Chapter 24 The Immune System

Pathogenicity of microbes Pathogens are microbes that can cause disease. Toxins are small organic molecules or pieces of protein or bacterial cell wall that are released when bacteria die.

How do pathogens get in? Adhesion Factors Adhesion factors allow a pathogen to bind to certain cells. Viruses have spikes that bind to host cell surfaces. Invasive mechanisms determine the extent of a disease in the body. Localized vs. Systemic.

Epidemiology The study of the factors that influence transmission of diseases in human populations. Infectious diseases; illnesses caused by pathogens, or their products. Highly transmissible pathogens (virus, bacterial) are contagious.

Transmission of Diseases

Viral Diseases Influenza (the flu)- fever, chills, vomiting, cold symptoms. Influenza or "flu" is an infection of the respiratory tract that can affect millions of people every year. It is highly contagious

Body Defenses: Overview Physical barriers: skin & epithelial linings & cilia Immune defenses – internal Innate, non-specific, immediate response (min/hrs) Acquired – attack a specific pathogen (antigen)

Lymphatic System: Overview of Immune Defense Organs & Cells Figure 24-2 ab: Anatomy of the immune system

The Composition of Whole Blood (4-6L in an adult) The percentage ranges for white blood cells indicate the normal variation seen in a count of 100 white blood cells in a healthy individual.

White Blood Cells (leukocytes) (0.1% of formed elements) Defend the body against pathogens Two classes Granular leukocytes Neutrophils (polymorphonuclear leukocytes) Eosinophils Basophils Agranular leukocytes Monocytes Lymphocytes

Neutrophils Neutrophils Acute inflammation Highly mobile phagocytes Containing bacteria-killing enzymes Multi-lobular nucleus

More Granular Leukocytes (granulocytes) Eosinophils (acidophils) Stain with an acidic red eosin stain Attracted to foreign compounds reacted with antibodies They kill pathogens by releasing substances that kill them. 2-lobed nucleus

Basophils Stain with a deep purple or blue basic dye Migrate to damaged tissue and release their granules Release histamines. Inflammatory response; increase capillary permeability.

Agranular Leukocytes (agranulocytes) Monocytes Migrate into peripheral tissues Are precursors to macrophages. Highly mobile phagocytic cells Oval, kidney-bean shaped nucleus

Agranular Leukocytes (agranulocytes) Lymphocytes (specific immunity) Primary cell of the lymphatic system T-cells attack foreign cells directly B-cells produce antibodies that bind foreign particles NK cells; immunological surveyors. Always remain in circulation. They don’t take up residence in tissues. Large round, purple staining nucleus.

The immune response. Two types INNATE IMMUNITY: NON-SPECIFIC ACQUIRED IMMUNITY: SPECIFIC

Innate Immunity: Phagocytosis & Inflammation Phagocytosis: Just eat it. THE PHAGOCYTES macrophages, neutrophils, NK cells Engulf and digest recognized "foreign" cells – molecules

Our immune system tags the foreign particles Opsonins- are the tagging proteins that make unrecognizable particles into “food” for phagocytes.

Innate Immunity: Phagocytosis & Inflammation Figure 24-6: Phagocytosis

Inflammatory Response: hallmark fo the innate immune pathway 1. acute phase attract immune cells to the infection site; neutrophils basophils to produce histamine to flush out the area;edema swollen redness. 2. produce a physical barrier to retard spread of infection. 3. promote tissue repair post-infection; not an immune function. Histamines: from mast cells  swelling, edema, b. v . dilation Interleukins: Secreted by macrophages Stimulate liver production of acute phase proteins (opsonins) Alter the blood endothelium to ease the passage of WBCs. Bradykinin: stimulates pain & swelling to draw attention to the wound Membrane attack complex proteins (25 complement proteins). . .

Inflammatory Response: Cytokines Signal Initiation Figure 24-8: Membrane attack complex

Some complement proteins are “warning proteins” Interferon is one such warning protein. Virus-infected cells produce this protein which in turn binds to receptors of noninfected cells causing them to prepare for possible attack. interferon Virus infected cell Watch Out guys

Acquired Immunity: Lymphocytes B cell and T cells lymphopoiesis

Lymphocytes Cytotoxic T cells Attack foreign cells or bodies infected with viruses Cell-mediated immunity Regulatory T cells Helper or suppressor T cells Regulate and coordinate immune response Memory T cells Remain “on reserve”

Lymphocytes B cells Plasma cells produce antibodies Antibody-mediated immunity B cells Plasma cells produce antibodies React to specific antigens Immunoglobins Antibody mediated immunity Memory B cells

Acquired Immunity: Antigen-Specific Responses Figure 24-13: Functions of antibodies

T Lymphocytes: One more detail. . . Major histocompatability complex (MHC) These incorporate antigen gragments and present them to the T cells; they come in two flavors: MHC class I MHC class II

Non-self proteins HLA antigens (MHC proteins) Self-proteins. Antigen Being Presented To the T-cell. HLA antigens (MHC proteins) Self-proteins.

T Lymphocytes: Cell Mediated Immunity Figure 24-16: T lymphocytes and NK cells

Blood Types: Like Antibodies & antigens will agglutinate Antigens on RBCs (A, B, AB or none = O) Antibodies in plasma (anti A, anti B, anti AB) Rh antigens & antibodies

Blood typing depends on RBC antigens Presence or absence of specific surface antigens on RBC cell membranes. An antigen is a genetically determined glycoprotein. There are 3 antigens we type for: A, B, and D (Rh) Antibodies attack “foreign” surface antigens. YOUR antibodies NEVER attack your antigens.

Blood Type A person with: Type A blood Surface antigen A, anti-B antibodies Type B blood Surface antigen B, anti-A antibodies Type AB blood Surface antigens A and B, no A or B antibodies Type O blood No surface antigens, both anti-A, anti-B antibodies Rh positive has the Rh surface antigens and no Rh antibodies

Figure 20.4 Blood Typing The blood type depends on the presence of agglutinogens on RBC surfaces.

Blood Typing

INDUCED IMMUNITY

INDUCED IMMUNITY ACTIVE IMMUNITY- inject a bit of the antigen (vaccine) and let the body’s immune system make antibodies against it. IMMUNIZATION

“BOOSTER”

Active Immunity. Dependent upon the presence of memory B and T cells capable of responding to lower antigen doses.