Immunology Lesson 13 - F24 PDF

Immunology DISP Biology Innate vs. adaptive immunity? Innate immunity (all animals) Barrier defences -first line of defense Mechanical Body coverings (i.e. skin, Ciliated cells on exoskeleton) the surface of th...

Immunology DISP Biology Innate vs. adaptive immunity? Innate immunity (all animals) Barrier defences -first line of defense Mechanical Body coverings (i.e. skin, Ciliated cells on exoskeleton) the surface of th Mucous protects mucous membranes trachea Ciliated cells line mucous membranes and clear mucous Photo by Gabrielle Tompkins Chemical Lysozyme in tears, saliva, mucous Stomach acid Low pH (3-5) secretions from oil/sweat glands Innate immunity Pathogens which breech barriers are detected Receptors bind fragments of molecules found in pathogens, not animal cells Example pathogen molecules Flagellin (bacteria) Lipopolysaccharide (bacteria) dsRNA (viruses) Receptors detect molecules common to pathogen group, not specific pathogen “Toll-like receptors (vertebrates) Innate immunity Internal responses to pathogens Once detected, pathogens pathogen targeted by: 1. Phagocytosis – immune cells ingest (engulf) and break down pathogen Macrophages (“big eaters”) Neutrophils (circulate in blood) Dendritic cells (vertebrates, in skin layer) 2. Antimicrobial peptides or proteins  Innate immunity Internal responses to pathogens Inflammatory response 5. 6. Neutrophils Neutrophi 1. Mast (phagocytic ls cells cells) phagocyto release migrate out se histamine of capillaries invading bacteria 2. Macrophag es release cytokines 3. Histamine and 4. Dilation and cytokine release at increased permeability injury site leads to… of capillaries ↑ fluid to site ↑ neutrophils to site Neutrophils crawl toward chemical cues Adaptive immunity (vertebrates) AKA Acquired immunity Remember pathogen; recognize it; mount a larger immune response on second exposure Respond to specific pathogens Involves T cells and B cells (white blood cells called lymphocytes) Large diversity of T and B cell receptors  B-cell and T-cell receptors T and B cells have surface receptors that recognize and bind antigens: Any substance that triggers immune response by B or T cell (i.e. bacterial or viral proteins or 2 identical antigen polysaccharides) 1 antigen binding sites per binding site per receptor receptor B-cell T-cell ~100,000 identical receptors on each B or T- Receptor diversity by combining different subunits ~1 million different B cell antigen receptors ~10 million different T cell antigen receptors Diversity arises from only 20,000 genes Variable (1 of 40) Joining (1 of 5) Constant igen receptors form during differentiation of B and T Lymphocytes maturing in thymus become T cells Lymphocyte s maturing in bone marrow become B cells s and B cells with self-reactive antigen receptors are marked for apoptos How is adaptive immune response generated? Pathogen must contact matching lymphocyte receptor Only small number receptors will match a given antigen Lymph vessel Pathogens to lymph Capillary nodes via lymph vessels Pathogen exposed to lymphocytes until antigen is matched to receptor Lymph node packed Antigen receptor with lymphocytes (B and T cells) match triggers cell division and B cells are activated “directly” by binding antigen Binding of antigen to B cell receptor triggers clonal selection: Stimulates cell to divide to make clone of cells with matching Many B cells receptors with receptor matching the antigen Clone of cells differentiate to: Memory cells (long lived) Population of cells that could recognize, respond to same antigen in the future Effector cells (short lived) Act on antigen (pathogen) Plasma cells with B cells Immunological memory Prior exposure to an antigen alters the speed, strength and duration of the immune response Primary immune response peak – 10-17 days Secondary immune response peak – 2-7 days Reservoir of long-lived T and B memory cells (can last decades) give rise to many more effector cells if pathogen is encountered again Immunological Memory Animation: Role of B Cells Copyright © 2025 Pearson Canada, Inc. 43 - 15 Immunological memory Use information on previous 2 slides to explain the biological basis for the differences in primary and secondary immune responses to antigen A. Note that antibodies are released by effector cells Effector cells fight infections Plasma cells are effector cells produced from B cells Produce and secrete antibodies Antibodies travel in body fluids (blood and lymph) where they neutralize or destroy pathogens/toxins - humoral response ​ ​Cytotoxic T cells are effector cells produced by T cells Secrete granzymes to poke holes in infected cells (kill infected cells) tibodies from plasma cells fight infection Neutralization Neutralizati Opsonizatio Activation of on n complement Pathogen with Antibodies markproteins and pore antibody bound pathogen for phagocytosis formation is “blocked” Targets a “membrane and can aggregate attack complex” to pathogens pathogen cell membrane Effector cells from T cells are Cytotoxic T cells Cytotoxic T cells activation by activated Helper T cells How are Helper T cells activated? Helper T cells activated after binding to an antigen presenting cell Phagocytic cell like dendritic cell or macrophage displays antigen on surface Activated helper T cells divide to make more T cells​ 1) Activated helper T cells 2) Memory helper T cells 3) Cytotoxic T cells Activated helper T cells release cytokines which stimulate: B cells Cytotoxic T cells  B cells also present antigens to Helper T cells In addition to antigens binding to B cell receptors, B cells can present the antigen to a helper T cell. Cytokines released from activated helper T cells stimulate division of B cells with matching antigens.  Cytotoxic T cells – two step activation 1) Activated by cytokines (from Activated helper T cells ) 2) AND attaching to antigen presenting cell displaying matching antigen Destroy infected cells by poking holes with proteins including perforin and Granzymes Vaccines trigger primary immune response and immunological memory Preparations of antigen with dead/deactivated pathogen or genes that encode proteins. Examples: inactivated toxins virus capsule proteins genes for microbial proteins mRNA vaccines – mRNA is converted to protein by host cells If pathogen with antigen encountered there will be a strong and rapid secondary immune response "Syringe and Vaccine" by NIAID is licensed under CC BY 2.0 mmunization programs reduce disease inciden COVID-19 Vaccines Moderna US trial: 30,000 participants Placebo 185/15,000 developed COVID 19 symptoms (30 severe) Vaccine 11/15,000 developed COVID 19 symptoms (0 severe) https://www.sciencemag.org/news/2020/11/absolutely- remarkable-no-one-who-got-modernas-vaccine-trial- developed-severe-covid-19 Moderna and Pfizer vaccine: COVID 19 mRNA Lyme Disease Vaccine | Lyme Disease