NURS 230 TRW Lec5b Immune System PDF

Topic 5b: Adaptive Immune Defenses/ Blood Types https://www.pinterest.ca/dr9018/immunology-humor/ CHAPTER 21 AND PART OF CHAPTER 17 IN TEXT Objectives for this Section Adaptive Immunity and Blood Groups - Chapter 21 and sections of Chapter 17 1. What is an antigen? P 791 2. What are antige...

Topic 5b: Adaptive Immune Defenses/ Blood Types https://www.pinterest.ca/dr9018/immunology-humor/ CHAPTER 21 AND PART OF CHAPTER 17 IN TEXT Objectives for this Section Adaptive Immunity and Blood Groups - Chapter 21 and sections of Chapter 17 1. What is an antigen? P 791 2. What are antigen-presenting cells? P 794-795 3. Explain the clonal selection of B cells and humoral response P 796-797 4. Differentiate between active and passive humoral immunity P 797-798 5. Describe the structure of an antibody and their targets and functions P 798-801 6. Explain the process of T-cell activation (including the role of MHC proteins). P 804-805 Objectives for this Section Adaptive Immunity and Blood Groups - Chapter 21 and sections of Chapter 17 7. Explain how Helper T cells function. P 806 8. Explain how Cytotoxic T cells and Treg cells function. P 807-808 9. Understand the examples of immune disorders covered in class: ◦ AIDS P 811 ◦ Immediate hypersensitivities (allergies) P 812-813 ◦ Systemic Lupus (covered as one of the presentations) 10. Explain the ABO blood groups P 663-665 11. What are the Rh blood groups? P 664 Introduction to Adaptive Immunity: Third Line of Defense Differs from Innate system: ◦ Specific to particular pathogens ◦ Systemic: not restricted to infection site ◦ Memory: recognizes pathogens after first exposure ◦ Amplifies inflammatory response ◦ Activates complement However, takes time, must be “primed” after initial exposure ◦ Vaccines can be the primer ◦ Previous exposure to foreign material  Much of Current Medical Care/ Research Targets Adaptive Immune Response Edward Jenner in 1796 ◦ Cowpox and smallpox are related viral infections ◦ Milkmaids, exposed to cowpox, were ‘immune’ to smallpox ◦ Inoculation with cowpox material created vaccination for smallpox Vaccine: ◦ Usually weakened or dead forms of microbe (antigen) ◦ Stimulates weaker immune response, before exposure with disease causing antigen ◦ Target adaptive immune system Nabel GJ. N Engl J Med 2013; 368:551-560. DOI: 10.1056/NEJMra1204186 Introduction to Adaptive Immunity Two main branches of adaptive system: 1. Humoral immunity ◦ Antibody-mediated immunity ◦ Antibodies, produced by lymphocytes, circulate freely in body fluids ◦ Bind temporarily to target cell ◦ Temporarily inactivate ◦ Mark for destruction by phagocytes or complement ◦ Humoral immunity has extracellular https://globalbiodefense.com/2015/02/04/scientists-call-antibody-bar-code-system/ targets Introduction to Adaptive Immunity 2. Cellular (Cell-Mediated) Immunity ◦ Lymphocytes act against target cell ◦ Directly—by killing infected cells ◦ Indirectly—by releasing chemicals that enhance inflammatory response; or activating other lymphocytes or macrophages ◦ Cellular immunity has cellular targets  Subcategories of the Adaptive immune response HUMORAL IMMUNITY CELL-MEDIATED IMMUNITY Carried out by Carried out by cells antibodies Directed against Directed against intracellular antigens extracellular antigens Requires antigen Antibodies recognize presenting cells antigens Uses B-lymphocytes Uses T-Lymphocytes https://d2jmvrsizmvf4x.cloudfront.net/ WhlY5N7HQ8KDXRWWD12F_Immune+response.jpg  Distinguishing properties of the adaptive immune response Property Significance for Immunity Specificity The ability to recognize multiple different antigens, but only one at a time Memory Stronger/enhanced response upon repeat exposure Clonal expansion of lymphocytes Rapid proliferation to tackle microbial expansion, using B and T lymphocytes (not involved in innate immunity) Specialization Optimized response to different antigens Systemic Not restricted to the infection site Speed Adaptive immune response is slower than the innate immune response Antigens Antigen: antibody generation, or any macromolecular that activates B or T lymphocytes Substances that can mobilize adaptive defenses and provoke an immune response Targets of all adaptive immune responses Most are large, complex molecules not normally found in body ◦ Recognized as intruders - “Nonself” Can be complete or incomplete Complete Antigens 2 Important properties Immunogenicity: ability to stimulate proliferation of specific lymphocytes Reactivity: ability to react with activated lymphocytes and antibodies released by immunogenic reactions Examples: foreign proteins, polysaccharides, lipids, and nucleic acids Figure 21.7 Incomplete Antigens (Haptens) Very small molecules, not immunogenic by themselves ◦ Eg: small peptides, nucleotides, some hormones May become immunogenic if hapten attaches to body’s own proteins http://www.creative-diagnostics.com/blog/index.php/immunogen-antigen-hapten-epitope-and-adjuvant/ ◦ Combination of protein and hapten is then seen as foreign ◦ May cause harmful immune response ◦ Eg. Poison ivy, animal dander, detergents, some cosmetics, etc. http://www.md-health.com/Cat-Allergies.html Antigenic Determinants Parts of antigen that antibodies or lymphocyte receptors bind to Most naturally occurring antigens have numerous antigenic determinants that: ◦ Mobilize several different lymphocyte populations ◦ Form different kinds of antibodies against them Large, chemically simple Figure 21.7 molecules (such as plastics) have little or no immunogenicity Self-Antigens: MHC Proteins Self-antigens: all cells covered with surface proteins that are not antigenic to self ◦ May be antigenic to others in transfusions or grafts One set of important self-proteins are group of glycoproteins called MHC proteins ◦ Coded by genes of major histocompatibility complex (MHC) ◦ Millions of gene combinations makes MHC unique to each individual ◦ Contain groove that can hold piece of http://bio1152.nicerweb.com/Locked/media/ch43/mhc.html self-antigen or foreign antigen for presentation Lymphocytes and Antigen- Presenting Cells Adaptive immune system involves three crucial types of cells: ◦ Two types of lymphocytes ◦ B lymphocytes (B cells)—humoral immunity ◦ T lymphocytes (T cells)—cellular immunity ◦ Antigen-presenting cells (APCs) ◦ Do not respond to specific antigens ◦ Play essential auxiliary roles in immunity ◦ T cells cannot recognize antigens without APCs http://intranet.tdmu.edu.ua/data/kafedra/internal/patologanatom/classes_stud/en/med/lik/ptn/Pathomorphology/ 3/04_Pathomorph_immune_syst.htm B and T Lymphocyte Comparison Table 21.4 Cell types of the Adaptive immune system Lymphocytes: Nucleated white blood cells B Cells: mature in bone marrow T Cells: mature in thymus Figure 21.8 Antigen receptor diversity ◦ Genes, not antigens, determine which foreign substances the immune system will recognize (determined before exposure to antigens) ◦ Variety of immune cell receptors are result of acquired genetic knowledge of microbes ◦ Different genes code for up to a billion different types of lymphocyte antigen receptors ◦ Huge variety of receptors: gene segments are shuffled around, resulting in many combinations ◦ Only certain lymphocytes activated, depending on which antigens they contact Antigen-Presenting Cells (APCs) Engulf antigens Present fragments of antigens to naïve T cells for recognition Major types ◦ Dendritic cells ◦ Macrophages ◦ B cells http://immense-immunology-insight.blogspot.ca/2013/10/question-antigen-presenting-cells.html Antigen-Presenting Cells (APCs) Dendritic cells: ◦ Found at body frontiers (ie - epidermis) ◦ Phagocytize pathogens that enter tissues, then enter lymphatic system to present antigens to T cells in lymph node ◦ Most effective antigen presenter ◦ Key link between innate and adaptive immunity Figure 21.10 Antigen-Presenting Cells (APCs) Macrophages: ◦ Widely distributed in connective tissues and lymphoid organs ◦ Present antigens to T cells, which not only activates T cell, but also further activates macrophage http://medical-dictionary.thefreedictionary.com/macrophage  Antigen-Presenting Cells (APCs) B lymphocytes: ◦ Do not activate naive T cells ◦ Present antigens to helper T cell to assist their own activation https://immense-immunology-insight.tumblr.com/page/10 Humoral Immune Response When B cell encounters target antigen, it provokes humoral immune response ◦ Antibodies specific for that particular antigen are then produced Immunocompetent, but naïve, B lymphocytes are activated when antigens bind to surface receptors, cross-linking them Triggers receptor-mediated endocytosis of cross-linked antigen-receptor complexes (clonal selection), leading to proliferation (clonal expansion) and differentiation of B cell into effector cells  Activation and Differentiation of B Cells Most activated clone cells become plasma cells (the antibody secreting effector cells) ◦ Secrete the same, specific antibodies for 4 to 5 days, then die ◦ Antibodies circulate in blood or lymph Figure 21. 11 Activation and Differentiation of B Cells Remaining clone cells become memory cells ◦ Provide immunological memory ◦ Can mount an immediate response in future Figure 21.11 Immunological Memory Primary immune response: ◦ cell proliferation and differentiation upon exposure to antigen for the first time ◦ Lag period: 3 to 6 days ◦ Peak levels of plasma antibody are reached in 10 days ◦ Antibody levels then decline Figure 21.12 Immunological Memory Secondary immune response ◦ Re-exposure to same antigen gives faster, more prolonged, more effective response ◦ Sensitized memory cells provide immunological memory ◦ Respond within hours, not days ◦ Peak at higher levels ◦ Bind with greater affinity ◦ Antibody level can remain high for weeks to months Figure 21.12 Active and Passive Humoral Immunity Active humoral immunity occurs when B cells encounter antigens and produce specific antibodies against them Two types of active humoral immunity: 1. Naturally acquired: formed in response to actual bacterial or viral infection 2. Artificially acquired: formed in response to vaccine of dead or attenuated pathogens ◦ Provide antigenic determinants that are immunogenic and reactive ◦ Spare us symptoms of primary response Active and Passive Humoral Immunity Passive humoral immunity occurs when ready-made antibodies are introduced into body ◦ B cells are not challenged by antigens ◦ Immunological memory does not occur ◦ Protection ends when antibodies degrade 2 types: ◦ 1. Naturally acquired (from mother) ◦ 2. Artificially acquired (injections) ◦ Antivenoms, antitoxins Figure 21.13 Antibodies Antibodies—also called Immunoglobulins (Igs)— are proteins secreted by plasma cells ◦ Make up gamma globulin portion of blood Capable of binding specifically with antigen detected by B cells Figure 21.14 Basic antibody structure Variable Antibody monomer consists of region four looping polypeptide chains linked by disulfide bonds Four chains consist of: ◦ Two identical heavy (H) chains with hinge region at “middles” ◦ Two identical light (L) chains ◦ Variable (V) regions form two identical antigen-binding sites ◦ Allows for binding to different antigenic determinants Figure 21.14 Basic antibody structure Stems makeup constant (C) regions ◦ Area that determines antibody class ◦ Considered effector region of antibody ◦ Serves common functions in all antibodies by dictating: 1. Type of cells and/or chemicals that antibody can bind 2. How antibody class functions to eliminate antigens ◦ Eg. fix complement, circulate in blood, etc. Figure 21.14 Five Antibody Classes (MADGE) IgM ◦ Pentamer (larger than others); first antibody released during primary response ◦ Potent agglutinating agent ◦ Readily fixes and activates complement IgA (secretory IgA) ◦ Usually dimer (sometimes monomer); found in mucus and other secretions ◦ Helps prevent entry of pathogens Table 21.5 Five Antibody Classes IgD ◦ Monomer attached to surface of B cells ◦ Functions as B cell receptor IgG ◦ Monomer; 75–85% of antibodies in plasma, circulating antibody ◦ From secondary and late primary responses ◦ Crosses placental barrier IgE ◦ Monomer active in some allergies and parasitic infections ◦ Causes mast cells and basophils to release histamine Table 21.5 Antibodies Plasma B cells can switch from making one class of antibodies to another ◦ Retain specificity for same antigen IgM is released during primary response, but plasma cell can switch to IgG for secondary response ◦ Almost all secondary responses are IgG ◦ Switching from IgM to IgA or IgE can also occur  Antibody targets and functions ◦ Antibodies do not destroy antigens; they inactivate and tag them ◦ Form antigen-antibody (immune) complexes ◦ Defensive mechanisms used by antibodies ◦ Neutralization ◦ Agglutination ◦ Precipitation ◦ Complement fixation Figure 21.15 Antibody targets and functions Neutralization ◦ Simplest, but one of most important defensive mechanism ◦ Antibodies block specific sites on viruses or bacterial exotoxins ◦ Prevent antigens from binding to receptors on tissue cells ◦ Antigen-antibody complexes undergo Figure 21.15 phagocytosis Antibody targets and functions Agglutination ◦ Antibodies can bind same determinant on two different antigens at the same time ◦ Each antibody has two arms, each containing a variable region capable of binding to one antigen ◦ Allows for antigen-antibody complexes to become cross-linked into large lattice-like clumps Figure 21.15 ◦ Process referred to as agglutination ◦ Example: clumping of mismatched blood cells Antibody targets and functions Precipitation ◦ Soluble molecules (instead of cells) are cross-linked into complexes ◦ Complexes precipitate out of solution ◦ Precipitated complexes are easier for phagocytes to engulf Figure 21.15 Antibody targets and functions Complement fixation and activation: ◦ Main antibody defense against cellular antigens (bacteria, mismatched RBCs) ◦ When several antibodies are bound close together on same antigen, complement-binding sites on their stem regions are aligned ◦ Alignment triggers complement fixation, cell lysis and other complement functions Figure 21.15 Summary of antibody actions Antigen-antibody complexes do not destroy antigens ◦ Prepare them for destruction by innate defenses Antibodies go after extracellular pathogens; not solid tissue unless lesion is present https://i.pinimg.com/736x/70/c9/47/70c9479793ee8dd9c448780f4c042450--bacteria-cartoon-science-comics.jpg Uses of the immune system in a laboratory setting (for interest) Zebrafish, phagocytosis by leukocytes Antibody staining for a protein of interest Whitesell et al. 2014 PLOS One 9(3): e90590 https://www.cusabio.com/manage/upload/image/ 20180723/20180723113150_45063.png Ellett et al. 2011 Blood 17:e49-e56 Cellular Immune Response T cells provide defense against intracellular antigens ◦ Eg. cells infected with viruses or bacteria, cancerous or abnormal cells, foreign (transplanted) cells Antigen needs to engulfed by an antigen presenting cell (APC) ◦ APC can be a professional APC: Macrophage or dendritic cell ◦ Non-professional APCs are any infected cells Some T cells directly kill cells; others release chemicals that regulate immune response T cells are more complex than B cells both in classification and function  Cellular Immune Response: T Cells Two populations of T cells ◦ based on which cell differentiation (CD) glycoprotein receptors are displayed on their surface ◦ T cells mature in the thymus 1. CD4 cells usually become helper T cells (TH) 2. CD8 cells become cytotoxic T cells (TC) Helper, cytotoxic, and regulatory T cells are activated T cells Naive T cells are simply termed CD4 or CD8 Figure 21.16 cells Cellular Immune Response: T Cells 1. CD4 cells usually become helper T cells (TH) ◦ Interact with Class II MHC proteins displaying antigens on APCs ◦ Can activate B cells, other T cells, and macrophages; direct adaptive immune response ◦ Some become regulatory T cells, which moderate immune response ◦ Can also become memory T cells Figure 21.16 Cellular Immune Response: T Cells 2. CD8 cells become cytotoxic T cells (TC) ◦ Capable of destroying cells harboring foreign antigens ◦ Also become memory T cells ◦ Interact with Class I MHC proteins displaying antigens on APCs Figure 21.16 MHC Proteins and Antigen Presentation T cells respond only to processed fragments of antigens displayed on surfaces of APCs by major histocompatibility complex (MHC) proteins Antigen presentation is vital for activation of naive T cells and normal functioning of effector T cells Two classes of MHC proteins: Class I MHC proteins, Class II MHC proteins (won’t discuss the details) Activation and Differentiation of T cells T cells can be activated only when antigen is presented to them Activation is a two-step process 1. Antigen binding 2. Co-stimulation Both occur on surface of same APC Both are required for clonal selection of T cell Example will be CD4 activation, but CD8 is similar Activation and Differentiation of T cells T cells only activated by APCs Antigen binding ◦ T cell antigen receptors (TCRs) bind to antigen-MHC complex on APC surface ◦ TCR must perform double recognition by recognizing both MHC and foreign antigen it displays ◦ Activation begins Figure 21.17 Activation and Differentiation of T cells Co-stimulation ◦ Binding to one or more co- stimulatory signals on surface of APC ◦ Requires double recognition to activated T cells ◦ This safeguards against unwanted T cell activation Figure 21.17 Activation and Differentiation of T cells Proliferation and differentiation: ◦ T cells that are activated enlarge and proliferate (clonal expansion) ◦ Differentiate and perform functions according to their T cell class ◦ Response peaks within a week, apoptosis occurs between days 7 and 30 ◦ Memory T cells remain and mediate secondary responses Figure 21.17 Cytokines ◦ Chemical messengers of immune system ◦ Mediate cell development, differentiation, and responses in immune system ◦ Examples: interferons and interleukins ◦ Other cytokines amplify and regulate innate and adaptive responses ◦ Example: gamma interferon—enhances killing power of macrophages Summary of Cytokines Questions Explain how a vaccine would target the humoral immune response and why this is helpful fighting disease. What types of cells can CD4 cells become? CD8? How are antigens presented to developing T cells? What is double recognition? Why is it important in T-cell development? Roles of Helper T (TH) cells Play central role in adaptive immune response Activate both humoral and cellular arms Once primed by APC presentation of antigen, helper T cells: ◦ Help activate B cells and other T cells ◦ Induce T and B cell proliferation ◦ Secrete cytokines that recruit other immune cells Without TH, there is no immune response Roles of Helper T (TH) cells: Activation of B cells Helper T cells interact with B cells displaying antigen fragments bound to MHC receptors Stimulate B cells (via cytokines) to divide more rapidly and begin antibody formation B cells may be activated without TH cells by binding to T cell– independent antigens ◦ Response is weak and short-lived © 2016 PEARSON EDUCATION, INC. Figure 21.18  Roles of Helper T (TH) cells: Activation of CD8 cells CD8 cells require TH cell to become activated into cytotoxic T cells Cause dendritic cells to express co-stimulatory molecules required for CD8 cell activation Figure 21.18 Roles of Helper T (TH) cells: Amplification of innate defenses Amplify responses of innate immune system ◦ Release of cytokines Activate macrophages, leading to more potent killers Mobilize lymphocytes and macrophages and attract https://www.pinterest.ca/pin/32228953562422483/ other types of WBCs Regulatory T (Treg) cells Related to T helper cells Dampen immune response by direct contact or by secreting inhibitory cytokines Important in preventing autoimmune reactions ◦ Suppress self-reactive lymphocytes in periphery (outside lymphoid organs) ◦ Research into using them to induce tolerance to transplanted tissue  Cytotoxic T (TC) cells ◦ Directly attack and kill other cells ◦ Activated TC cells circulate in blood and lymph and lymphoid organs in search of body cells displaying antigen they recognize ◦ Activated TC cells target: ◦ Virus-infected cells ◦ Cells with intracellular bacteria or parasites ◦ Cancer cells ◦ Foreign cells (transfusions or transplants) Figure 21.19 Cytotoxic T (TC) cells Cytotoxic T cells deliver lethal hit using two mechanisms: 1. TC cell releases perforins and granzymes by exocytosis ◦ Perforins create pores through which granzymes enter target cell ◦ Granzymes stimulate apoptosis 2. TC cell also binds specific membrane receptor on target cell and stimulates apoptosis (not shown) Figure 21.19 Cytotoxic T (TC) cells Differences between NK cells and Tc cells: ◦ Natural killer cells recognize other signs of abnormality that cytotoxic T cells do not look for, such as: ◦ Cells that lack class I MHC proteins entirely ◦ Antibodies coating target cell ◦ Different surface markers seen on stressed cells ◦ NK cells use same key mechanisms as TC cells for killing their target cells ◦ Both perform immune surveillance Summary Focus Figure See Focus Figure 21.1 on pages 808 and 809 for a great review of the immune system (innate and adaptive) Immune Problems *Note: an example of an autoimmune disease (systemic lupus) will be given by classmates We will look at one example of an Immunodeficiency and a hypersensitivity disorder Immunodeficiencies: congenital or acquired conditions that impair function or production of immune cells or molecules We will look at one example: Acquired immune deficiency syndrome (AIDS) Immunodeficiencies: AIDS Human immunodeficiency virus (HIV) cripples immune system by interfering with activity of helper T cells Characterized by severe weight loss, night sweats, and swollen lymph nodes Opportunistic infections occur, including Pneumocystis pneumonia and Kaposi’s sarcoma HIV is transmitted via body fluids: blood, semen, and vaginal secretions HIV can enter the body via: ◦ Blood transfusions; blood-contaminated needles; sexual intercourse and oral sex; mother to fetus HIV multiplies in lymph nodes throughout asymptomatic period, ∼10 years if untreated  Immunodeficiencies: AIDS HIV-coated glycoprotein complex attaches to CD4 receptors HIV enters cell and uses reverse transcriptase to produce DNA from its viral RNA ◦ HIV reverse transcriptase is prone to frequent errors, leading to high mutation rate and resistance to drugs The DNA copy (a provirus) directs host cell to make viral RNA and proteins, enabling virus to reproduce No cure for AIDS found; four major classes of antivirals in combination help but can fail as virus becomes resistant http://www.interactive-biology.com/3574/aids-and-mechanism-of-hiv-infection/ Hypersensitivities: Allergies http:// www.organizeit.co.u Hypersensitivities: immune k/natural-remedies- hayfever-allergy- responses to perceived (otherwise types/ harmless) threat that cause tissue damage Antibodies cause immediate and subacute hypersensitivities Allergies are known as Immediate hypersensitivity or acute (type 1) hypersensitivity, several steps: ◦ Initial contact with allergen is asymptomatic but sensitizes person ◦ Activated IgE against antigen binds to mast cells and basophils Figure 21. 20  Hypersensitivities: Allergies Figure 21. 20 ◦ Later encounter with same allergen causes flood of histamine release from IgEs ◦ Histamines causes vasodilation, leakiness of the vessels, leading to symptoms ◦ Asthma can occur if allergen is inhaled ◦ Allergic reactions can be local or systemic ◦ Systemic response: anaphylactic shock ◦ Usually seen with injected allergens ◦ Bronchioles constrict, making breathing difficult Review Questions What are the differences between helper T cells and cytotoxic T cells in terms of function? Which type of cell is important for preventing autoimmune disorders? What mechanisms do Tc cells use to destroy pathogens? How does HIV infect and affect the immune system of its host? Human blood groups (Chapter 17) ◦ RBC membranes bear different many antigens ◦ RBC antigens are referred to as agglutinogens because they promote agglutination ◦ Humans have at least 30 naturally occurring RBC antigens ◦ Presence or absence of each antigen is used to classify blood cells into different groups ◦ Not the presence of plasma antibodies https://www.healthtap.com/topics/abo-group-rh-type Human blood groups ◦ Antigens of ABO and Rh blood groups cause most vigorous transfusion reactions; therefore, they are major groups typed ◦ Some blood groups (MNS, Duffy, Kell, and Lewis) are only weak agglutinogens ◦ Not usually typed unless patient will need several transfusions https://www.pinterest.ca/pin/133067363959444860/ ABO blood groups Based on presence or absence of two agglutinogens (A and B) on surface of RBCs ◦ Type A has only A agglutinogen ◦ Type B has only B agglutinogen ◦ Type AB has both A and B agglutinogens ◦ Type O has neither A nor B agglutinogens https://usercontent1.hubstatic.com/6637132_f520.jpg ABO blood groups Blood plasma may contain preformed anti-A or anti-B antibodies (agglutinins) ◦ Act against transfused RBCs with ABO antigens not present on recipient's RBCs, therefore: ◦ Type A has anti-B antibodies ◦ Type B has anti-A antibodies ◦ Type AB has non antibodies ◦ Type O has both A and B antibodies Anti-A or anti-B form in blood at http://www.mrwiggersci.com/bio/lecture-notes/blood-type_files/image001.gif about 2 months of age, reaching adult levels by 8–10 years of age ABO blood groups Table 17.4 Rhesus (Rh) blood groups 52 named Rh agglutinogens (Rh factors) ◦ C, D, and E are most common Rh+ indicates presence of D antigen ◦ 85% Americans are Rh+ Anti-Rh antibodies are not spontaneously formed in Rh– individuals (unlike ABO) https://pleasepressreset.com/home/shit-we-forgot/rh-blood-type/  Rh blood groups First Exposure Upon first exposure, Anti-Rh antibodies form if: ◦ Rh– individual receives Rh+ blood, ◦ Or Rh– mother is carrying Rh+ fetus First exposure, takes time to mount an immune response Second exposure, hemolysis occurs https://immense-immunology-insight.tumblr.com/post/67742352535/the-rh-incompatibility-comic-is-here-think-of  Rh blood groups Second Exposure Second exposure to Rh+ blood will result in typical transfusion reaction Known as Erythroblastosis fetalis if in pregnant woman ◦ Fetal RBCs are attacked, baby may be anemic, death may even occur ◦ Mother treated with a serum that contains anti-Rh antibodies https://immense-immunology-insight.tumblr.com/post/67742352535/the-rh-incompatibility-comic-is-here-think-of Transfusion reactions Occur if mismatched blood is infused Donor’s cells are attacked by recipient’s plasma agglutinins ◦ Agglutinate and clog small vessels ◦ Rupture and release hemoglobin into bloodstream Result in: ◦ Diminished oxygen-carrying capacity ◦ Decreased blood flow beyond blocked vessel ◦ Hemoglobin in kidney tubules can lead to renal failure Symptoms: fever, chills, low blood pressure, rapid heartbeat, nausea, vomiting Transfusion reactions Treatment: preventing kidney damage with fluids and diuretics to wash out hemoglobin Type O universal donor: no A or B antigens Type AB universal recipient: no anti-A or anti- B antibodies ◦ Misleading: other agglutinogens that cause transfusion reactions must also be considered Autologous transfusions: patient predonates own blood that is stored and available if needed Excellent Summary Video: https://www.youtube.com/watch?v=tiIRU_ZpVP0 Questions How can you explain that an incompatible ABO blood group will generate a transfusion reaction the first time a transfusion is given, while Rh incompatibility creates a problem the second time a transfusion is given? What type(s) of blood can a person with Type A blood receive? What are the Rh and ABO combinations which are “universal donors”? “Universal acceptors”?