to pathogens to develop immunity Exposure via environment or premeditated (vaccine) Has memory Key difference between acquired immunity and natural immunity Systemic instead of localized. B-Lymphocytes Made in bone marrow Matured in bone marrow Develops “immunocompetence” Ability to recognize and bind to pathogens/antibodies but ignore body’s cells Displays approx. 10,000 proteins (antibodies) on it’s surface Called membrane-bound antibodies Each B-cell has unique membrane-bound antibodies Overwhelm antigens by shear number and variety. More unique antibodies, more likely a “match” to and antigen for recognition B-Lymphocytes Once “mature” they reside in the lymph nodes, lymph and blood “humors” = Fluids Not truly activated until they are exposed to their “perfect match” antigen. Humoral Immunity – Binding and Activation Binds to “matching” antigen and “activates” (SEE SLIDE 26) Clones itself producing new cells with same specific antibody for that specific antigen. Most are “Effector” cells (Plasma cells). These are the active fighters Mass produce antibodies and “spew” them out into the fluids Few are long-lived Memory B-cells. Memory B-cells remember genetic code for that antibody Stronger, faster response for next exposure Humoral Immunity – Effects on antigens Antibodies in the fluids bind to antigens “mark them” for destruction Antibodies do not destroy invaders themselves Neutralization- Block all binding sites on the antigens so they cannot bind to body cells and reproduce Agglutination- Antibodies have multiple binding sites. Can attach to multiple antigens at once causing them to “clump” together Easier for macrophages to destroy Also send out chemical messengers to attract phagocytes and lymphocites to destroy the marked antigens. Agglutination Humoral Immunity – Limitations Some pathogens mutate frequently making memory cells ineffective. Example: Influenza, covid Others do not mutate frequently and therefore memory cells more affective. Example: Mumps, polio Humoral Immunity – Passive Immunity Fetus receives pre-formed antibodies from mother across the placenta. Later receives antibodies via breast milk. Short-lived as there are no memory cells involved. Humoral Immunity – Exogenous antibodies A person is exposed to a pathogen and develops antibodies. That person’s blood plasma containing antibodies can be given to another person aiding in their immune response. Examples: Ebola, COVID-19 Antibodies (1 of 2) Immunoglobulins (antibodies) Classes: IgG IgA IgM IgE IgD Characterized by differences in structure and function Immunoglobulin G (IgG) Most abundant class (80%-85%) Accounts for most of the protective activity against infections Transported across the placenta to protect newborn child Immunoglobulin A (IgA) IgA molecules are found predominantly in the blood IgA-2 (secretory IgA) molecules are found predominantly in bodily secretions (most important) Dimer anchored by a J chain and a “secretory” piece Secretory piece may function to protect IgAs against enzyme degradation Immunoglobulin M (IgM) Largest of the immunoglobulins Pentamer stabilized by a J chain First antibody produced during the primary response to an antigen Synthesized early in neonatal life Immunoglobulin D (IgD) Low concentration in the blood Function as one type of B cell antigen receptor Immunoglobulin E (IgE) (1 of 2) Low concentration in the blood Defense against parasitic infections Initiates an inflammatory reaction to attract eosinophils When produced against innocuous environmental antigens, they are a common cause of allergies Fc portions of IgEs are bound to mast cells Class Switch Change in antibody production from one class to another B cells start off producing IgM and IgD During clonal selection, B cell can switch to secrete IgG, IgA, or IgA Population of plasma cells capable of producing many antibody classes is created Cellular immunity / Cell-mediated immunity Last effort by the body to defend the body from invaders Natural immunity and Humoral immunity have failed to stop invader Cells are breached by invading antigens/pathogens  Cellular Immunity – Antigen Presenting Cells (APCs) Phagocytes/Macrophages engulf and break up invading antigens Present or display the pieces on their exterior surface attached to Major Histocompatibility Complexes All cells have a different type of MHC that tells the bodies immune system to “leave them alone”. Cellular Immunity - Tcells Made in the bone marrow but matured in the Thymus gland Tcells can only recognize antigens in the “broken up” form on the MHC There are many types of Tcells: Helper (Th), Cytotoxic (Tc), Memory (Tm), Regulatory (TR), and Natural Killer We will focus on the Helpers, cytotoxic and memory Cellular Immunity – Helper Tcells Cannot directly destroy antigens Can bind to only 1 specific combination of antigen fragment/MHC. Once bound it can “activate” Like Bcells it will copy itself Memory Tcells Helper Tcells Regulatory Tcells Releases chemical messengers call Cytokines Cellular Immunity - Cytokines Cause multiplication of Helper Tcells Cause activation of Cytotoxic Tcells Cytokines also help to activate Bcells in the humoral immune response Bcells are still not fully activated upon binding to antigen Bcell antibody receptors are so varied they could bind to your healthy cells and cause their destruction Once bound to an antigen it waits for Helper Tcell to “inspect” it. If pathogenic T H will release cytokines to fully activate it Cellular Immunity – Cytotoxic Tcells Reside in blood and lymph fluids Locate cells with antigen fragments on their MHC If receptors match they will bind to the cell Release enzymes that puncture the cell membrane of damaged cell, killing the cell. Releases from cell and continues to hunt for more cells with that antigen/MCH combination Cellular Immunity – Regulatory Tcells Release inhibitory Cytokines Stops immune response once the threat has been managed Without = autoimmune diseases Helpful Videos https://www.youtube.com/watch?v=2DFN4IBZ3rI https://www.youtube.com/watch?v=rd2cf5hValM