IMMUNITY

Three Lines of Defense (1) Barriers at body surfaces ◦ Intact skin and mucous membranes ◦ Lysozyme ◦ Normal bacterial flora ◦ Flushing effect and low pH of urine

Barriers at Body Surface

Three Lines of Defense (2) Nonspecific Responses ◦ Lymph nodes trap and kill pathogens ◦ Natural killer cells attack a range of targets ◦ Inflammation

Inflammation Nonspecific response to foreign invasion, tissue damage, or both Purpose of inflammation ◦ Destroys invaders ◦ removes debris ◦ promotes healing Characterized by ◦ redness ◦ swelling ◦ warmth ◦ pain

Inflammation Mast cells release histamine Capillaries dilate and leak Complement proteins attack bacteria White cells attack invaders and clean up

Chemical Weapons in Immunity

Three Lines of Defense (3) Features of Immune Responses ◦ Self / non-self recognition ◦ Self ◦ proteins and other molecules that belong to the body ◦ Non-self ◦ Molecules not recognized as belonging to the body ◦ Antigens (foreign substances) ◦ Specificity ◦ Diversity ◦ Memory

Autoimmune Disorders Immune system makes antibodies against self antigens Grave’s disease ◦ hyperthyroidism Myasthenia gravis ◦ body produces antibodies that prevent muscles from receiving message from nerve cell Type I Diabetes Celiacs ◦ Villi becomes damaged due to gluten

neutrophil mast cell T lymphocyte B lymphocyte basophileosinophil NK cell Cells Involved in Immune Responses

dendritic cell macrophage

Memory and Effector Cells When a B or T cell is stimulated to divide, it produces more than one cell type ◦ Memory cells  set aside for future use ◦ Effector cells  engage and destroy the current threat

Steps in Immune Response Recognition of an antigen Rounds of cell division that form huge populations of lymphocytes Specialization of lymphocytes into effector and memory cells that have receptors for one kind of antigen

Key Components of Immune Response MHC markers ◦ Major histocompatibility complex ◦ Antigen-presenting cells T cells B cells Natural killer cells

antigen fragments MHC molecule antigen-MHC complex Formation of Antigen-MHC Complex

Immune Responses

5 Classes of Immunoglobulins IgG ◦ found in blood plasma ◦ all body fluids ◦ smallest but most common ◦ primary and secondary response IgA ◦ found in your nose, digestive tract, ears, eyes ◦ protects mucous membranes  saliva, mucus tears, breast milk

5 Classes of Immunoglobulins IgM ◦ found in the blood and lymph ◦ used to fight a new infection ◦ causes clumping of antigens, transfusion reactions IgE ◦ found in your lungs, skin ◦ responsible for allergic reactions IgD ◦ found in your stomach, chest ◦ very small amount

5 Classes of Immunoglobulins IgG, IgD, and IgEIgAIgM

Antigen-Receptor Diversity Gene sequences get shuffled, extensively and randomly, before they are expressed Each B cell or T cell bears only one type of antigen receptor

Antibody-Mediated Response Cell-mediated response

Antibody-Mediated Response Carried out by B cells Targets are intracellular pathogens and toxins Antibodies bind to target and mark it for destruction by phagocytes and complement

Antibody-Mediated Response  B cell becomes antigen- presenting cell  Helper T cell binds to antigen-MHC complex  Interleukins stimulate B cell division and differentiation  Effector cells secrete antibodies helper T cell antigen naïve B cell MHC molecule antigen- MHC complex antigen- presenting B cell effector B cell memory B cell interleukins antibody

Antibody-Mediated Response Antibody-mediated response

Clonal Selection Clonal selection of a B cell

Clonal Selection  Only the B cell with antigen-receptor that matches antigen is stimulated to divide  Mitosis yields many cells with that receptor antigen clonal population of B cells

Immunological Memory Memory cells specific for an antigen are quickly activated to divide upon subsequent exposure to that antigen Primary Immune Response: Secondary Immune Response: effector cellsmemory cells effector cellsmemory cells naïve T or B cell

Immune Memory

Primary response ◦ Initial reaction ◦ 1 st exposure Secondary response ◦ If same pathogen enters the body a 2 nd time  memory B-cells launch a rapid and intense response  faster than primary

Primary and Secondary Immune Response

Cell-Mediated Response Cell-mediated response

Cell Mediated Response Carried out by T-cells Stimulated by Antigen-MHC complex most effective against ◦ Virus-infected cells ◦ Cancer cells ◦ Foreign tissue cells  transplant rejection ◦ Fungi ◦ Protozoan parasites

4 subgroups of T-cells ◦ Killer T-cells  directly destroy cells with antigen ◦ Helper T-cells  promote immune response  activates B-cells ◦ Supressor T-cells  inhibit immune response and B-cell production ◦ Memory T-Cells  remember specific antigens  stimulate a faster and more intense response

cytotoxic T-cell tumor cell Cytotoxic T Cell

Organ Rejection Cytotoxic T cells can contribute to rejection They recognize a portion of the donor cell’s MHC complex as self, view a portion as foreign Treat the combination as an antigen-MHC complex and attack donor cells

Hepatitis B Hepatitis B booster 1 Hepatitis B booster 2 Hepatitis B assessment DTP (Diphtheria; Tetanus; and Pertussin, or whooping cough) DTP booster 1 DTP booster 2 DT HiB (Hemophilus influenzae) HiB booster Polio Polio booster 1 Polio booster 2 MMR (Measles, Mumps, Rubella) MMR booster MMR assessment Pneumococcal Pneumococcal booster 1 Pneumococcal booster 2 Varicella Varicella assessment Hepatitis A (in selected areas Birth–2 months 1–4 months 6–18 months 11–12 years 2, 4, and 6 months 15–18 months 4–6 years 11–16 years 2, 4, and 6 months 12–15 months 2 and 4 months 6–18 months 4–6 years 12–15 months 4–6 years 11–12 years 2, 4, and 6 months months 1-18 years 12–18 months 11–12 years 1-12 years RECOMMENDED VACCINES RECOMMENDED AGES Vaccines

Allergies Immune reaction to a harmless substance Genetic predisposition IgE responds to antigen by binding to mast cells and basophils These cells secrete the substances that cause symptoms

Anaphylactic Shock A life-threatening allergic reaction Caused by the release of histamine by many mast cells and basophils Airways constrict and blood pressure drops as capillary permeability soars

AIDS Combination of disorders that follows infection with HIV Includes ◦ Yeast (Candida) infections ◦ Pneumocystis pneumonia ◦ Karposi’s sarcoma

HIV Life Cycle HIV replication cycle

T Cell Decline Release of new viral particles kills the host T cell The body is constantly making new T cells, but cannot outpace the rate of destruction As infection proceeds, T cell numbers inevitably decline

Effect of T Cell Decline CD4 helper T cells play a vital role in immune function They are required for both cell-mediated and antibody-mediated immunity Infected individual becomes vulnerable to other infections, which eventually result in death

Transmission of HIV HIV does not live long outside human body Most often spread by exchange of bodily fluids with an infected person Can travel from mothers to offspring during pregnancy, birth, or breast-feeding Not known to be transmitted by food, air, water, casual contact, or insect bites

Treatment No cure Once HIV genes are incorporated, no way to get them out AZT and other drugs slow the course of the disease and increase life span Researchers continue to develop drugs and to work toward an AIDS vaccine

Impacts, Issues Video The Face of AIDS