Innate Immunity
that which is present at birth, before contact with microbes or their products;
First Line of Defense
Include the Skin and Mucous Membranes of the Respiratory, Digestive, Urinary, and Reproductive Systems
Dendritic Cells in skin
phagocytize Pathogens
Perspiration secreted by Sweat Glands
- Salt inhibits growth of many Pathogens by drawing water from them
- Antimicrobial Peptides (Defensins) act against microorganisms
- Lysozyme (enzyme) destroys Cell Wall of Bacteria
Sebum secreted by Sebaceous (Oil) Glands
Helps keep skin pliable and less likely to break or tear
Lowers skin pH to a level inhibitory to many bacteria
Lacrimal Apparatus
- Produces and drains tears
- Blinking spreads tears and washes surface of the eye
- Lysozyme in tears destroys bacteria
Plasma
Mostly water containing Electrolytes, dissolved gases, nutrients, and proteins
Formed Elements (3 types)
the Cells & Cell Fragments in the Plasma.
Types- Erythrocytes, Platelets, Leukocytes.
Viral infections show increase in
Lymphocytes
Bacterial diseases often show increase in
Leukocytes and Neutrophils
Increased Eosinophils indicate Allergies or Parasitic Worm Infection
(Eosinophils attack multi-cellular parasites)
Six stages of phagocytosis
Chemotaxis
Adhesion
Ingestion
Maturation
Killing
Elimination
Chemotaxis
movement in response to a chemical stimulus
Adherence
binding of Phagocyte to microbe by attaching to complementary molecules on its surface (such as Glycoproteins)
Ingestion
envelopment of microbe by Phagocyte via its Pseudopodia, and taking it in by Endocytosis
Maturation/Killing
destruction of microbe by digestive enzymes which added to maturing Phagosome when Lysosome fuses with it forming a Phagolysosome; these also contain toxic forms of oxygen, and an acidic pH which usually kill microbe
Elimination
excretion of microbial cell remains from Phagocyte by Exocytosis
Nonphagocytic Killing
Killing by Eosinophils
Attack parasitic Helminths (worms) by adhering to their surface, and secreting Toxins that weaken or kill the Helminth
Nonphagocytic Killing
Killing by Natural Killer Lymphocytes (NK Cells)
large Lymphocytes that attach foreign cells (those that are not part of the body) & abnormal body cells (tumor cells), but do not target specific microbes, as do other Lymphocytes
Nonphagocytic Killing
Killing by Neutrophils
Usually phagocytic, but can destroy microbes without phagocytosis
Produce chemicals that kill nearby invaders
Have enzymes that form Superoxide Radicals & H2O2 (Hydrogen Peroxide) - Oxidants
Also an enzyme that converts that converts these Oxidants into H
Interferons
Protein molecules released by virus-infected host cells to nonspecifically inhibit the spread of viral infections
Type 1 (Alpha & Beta)
- Alpha Interferons produced by infected Monocytes, Macrophages, & some Lymphocytes;
- Beta Interferons - produced by infected Fibroblasts
Type 2 ( Gamma)
produced by activated T Lymphocytes & NK Cells
Gamma Interferon (Macrophage Activation Factor)
stimulates activity of Phagocytes - both Macrophages & Neutrophils, but small role in protecting cells against viral infections
complement cascade
sequence of enzymatic reactions involving Complement Proteins in which the product of one reaction is the enzyme that catalyzes the next reaction
Membrane Attack Complexes
end products of the Complement Cascade which punch holes in foreign cell's Cytoplasmic Membrane allowing water to flow in ? Cell Lysis
Gram - more affect then Gram +
Lectins
chemicals that bind to specific sugar subunits of polysaccharide molecules; in this case to Mannose in Mannan Polysaccharide on the surfaces of Bacteria, Fungi, & Viruses, but rare on Mammalian Cells
Difference in 3 path ways? (Classical, Alternative, Lectins)
- Classical starts with antigens and antibodies binding.
- Alternative (useful in early stage of infection) Complement Proteins (B, D, & Properdin) bind to Endotoxins or Glycoproteins
- Lectins by the binding Lectins to surface microbial Polysaccharides
Inflammation (4 examples)
- a Nonspecific, Localized Response to tissue damage resulting from various causes - chemicals, heat, UV, trauma, and Pathogens
- Characterized by Redness, Heat, Swelling, and Pain
Acute Inflammation (3 examples)
- Dilation and Increased permeability of the Blood Vessels
- Migration of Phagocytes
- Tissue Repair
Chronic Inflammation (3)
- Vasodilators: Serotonin
- Increase Capillary Permeabilty: Leukotrienes
- Chemotactic Factors:
Increase in Body Temp by Fever (3)
1) Muscle Contractions (shivering)
2) Increased Metabolic Activity
3) Constriction of Blood Vessels
Crisis (3)
Return temp to normal
1) Sweating,
2) Skin Blood Vessel Dilation, &
3) ? in Metabolic Rate
Type I (Immediate) Hypersensitivity
- Localized or Systemic Reactions
- Develops within seconds or minutes
- Commonly called Allergies
- The Antigens that stimulate it are called Allergens
(Mast Cells) Degranulation
release of Inflammatory Chemicals
Basophils
Sensitized Basophils Degranulate like Mast Cells when Allergens attach to IgE (Ab) on their surface
Eosinophils
Sensitized Eosinophils in the bloodstream can Degranulate when Allergen binds to IgE (Ab) molecules on their surface
Type II (Cytotoxic) Hypersensitivity
- Results when cells are destroyed by an Immune Response, often due to the combined activities of Complement and Antibodies
- A component of many Autoimmune Diseases
Type II Transfusion Reactions
destruction of blood cells following an incompatible blood transfusion
Type II Hemolytic Disease of the Newborn
destruction of fetal red blood cells when an Rh+ fetus is carried by a sensitized Rh- mother
Type III (Immune Complex-Mediated) Hypersensitivity
Caused by formation of Immune Complexes (Complexes of Antigen bound to Antibody)
Type IV (Delayed or Cell-Mediated) Hypersensitivity
Inflammation 12-24 h after contact with certain Antigens
Results from the actions of Antigen, APCs (Antigen-Presenting Cells), and T Cells
Autograft
tissue moved to a different location within the same individual
Isograft
that from a genetically identical individual
Allograft
that from different organism of the same species
Xenograft
that from an organism of a different species
If Donor and Recipient differ in MHC Class I Molecules
the Grafted T Cells attack all of the Recipient's Tissues ? destructive lesions in skin and intestines
If Donor and Recipient differ in MHC Class II Molecules
then Grafted T Cells attack the Host's APCs (Antigen-Presenting Cells) ? Immunosuppression
Secondary Lymphoid Organs & Tissues
Lymph Nodes
Spleen
Tonsils
Mucosa-Associated Lymphoid (Lymphatic) Tissue (MALT)
Primary Lymphoid Organs
Red Bone Marrow, Thymus
Hapten
molecule too small to be antigenic, but when it binds to larger carrier molecule (usually a Protein) can elicit an Adaptive Response
Exogenous Antigens
those on microbial components (cell walls, membranes, flagella, & pili), toxins, or secretions from microbes outside body cells
Endogenous Antigens
those produced by microbes inside body's cells that are incorporated into host cell's Cytoplasmic Membrane
Autoantigens (Self-Antigens)
those on normal uninfected body cells; usually ignored by the Immune System, but occasionally mistaken for Foreign Antigens and elicit an Autoimmune Response
Class I MHC
Present on all normal body cells except Red Blood Cells
Class II MHC
Present only on Antigen-Presenting Cells (APCs)
Include Macrophages, Dendritic Cells, & B Cells
Cytotoxic T Lymphocyte (Tc or CD8 Cells)
Distinguished by the CD8 cell-surface Glycoprotein (CD = Cluster of Differentiation)
Directly kills other cells: those infected with Viruses & other Intracellular Pathogens; Abnormal Cells, such as Cancer Cells
Helper T Lymphocyte
Helps regulate activity of B Cells and Cytotoxic T Cells
Includes Type 1 and Type 2 Helper T Cells
Type 1 Helper T Cells (Th1 Cells)
help in activating Cytotoxic T Cells by secreting certain Cytokines (soluble protein messengers)
Have Cytokine Receptor CCR5
Type 2 Helper T Cells (Th2 Cells)
help activate B Cells by secreting other Cytokines
Have Cytokine Receptors CCR3 & CCR4
Helper T Cells thus determine which Immune Response will be activated
Regulatory T Lymphocyte (Tr Cells)
Also known as Suppressor T Cells
Have both CD4 & CD25 cell-surface Glycoproteins
Represses Adaptive Immune Responses
Activated by contact with other immune cells, and secrete different Cytokines than Helper T Cells
IgG (Immunoglobulin G)
most prevalent
Crosses Placenta to Fetus, providing Passive Immunity to newborn
Activates Complement ? Cell Lysis
Enhances Phagocytosis (by Opsonization)
Neutralizes Toxins and prevents attachment of Pathogens to host cells
IgM
first antibody produced, pentamer. 3rd most common
IgA (Immunoglobulin A)
Monomer in Plasma & a Dimer in other body fluids
- 2nd most common
- Helps prevent attachment of Pathogens to Mucous Membranes in G.I., Respiratory, Urinary and Reproductive Tracts
- In breast milk provides Passive Immunity to baby against Enteric Pathoge
IgE (Immunoglobulin E)
Inflammatory Response
4th common
IgD
Most on B Cell Membranes; may act as BCR.
least common
Naturally Acquired Active Immunity
body's immune response to Antigens encountered in daily life; immunity resulting from having had and recovering from a disease
Artificially Acquired Active Immunity
body's immune response to Antigens introduced into body via a Vaccine (immunization to protect against a disease)
Naturally Acquired Passive Immunity
that from the transfer of Antibodies across the placenta (IgG), or in the breast milk (IgA) from mother to fetus or baby
Artificially Acquired Passive Immunity
that from the injection into the body of an Antiserum or Antitoxin (containing Antibodies) from an immune person or other animal